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 +1  (free120#27)

To those wondering how a CFTR mutation is not detected:

CF can result from more than a thousand different mutations.[45] As of 2016, typically only the most common mutations are tested for, such as ΔF508[45] Most commercially available tests look for 32 or fewer different mutations.

Wikipedia


 +1  (free120#31)

A single-nucleotide polymorphism is a single nucleotide substitution that is present in at least 1% of the population (in this question, it is 7.5%). This fits the definition.

I'm not sure how to rule out variant of unknown significance. I guess since we known that the protein is unchanged, we can say that it is not significant (and therefore the significance is not unknown).


 +1  (free120#7)

To those wondering what alveolar proteinosis is, it is a rare lung disorder characterized by abnormal accumulation of surfactant-derived lipoproteins within the alveoli. Sometimes it can occur secondary to lung infections, although usually it is an autoimmune process.


 +0  (free120#2)

Other answer choices

B) Femoral nerve supplies none of the muscles below the knee, although the saphenous nerve, one of its branches, travels medial to the tibia (like the great saphenous vein). The femoral nerve supplies the quads, sartorius, iliacus, and pectineus muscles.

C) Obturator nerve, again, supplies none of the muscles below the knee. It innervates the obturator externus, pectineus (dual innervation), the three adductor muscles, and the gracilis muscle. Contrary to intuition, the obturator nerve does not innervate the obturator internus muscle, which is innervated by "nerve to obturator internus."

D) The sural nerve supplies only cutaneous innervation. It is a branch of both the common fibular and the tibial nerves, so maybe it will be injured in this case, but it won't cause muscular deficits.

E) The tibial nerve is the most tempting alternative option. It supplies the muscles of the calf, which effect plantar flexion and ankle inversion.


 +0  (free120#1)

Couldn't find this in FA or SketchyMicro, but it seems that

"the role of aminoglycosides in the treatment of infective endocarditis is well established. The combination of a beta-lactam with an aminoglycoside shortens the treatment of endocarditis due to... streptococci" 1996 https://www.ncbi.nlm.nih.gov/pubmed/8677414

and "Aminoglycosides are often used in combination with glycopeptides (such as vancomycin) and β-lactams for the treatment of bacterial endocarditis caused by α-haemolytic streptococci, staphylococci and enterococci." 2002 https://academic.oup.com/jac/article/49/3/437/727559





Subcomments ...

CNS amoebiasis is most notoriously caused by Naegleria fowleri, which I encourage you to memorize as the “brain-eating amoeba.” Found in fresh-water bodies of water like ponds and lakes, it has three forms: a cyst, a trophozoite (ameboid), and a biflagellate (i.e. has two flagella). Infection is via olfactory cell axons through the cribriform plate to the brain.

mullerplouis  To add to this it causes Meningoencephalitis. Look out for confusion and brain signs mixed with signs of meningitis. Only a handful of organisms that cause both. +2  
osler_weber_rendu  Am I the only one who thought portal of entry cant be through a nerve and just ignored all the nerves? +10  
luciana  @osler_weber_rendu I thought the same... I knew it was through cribriform plate, but not that was actually through the nerve +3  
paperbackwriter  @osler_weber_rendu yeah same here, otherwise would have been a much simpler question +  
melchior  In line with the thinking above, SketchyMicro teaches it as if it just passes through the cribriform plate, ignoring the nerves. Wikipedia says that it actually enters the nerves, then passes through the plate. +1  


Subacute combined degeneration never produces exagerated reflexes. It's one of the causes of babinski + with absent ankle reflex.

melchior  From googling it, it seems that B12 deficiency can produce either hyperreflexia or hyporeflexia. This makes sense, because it causes both UMN lesions (causing hyperreflexia), but it also affects the afferent pathways. https://www.hindawi.com/journals/crinm/2013/159649/ +1  


Schistosomiasis is a parasitic worm particularly endemic in Africa (Egypt, in particular, comes up the most on questions) that is most associated with chronic cystitis. Calcifications of the bladder wall are essentially pathognomonic. Chronic infection is associated with an increased risk of squamous cell carcinoma of the bladder (as opposed to the usual urothelial/transitional cell).

takayasuarteritis  Why does his cell differential show no eosinophilia? Schistosoma is a worm..? +  
takayasuarteritis  It also says in FA that SCC of bladder is associated with painless hematuria. My dude in the question stem is having "pain with urination that has increased in severity during the past month." +  
melchior  @Takayasuarteritis, technically he does have eosinophilia. Reference range is 1 - 3%. His is 5%. Also, although SCC of bladder presents with painless hematuria, schistosomiasis itself can have hematuria, and that hematuria can be painful. +  


DI is an important complication of some skull base fractures and can be treated with DDAVP. You probably remember that this works via the activation of aquaporin channels, but these are moved from intracellular vesicles to the apical membrane surface as a result of a DDAVP-mediated increase adenylate cyclase via a stimulatory G protein that increases intracellular cAMP.

aneurysmclip  Page 332 FA 2019; cAMP signaling pathway, thus increase adenylyl cyclase was best option imo +  
melchior  Page 337 FA 2020; This is working via V2 receptor, which uses the Gs pathway to generate cAMP. Reminder: V1 works via Gq. V1 is present on the blood vessel smooth muscle +3  


(Unstable) angina. Most immediate treatment is nitro.

melchior  Nitrates, such as nitroglycerin, increase nitric oxide, which then increases cGMP (not cAMP) +  


The patient’s chronic inflammatory pneumonitis is killing off his lung parenchyma (composed primarily of type I pneumocytes). Type II pneumocytes, in addition to making surfactant, can replicate in order to replace type I pneumocytes, so they will be increased. Chronic interstitial inflammation results in fibrosis, hence an increase in fibroblasts.

len49  UW ID 666 has a great explanation. +1  
melchior  From the UW ID 666 explanation, although type II pneumocytes normally differentiate into type I pneumocytes after proliferation, they do not differentiate in idiopathic pulmonary fibrosis due to altered cell signals and altered basement membrane, which is why type II pneumocytes are increased. +1  


Functional parathyroid adenomas can cause elevated parathyroid hormone (PTH), which results in hypercalcemia and hypophosphatemia. Hypercalcemia is characterized by the rhyming symptoms: stones (renal, biliary), bones (including bone pain to osteitis fibrosa cystica), groans (abdominal pain, n/v), thrones (polyuria, constipation), and psychiatric overtones (from depression to coma).

drmohandes  Great explanation, thanks. Does anyone know why this patient is anemic though? Is there some link between hyperparathyroidism and anemia I am missing? +  
drmohandes  *Patient erythryocytes = 3million/mm3 (normal 3.5 - 5.5) +  
melchior  From googling, it looks like it just happens. One author says that high concentrations of parathyroid hormone downregulate erythropoietin receptors. Regardless, it corrects after parathyroidectomy, showing that parathyroid hormone likely causes it, somehow. https://www.ncbi.nlm.nih.gov/pubmed/10790758 https://academic.oup.com/jcem/article/97/5/1420/2536309 +  


submitted by trump2020(4),

How do we know the inferior aspect of the tube doesnt rupture, releasing fluid down in between the layers of the broad ligament?

melchior  What is special about the Pouch of Douglas is that it is the lowest point of the peritoneal cavity, so even if blood gets in between the layers of the broad ligament (which I agree with you, it looks like it should), I bet it somehow makes its way down to the Pouch of Douglas due to gravity. +1  


submitted by hungrybox(585),

Other answers:

sebaceous gland → acne, Cutibacterium acnes (formerly Propionibacterium acnes)

apocrine gland (aka sweat gland) → The substance secreted is thicker than eccrine sweat and provides nutrients for bacteria on the skin: the bacteria's decomposition of sweat is what creates the acrid odor.

eccrine gland → used to secrete stuff inside the body (ie salivary glands, pancreatic glands)

dermis → middle layer of skin.

melchior  To tweak the above a little, eccrine glands are more commonly known as "sweat glands," although sweat glands that are apocrine do exist in the armpits and perineal area, though they do not contribute to cooling. +  


Malonyl-CoA inhibits the rate-limiting step in the beta-oxidation of fatty acid. Logically, resting muscle requires less energy (and thus less need for fatty acid breakdown) than active muscle.

zpatel  it inhibits Carnitine acyltransferase-1 in beta-oxidation. +3  
melchior  FA 2020 pg 89 +  


CD80 is also known as B7. Question is asking if you know that CD28 (T-cells) interacts with B7 (APC) as a co-stimulatory signal to activate the T-cell.

Looks like the picture is demonstrating contact dermatitis (due to her recent use of new hair dye) which is a type IV HSR

I usually remember that B-7 is on the B-cell (an APC)

melchior  Reminder: CTLA-4 on T-cells also binds to B-7, and the effect is opposite that of CD28 (inhibits T cell activation) FA 2020 pg 222 +  


Narcotic use for acutely painful conditions is both reasonable and important. Short-term use (immediately post-surgical) does not lead to long-term dependence (or so people have thought…). And yes, drugs addicts should also receive narcotics to control pain.

drdoom  prefer “patients with hx of substance abuse” over more conveniently typed but less redemptive “drug addict” +8  
sugaplum  I don't see why switching her to oral pain meds when she is ready would be incorrect. Clearly she is worried about being on the pain meds, I feel making a proclamation that she has a low risk of addiction would be profiling just because she doesn't have a history. The opioid epidemic also affects people who didn't have a previous history of drug abuse. Just a thought, not trying to push any buttons. Maybe I am thinking to hard about this, but I don't see the clear A vs B line for this question. +21  
nbme4unme  @sugaplum I thought the exact same thing as you and chose the acetaminophen answer accordingly. I maintain that I am correct, my score be damned! +5  
sushizuka  I had a similar question on UW and the explanation stated that the correct answer choice was the only one that addressed the patient's concern and answered her question. The rest were just alternative treatments, so they were incorrect. But I too answered with oral pain meds. +2  
angelaq11  couldn't agree more with you all. I chose acetaminophen because opioid abuse is NO joke. The crisis is still going strong because of answers like this... +  
houseppary  I ruled out oral acetaminophen because they described in great detail the severity of her injuries, and indicated that she wasn't even fully conscious/aware when she asked this question about opioids. Rather than expose her to more pain, and possibly worsen her long-term pain prognosis, by switching to acetaminophen too early, in this case it makes sense to keep her comfortable because she's very seriously injured and not even fully lucid. It's kind to reassure her in this case. +  
anastomoses  I appreciate all of the passion for the opioid crisis, and the wording of the answer is definitely not ideal. However, PAIN is also very real, and there is no way acetaminophen alone would cut it in a case like this, not "as soon as she can take medications orally." Maybe I'm lucky to have 6 months in clinicals before STEP or had a mom who just went through urgent spine surgery for breast cancer mets, but there is a time and place for opioids and this is clearly one of them. Thank you for coming to my ted talk. +1  
llamastep1  I agree with anastomoses, cmon guys have you ever had serious pain? oral acetaminophen is NOT enough for that type of pain. +  
sora  I r/o oral acetaminophen b/c she's post-op for major GI surgeries so you might want to avoid PO meds for a while +  
melchior  As argument against the oral acetaminophen answer choice, it says "switch the patient to oral acetaminophen boldas soon as she can take the medication orallybold" This means you're just waiting for her swallowing inability from the facial fracture surgery to come back, which might not have much to do with her pain, and so it seems somewhat arbitrary. +  
drpee  Maybe logically/clinically A is true, but this seems like a "patient communication" question to me and I could NEVER imagine A being a good way to phrase this point IRL. +  


Electrical alternans on boards means a big pericardial effusion (and usually cardiac tamponade physiology). The heart cannot fill properly, preload decreases, hypotension and tachycardia ensue, fluid backup leads to elevated JVP. Underlying etiology in this patient is renal failure.

zpatel  Cardiac temponade. +  
melchior  Hypotension and jugular venous distension are two components of Beck's triad, which is associated with acute cardiac tamponade. The third component is muffled heart sounds, which is not addressed in this question. +1  


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