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Comments ...

 +0  (nbme20#2)

Norovirus is the most common cause of viral gastroenteritis in the USA due to vaccination. + Rotavirus is the most common cause of viral gastroenteritis in the rest of the world. In this question you had to know the most common cause


 +0  (nbme24#31)

Keywords from Dr. Turco from Kaplan:

  • Replication- DNA
  • Transcription- RNA
  • Translation- Protein

 +0  (nbme24#35)

Per American Lung Association: Bronchopulmonary dysplasia (BPD) is a form of chronic lung disease that affects newborns (mostly premature) and infants. It results from damage to the lungs caused by mechanical ventilation (respirator) and long-term use of oxygen. Most infants recover from BPD, but some may have long-term breathing difficulty. + Prematurely born infants have very few tiny air sacs (alveoli) at birth. The alveoli that are present tend to not be mature enough to function normal, and the infant requires respiratory support to breathe. Although life-saving, these treatments can also cause lung damage


 +0  (nbme23#48)

However weird, you have to respect the patient's beliefs as long as they aren't putting the newborn at harm. In these types of questions you have to build patient-physician relationships because the patient might become offended if you disregard their beliefs. So while the newborn most likely has gas and not "the evil eye", choice E is the least "offending" answer that suggests treatment.

charcot_bouchard  Exactly. If she was cracking the egg on Baby's head u stop her lol (i am cracking up on my own jokes)

 +2  (nbme22#6)

The question while stupidly written, asks how long the RBC's that carry the CO take to be removed from the circulation, not how long the CO takes to be removed from the RBC. Just asking the lifespan of RBCs in an stupidly complicated way. As we know, RBC's life span is about 120 days and then they are removed from our circulation. 120 days is about 4 months. Next time they will probably ask the RBC lifespan in weeks or in hours, who knows? smh


 +1  (nbme22#43)

FA 2018 page 107

C1 esterase inhibitor deficiency: Causes hereditary angioedema due to unregulated kvllikrein activation, which leads to increased bradykinin.


 +0  (nbme22#27)

Page 36 of FA 2018. Purine antagonist drugs are:

6-MP(Azathioprine is a prodrug of 6-MP), Mycophenolate, ribavirin.

sbryant6  I forgot what the MP stood for in 6-MP, so I chose methylprednisolone. Silly mistake.

 +1  (nbme22#19)

Important to know here is location. Apart from learning the histologic descriptions (which are boring as shit), neoplasia in the diaphysis is consistent with Ewing sarcoma. Osteosarcoma location is at the Metaphysis.


 +2  (nbme22#25)

Histamine causes arteriole vasodilation, causing a buildup of blood in the capillaries. The increased blood in the capillaries will cause the pressure there to rise. Filtration is dependent on pressure, the higher the pressure, the more the filtration.

Remember blood flow: veins to venules to capillaries to arterioles to arteries

yb_26  agree in all, except the blood flow - it is right the opposite [https://teachmeanatomy.info/the-basics/ultrastructure/blood-vessels/]
link981  I stand corrected @yb_26. Brainfart moment 🙈

 +1  (nbme22#17)

Marginal zone lymphoma is caused by CHRONIC INFLAMMATION. H-Pylori can cause chronic inflammation in the stomach.

Epstein barr virus is associated with BURKITT lymphoma, the JAW lesion in Africa.

Got it wrong because I thought H-Pylori only caused gastric cancer.


 +3  (nbme22#40)

Per First Aid 2018 (pg 421) & Merck Manual

a) CML is not the answer because in CML you have HIGH WBCs & Platelets. In the stem there is only high platelets. b) Is the answer because in Essential Thrombocythemia we have normal WBCs and RBCs, just high platelets. c) Myeloid metaplasia refers to well a metaplasia in myeloid cells which are basophils, eosinophils, etc. d) In Polycythemia Vera we have HIGH RBCs, WBCs, and Platelets. e) Reactive thrombocytosis- is a elevated platelet count that occurs secondary to another disorder like:

-Chronic inflammatory disorders (eg, rheumatoid arthritis, inflammatory bowel disease, tuberculosis, sarcoidosis, granulomatosis with polyangiitis) -Acute infection

-Hemorrhage

-Iron deficiency

-Hemolysis

-Cancer

-Splenectomy or hyposplenism

impostersyndromel1000  perfect response right here

 +2  (nbme21#39)

p^2 + 2pq + q^2 = 1 p+q= 1

q^2= 1/900 q= 1/30 p= 29/30 which rounds to 1

They are asking for carrier frequency which is 2pq.





Subcomments ...

submitted by beeip(60),

How to differentiate between Norovirus and Rotavirus here? Must be related to the the contagious nature of the illness?

strugglebus  You know it’s Noro because people are vaccinated against Rota at 2,4,6 months. +  
beeip  @strugglebus: I didn't know about the vaccine schedule. Thanks! +  
strugglebus  As an addendum, you know it’s not staph aureus b/c that is rapid onset within 4 hours. +  
asapdoc  @Beeip If you go to the vaccines page in first aid it gives you all the high yield vaccinations. I didnt realize to correlate that page to a lot of questions until I got this answer wrong +  
savdaddy  its norovirus b/c it can survive ~2 weeks without a host, which is why we see family members with symptoms 3 days after the initial virus. +  
savdaddy  ***after the initial outbreak +  
eacv  for me this was a discart qx: 1.Giardia lamblia not showed steatorrhea and it needs medication to go away. 2. Rotavirus normally in unvaccinated kids. 3. Shiguella VERY inflammatory stool test do not show anything 4.S areus is very FAST 2-6 hr after eat the contaminated food. +  
link981  Norovirus is the most common cause of viral gastroenteritis in the USA due to vaccination. + Rotavirus is the most common cause of viral gastroenteritis in the rest of the world. In this question you had to know the most common cause. +  


submitted by seagull(391),

This infant has oxygen toxicity due to free radical generation. Free radicals damage the lung parenchyma leading to fibrosis and dysplasia (abnormal growth).

link981  Per American Lung Association: Bronchopulmonary dysplasia (BPD) is a form of chronic lung disease that affects newborns (mostly premature) and infants. It results from damage to the lungs caused by mechanical ventilation (respirator) and long-term use of oxygen. Most infants recover from BPD, but some may have long-term breathing difficulty. + Prematurely born infants have very few tiny air sacs (alveoli) at birth. The alveoli that are present tend to not be mature enough to function normal, and the infant requires respiratory support to breathe. Although life-saving, these treatments can also cause lung damage. +  


Did anyone else go down the: she's hypotensive so maybe she'll get waterhouse friderichsen syndrome because nothing else is making sense to me at this point??? route -

Turns out, severe malaria can cause cardiovascular collapse and hypotension.

shriya goyal  yes I answered it like that +1  
redvelvet  me too :( +  
abigail  me three :( +  
yex  Me four :-/ +  
link981  Slowly raising my hand as well +  
tinydoc  Sammmme +  
bullshitusmle  same here!!!:@ +  


submitted by cbrodo(14),

The posterior columns (Fasciculus cuneatus/Fasciculus gracilis) carry information to the brain regarding proprioception, vibration, discriminative touch and pressure. Physical exam findings suggest a lesion here (the spinothalamic tract carries pinprick/pain and temperature, and these were normal). Since the patient has abnormal findings in the lower extremities, and normal findings in the upper extremities, the answer is Fasciculus gracilis. This is because information from body areas below the level of T6 is carried by gracilis and information from body areas above the level of T6 is carried by cuneatus.

kai  kick Goals (gracilis) with your feet Cook and eat (cuneatus) with your hands +2  
temmy  i remember gracilis is for legs by saying i have graciously long legs and they are inside while arms can spread out to remember their orientation on the spinal cord +  
jess123  I remember it as gracilis = grass so feet haha +  
link981  Just to add found on page 492 on FA 2018. +  
charcot_bouchard  Hey Temmy, I can spread my legs too :) +  
maxillarythirdmolar  I can't feel GRACIE's ~fine touch~ as she ~vibrates~ my balls. +  


submitted by lfsuarez(65),

During protein translation, the ribosome bind to mRNA to initiate trasncription starting at the N-terminus. The N-terminus peptide end contains a signal recognition particle that binds to the signal recognition particle receptor on the rough ER to allow the protein to be made into the RER.

link981  Rough endoplasmic reticulum- site of synthesis of secretory (exported) proteins. Smooth endoplasmic reticulum- site of STEROID synthesis and detoxification of drugs and poisons. Page 46 FA2018 +  


A normoblast is an immature RBC, so it's elevated in states of increased hematopoiesis.

sympathetikey  Don't mind me. Just sippin my dumb ass soda over here. +7  
someduck3  The term "Normoblast" isn't even in first aid. +6  
link981  NBME testing your knowledge of synonyms. Have to know 15 descriptive words of the same thing I guess. +  
tinydoc  I wish they would stop making it so every other question I know the answer and I can't find it among the answer choices because they decided to use some medical thesaurus on us. +1  


submitted by seagull(391),

Hardy-Weinberg equation = 1= P^2 + 2pq + q^2

P^2 = 1/10,000 = 1/100

Then remember P + q = 1 ------> 1/100 + q = 1 (q = 99/100)

Lastly plug back into Hardy-Weinberg Equation as:

2pq = Heterozygote carrier

(2 x 1/100 x 99/100 = 2/100 = 1/50)

link981  I think q should be 1/100. You got p and q mixed up. +  


submitted by ferrero(15),

A very similar question I have seen in Qbanks will ask why a patient with right heart failure does not develop edema and the answer is increased lymphatic drainage. I got this question wrong originally because I answered along this line of reasoning but I think in this case it all has to do with WHERE the extra pressure is coming from. In this question the pt has diastolic hypertension so you can think about the pressure as coming "forward" so constricting precapillary sphincters can prevent an increase in pressure in the capillary bed. However for right heart failure this extra fluid is coming from the OPPOSITE direction (backwards from the right heart) and constricting precapillary sphincters can do nothing (on opposite side of capillary bed) - the only way to prevent edema is to increase lymphatic drainage.

seagull  The question clearly lead us to think about Osmotic pressure by talking about protein and urine. I wonder how many people used that line of reasoning (like myself)? +10  
mousie  Great explanation, I chose lymphatic drainage for the same reasoning (similar Q on different bank) +1  
sympathetikey  My reasoning was much more simplistic (maybe too simple) but in my mind, systolic BP is determined by Cardiac Output and diastolic BP is determined by arterioles. Therefore, what comes before the capillary and regulates resistance? Arterioles. That's why I said that pre-capillary resistance. +12  
cr  the main difference between the 2 cases is that in this case the patient has high BP +  
link981  So in kindergarten language the question is essentially asking how high pressure in the arterial system is NOT transmitted to the venous system (which is where EDEMA develops). But you know they have to add all this info to try confuse a basic principle and make you second guess yourself. (Got it wrong by the way) because of what @ferrero said of Qbank questions. +  
hello  @ferrero what are you talking about? lymphatic drainage is the wrong answer... +  
hello  ok never mind. i got it. hard to understand b/c it was a big block of text. +  


submitted by link981(28),

Histamine causes arteriole vasodilation, causing a buildup of blood in the capillaries. The increased blood in the capillaries will cause the pressure there to rise. Filtration is dependent on pressure, the higher the pressure, the more the filtration.

Remember blood flow: veins to venules to capillaries to arterioles to arteries

yb_26  agree in all, except the blood flow - it is right the opposite [https://teachmeanatomy.info/the-basics/ultrastructure/blood-vessels/] +1  
link981  I stand corrected @yb_26. Brainfart moment 🙈 +  


submitted by yotsubato(234),

Although acetaminophen (Tylenol) is not considered an NSAID, it too may provoke an aspirin-like sensitivity.

meningitis  For that same reason (not an NSAID) it doesn't reduce inflammation so it cant be used for Gout. +1  
meningitis  And I think Indomethacin is associated with anaphylactic reactions in patients with aspirin-sensitive asthma and aspirin allergies. Can anyone confirm? +  
link981  How many other's like me didn't see "allergic to aspirin"? FML +1  
hyperfukus  OMFG me too i just got so mad and questioned my whole life at least its cuz i can't read not bc i don't understand :((((( +  


submitted by yotsubato(234),

p53 is mutated and cant bind the TATA box, so what happens to transcription of inhibitory proteins?

Is basically what this question is trying to ask...

So no TATA box promoter => Decreased binding of RNA polymerase

link981  You said it, they are "trying" to ask. Should use better grammar. +1  
titanesxvi  This is on first aid, and says that the promoter region is where RNApolymerase binds +  


submitted by seagull(391),

Did anyone need to read that last sentence like 50 times because the author refuses to use better grammar. Just frustrating.

link981  Author rationale: "What is grammar?" +  


submitted by seagull(391),

Which of the following reasons is why this question is bull?

1) Using the word "cyclic" instead of tricyclic for clarity

2) Knowing all of epidemiology of all drugs

3) having to reason out that anticholinergic effects are probably the worst over alpha1 or H1 effects to no certainty.

4) The crippling depression of studying for days-to-weeks on end to probably do average on the test.

nlkrueger  yo, re-fucking-tweet +4  
aesalmon  I agree, I picked H1 because such a common complaint for those on TCAs is Sedation, I figure it might be so commonly seen as to be the "most common" reason for noncompliance. I suppose the "hot as a hare...etc" effects would be more severe/annoying, but I didn't think they were more common. +2  
fcambridge  I just like to pretend that there's a reason this question is now in an NBME and no longer being used for the test. Hopefully they realized the idiocy of this question like we all do +  
link981  Since it said cyclic, I thought of using, discontinuing, then using again. These people who write these questions need take some English writing courses so they can write with CLARITY. Cyclic is not the same as Tricyclic. +1  


Two major mechanisms of action have been elucidated:

1) Flucytosine is intrafungally converted into the cytostatic fluorouracil which undergoes further steps of activation and finally interacts as 5-fluorouridinetriphosphate with RNA biosynthesis thus disturbing the building of certain essential proteins.

2) Flucytosine also undergoes conversion into 5-fluorodeoxyuridinemonophosphate which inhibits fungal DNA synthesis.

3) Thymidylate synthetase is an enzyme that catalyzes the conversion of deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP).

Thymidine is one of the nucleotides in DNA.

With inhibition of TS, an imbalance of deoxynucleotides and increased levels of dUMP arise. Both cause DNA damage.

(WIKI)

link981  Just look at page 36 of FA 2018 and memorize that shitty diagram o De novo pyrimidine and purine synthesis they ask so much about. No need for scientific explanations for this one unless you like to waste time. +2  


submitted by welpdedelp(70),

It was just asking the lifespan of RBCs (120 days)

haliburton  If I'm reading this right, this is just a tricky dicky question. I think CO binds 200x stronger than O2. But if an O2 cycles through binding / unbinding 200 times before a CO gets kicked off, this should still clear the CO from that cell sooner or later. strange to think it is 1. essentially permanently trapped in a cell, and 2. doesn't kill you and can be treated with O2 to resolution within a few hours or a day. They must just be thinking, until that last RBC dies, you've got original CO in a circulating cell. but just a fraction (because you didn't die). not sure how that CO isn't just passed on during recycling, based on this line of thinking. +3  
link981  The question while stupidly written, asks how long the RBC's that carry the CO take to be removed from the circulation, not how long the CO takes to be removed from the RBC. Just asking the lifespan of RBCs in an stupidly complicated way. As we know, RBC's life span is about 120 days and then they are removed from our circulation. 120 days is about 4 months. Next time they will probably ask weeks or in hours, who knows? smh +2  


I think the increase in plasma renin activity with NSAIDs has to do with inhibition of efferent artery dilation by prostaglandins (PGE2), since that's what NSAIDs do by inhibiting COX. This decreased renal blood flow leads to RAAS activation to conserve water and ultimately renin increases.

htballer55  Afferent artery dilation* +4  
link981  There is decreased afferent renal artery dilation (less blood flow) leads to increased renin release from the juxtaglomerular cells (located near the afferent artery) to try to increase blood flow. I got it wrong but after reviewing saw my idiotic mistake. +1  


This more likely to be diuretics rather than laxatives b/c

the lab study shows a renal dysfunction (BUN & Creatinine are elevated)

Most likely the patient abused loop diuretics; also knows to cause contraction alkaloids, along with renal problems such as interstitial nephritis

endochondral1  would laxatives also have the low potassium? +1  
link981  My question exactly. And what if they were taking Potassium sparing diuretics? Then laxatives would be more likely or am I mistaken? +  
link981  Also creatine is normal, it's at the higher limit of normal so we can't say there is renal dysfunction. The BUN is elevated because patient has metabolic alkalosis with respiratory acidosis. +  
sweetmed  very important to Remember this: Diarrhea causes metabolic acidosis[from bicarb loss in stool], vomiting & loop diuretics cause metabolic alkalosis. +1  
hello  @usmleuser007 not sure your approach is the best way to think about it. The serum Cr is at the upper limit of normal (1.2). And, even if you calculate the ratio of BUN/Cr, it's 21, which would be a PRE-renal issue. +  


This more likely to be diuretics rather than laxatives b/c

the lab study shows a renal dysfunction (BUN & Creatinine are elevated)

Most likely the patient abused loop diuretics; also knows to cause contraction alkaloids, along with renal problems such as interstitial nephritis

endochondral1  would laxatives also have the low potassium? +1  
link981  My question exactly. And what if they were taking Potassium sparing diuretics? Then laxatives would be more likely or am I mistaken? +  
link981  Also creatine is normal, it's at the higher limit of normal so we can't say there is renal dysfunction. The BUN is elevated because patient has metabolic alkalosis with respiratory acidosis. +  
sweetmed  very important to Remember this: Diarrhea causes metabolic acidosis[from bicarb loss in stool], vomiting & loop diuretics cause metabolic alkalosis. +1  
hello  @usmleuser007 not sure your approach is the best way to think about it. The serum Cr is at the upper limit of normal (1.2). And, even if you calculate the ratio of BUN/Cr, it's 21, which would be a PRE-renal issue. +  


submitted by keycompany(111),

Flow Rate = Velocity x Cross-Sectional Area

2 cm^2 x 20 cm/sec x 60 sec/min x 1 L/1,000 cm^3 = 2.4 L/min

1,000 cm^3 = 1 L

seagull  Well, I missed this one. I don't even feel bad. +7  
link981  @keycompany a small typo, 100 cm^3 = 1 L not 1000cm^3. 1000 mL^3= 1 L +  
hello  @keycompany how did you edit your original comment to fix your typo? +  


submitted by haliburton(81),

warfarin inhibits the synthesis of factors II, VII, IX, X, C, and S by blocking reduction of oxidized vitamin K. The enzyme Epoxide Reductase is inhibited by warfarin. The reduced (active) form of vit. K is a cofactor for gamma-glutamyl carboxylase.

link981  So factors II, VII, IX, and X are precursor proteins? GTFO +  


submitted by hello(59),

Knowing the LR+ value = 10 does not help to solve this Q because estimating where "10" should fall on an axis is arbitrary. Also, the data points are coordinates -- they have an X-value and a Y-value (X, Y).

The way to approach this Q is to know that a high specificity means that a positive result is very, very likely to be a true positive.

Suppose that the specificity is 0.99 -- this is 99% specificity. Then, you look at the graph. The X-axis is "1-specificity." So, suppose the best test has a specificity of 99%. Then, calculate 1-specificity = 1 - 0.99 = 0.10. You would then chose the datapoint that corresponds to having an "X-value" that is closest to the origin. In this problem, it corresponds to data point "A."

You don't even need to know a specific specificity value to solve this problem. All you need to do is understand that if the specificity is extremely high, you will need to find a datapoint that is closest to the origin -- at least for the value in the X-axis in the coordinate of the data point -- because the X-axis corresponds to a calculation of "1-specificity".

link981  Excellent explanation but a minor typo. 1-0.99 = 0.01 not 0.10 :) +1  


submitted by seagull(391),

out of curiosity, how may people knew this? (dont be shy to say you did or didnt?)

My poverty education didn't ingrain this in me.

johnthurtjr  I did not +  
nlkrueger  i did not lol +  
ht3  you're definitely not alone lol +  
yotsubato  no idea +  
yotsubato  And its not in FA, so fuck it IMO +  
niboonsh  i didnt +  
imnotarobotbut  Nope +  
epr94  did not +  
link981  I guessed it because the names sounded similar :D +2  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +2  
impostersyndromel1000  same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle. +  
jaxx  Not a clue. This was so random. +  
wolvarien  I did not +  
ls3076  no way +  
hyperfukus  no clue +  


submitted by meatus(1),

I'm sorry but what am I missing here... I thought the whole point of diuretics is to correct volume overload by diuresis? How would total volume be increased??

niboonsh  the question is asking what would happen to the URINARY ph, bicarb, and volume. dont worry, i misread the question too -_- +5  
link981  Also misread the question, thought about the lab volumes of the BLOOD smh +2  
hyperfukus  yooooo me too!!! this is the second NBME i did this on they purposely don't write urine on the arrow categories to mess u up i swear!!! AHHHHHH +  
medulla  missed this question for the same reason .. still pissed +  


submitted by hayayah(382),

Pregnancy + Hx of thrombosis --> think antiphospholipid syndrome

The PT and PTT are prolonged d/t interference from the antibodies to phospholipids. Thrombin time normal.

Had to find research articles about it so take it from here and don't waste your time...

monoloco  yeah, i’ve never heard of antiphospholipids increasing PT time ... +3  
goldenwakosu  Not sure if that little detail was to throw us off. I think the point of the question was to ID antiphospholipid syndrome based on the clinical criteria (spontaneous abortion + thrombosis) +1  
johnthurtjr  I actually went down a rabbit hole with this one recently - essentially in vitro findings =/= in vivo findings, clot-wise with anti-phospholipid antibodies. +1  
link981  No mention of lupus anticoagulant, anticardiolipin, or anti Beta 2 antibodies. FA mentios prolonged PTT but nothing on PT. What a piece of shit question. But thanks to the dudes above who explained it +3  
yb_26  UWorld mentioned "prolong aPTT (and sometimes PT)" in APS +1  


The description of bilateral lower limb loss of vibration implies DCML damage, and the absent DTRs + Romberg seem to me to be implying that he possibly has tabes dorsalis from syphilis (or something very similar in presentation).

As for the other answers, A is wrong because his motor function is intact, B is wrong because pain and temperature deficits are not mentioned, C is wrong because it implies a specific nerve is entrapped, but he has lost bilateral sensation in his entire lower extremities

D is the trickiest, and I’m not 100% sure, but I would think radiculopathy of the anterior (ventral) roots would cause motor deficits since they carry motor efferents. You might also expect that motor dysfunction to be unilateral, since it would be unlikely to have a problem with the nerve roots on both sides. also the DCML is not located near the anterior roots of the spinal cord, so if the anterior roots were affected you really wouldn’t expect to see vibratory loss.

So basically process of elimination, I do feel like sensory neuropathy is an extremely vague answer though and I wasn’t a fan of the question.

keycompany  This is a great rationale. I would like to add on that D is wrong because Radicular Neuropathy of the anterior lumbar roots would (1) be painful [radicular neuropathy is characterized by radiating pain (hence the word “Radicular”); this patient has numbness and tingling, not pain] and (2) because the anterior lumbar roots are the motor roots and do not carry sensory innervation. This patient is having a problem with his dorsal spinal cord (not anterior/ventral). +4  
hello  Want to clarify that "radiculopathy" is not synonymous with pain. Radiculopathy can cause pain, weakness, or numbness. I think the only reason Choice D. was incorrect because it discussed the "anterior lumbar roots", which would affect motor function. +3  
niboonsh  Radiculopathy is damage to the actual nerve itself, wouldnt that make it a LMN lesion and babinski would be negative? +1  
link981  Great explanation guys +  


submitted by neonem(245),

From centerwatch.com (never heard of it before but seems like a good explanation):

"Phase IV studies, often called Post Marketing Surveillance Trials, are conducted after a drug or device has been approved for consumer sale. Pharmaceutical companies have several objectives at this stage: (1) to compare a drug with other drugs already in the market; (2) to monitor a drug's long-term effectiveness and impact on a patient's quality of life; and (3) to determine the cost-effectiveness of a drug therapy relative to other traditional and new therapies. Phase IV studies can result in a drug or device being taken off the market or restrictions of use could be placed on the product depending on the findings in the study."

seagull  Well, I was not smart and put phase 1 since it was talking alot about adverse effects and withdrawl from the patients. But now I see I have 2 extra chromosomes...my bad. +  
link981  Phase 1- Determine if drug is SAFE Phase 4- Continous surveillance of a drug that is already on the market. The vignette clearly states the drug is marketed. That means it passed the clinical trials. Marketed drugs have passed Phase 3 +