Some recent contributions

... medbitch94 made a comment on nbme20/block3/q#42 (A 13-year-old girl has an episode of severe cellular...)
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submitted by medbitch94(0)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4946499/


... medbitch94 made a comment on nbme20/block3/q#26 (A 3-month-old boy is brought to the physician...)
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submitted by medbitch94(0)

FA2019 page 47: I-cell disease (inclusion cell disease/mucolipidosis type II)—inherited lysosomal storage disorder; defect in N-acetylglucosaminyl-1-phosphotransferase → failure of the Golgi to phosphorylate mannose residues (forming mannose-6-phosphate) on glycoproteins → proteins are secreted extracellularly rather than delivered to lysosomes. Results in coarse facial features, gingival hyperplasia, clouded corneas, restricted joint movements, claw hand deformities, kyphoscoliosis, and high plasma levels of lysosomal enzymes. Often fatal in childhood.


... medbitch94 made a comment on nbme20/block3/q#49 (A 92-year-old woman who was recently admitted to a...)
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submitted by medbitch94(0)

Full article: https://www.ncbi.nlm.nih.gov/books/NBK448130/


... medbitch94 made a comment on nbme20/block3/q#49 (A 92-year-old woman who was recently admitted to a...)
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submitted by medbitch94(0)

Actinic purpura results from extravasation of blood into the dermis. This phenomenon is due to the skin atrophy and the fragility of the blood vessels in elderly individuals, which is exacerbated by chronic sun exposure. Actinic purpura lesions are located on sun-exposed areas, like the arms, face, and neck.

Skin atrophy in dermatoporosis is due to an alteration of collagen, similar to that which is seen in osteoporosis. This pronounced skin atrophy caused by the photo-aging makes the dermal vascular network very sensitive to the slightest trauma or shearing force.


... medbitch94 made a comment on nbme20/block2/q#35 (A 36-year-old woman comes to the office because of a...)
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submitted by medbitch94(0)

WHY she has a huge ass liver too? I don't understand how you can choose big spleen over big liver or visa versa


... monoloco made a comment on nbme20/block1/q#27 (A 53-year-old woman comes to the physician because...)
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submitted by monoloco(2)

When you have a traveler who has intermittent abdominal symptoms and diarrhea, and who has traveled to the likes of northern Africa and such, Schistosomiasis needs to be on your radar. At least, that’s how I’ve incorporated this nugget into my mental space.


... drdoom made a comment on nbme20/block1/q#6 (A 16-year-old student has uncontrollable sleepiness,...)
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submitted by drdoom(6)

This is an interesting one. I like to remember it this way: in people with narcolepsy, all the “right kinds” of sleep are happening at all the “wrong times” of day. During the day, when a power nap would typically throw you immediately into REM, this kid is only entering Stage 1 or 2 (lightest sleep = slightest noises jar him back to reality). At night, when he should peacefully drift into Stage 1, 2, and so on, he instead completely zonks out. Classic narcolepsy.

From UpToDate: “Narcolepsy can be conceptualized as a disorder of sleep-wake control in which elements of sleep intrude into wakefulness and elements of wakefulness intrude into sleep.”


... drdoom made a comment on nbme20/block1/q#11 (The sequence surrounding the first two exons of the...)
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submitted by drdoom(6)

As described in the question stem, this mutation occurs within an intron (a gene segment which is transcribed [DNA->RNA] but not translated). RNA splicing enzyme(s) grab RNA and “loop it”; an intron is cut out and the exons on either side of the intron are adjoined, like this:

exon1—intron—exon2 => exon1—exon2

Typically, this splicing occurs at the very edges of the intron (what I denoted with the “—” character). But in our case, a mutation within the intron is causing RNA splicing enzyme to recognize a new site: the splicer cuts within the intron (instead of at the very edge, as it should). So, we get something that looks like this:

exon1—intr—exon2

That’s a totally different mRNA molecule, and it's going to make our β-globin protein look (and behave) awfully strange.


... monoloco made a comment on nbme20/block1/q#11 (The sequence surrounding the first two exons of the...)
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submitted by monoloco(2)

This has to do with intron splicing. Remember GTAG. This mutation induced an AG closer where it was supposed to be, so some of that intron just became an exon.


... monoloco made a comment on nbme20/block1/q#32 (A 56-year-old woman is brought to the emergency...)
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submitted by monoloco(2)

This is the only choice that comes close to nicking the thoracic duct, specifically at its inlet, the left subclavian.


... monoloco made a comment on nbme20/block2/q#14 (A 23-year-old woman has had fever, hypotension, and...)
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submitted by monoloco(2)

Encapsulated organisms run rampant in patients who have no spleen, whether physically or functionally. (Recall the wide-array of sequalae sickle cell patients experience thanks to their functional autosplenectomy.)


... monoloco made a comment on nbme20/block2/q#28 (At a postnatal checkup, a 6-week-old female newborn...)
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submitted by monoloco(2)

Annular pancreas is the only answer that accounts for the bile in the vomit; of the choices, it is the only obstruction distal to where bile enters the GI tract.


... monoloco made a comment on nbme20/block2/q#10 (A 70-year-old woman is transferred to a...)
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submitted by monoloco(2)

This is indirectly asking about peak bone density. That whole thing about weight-bearing exercises, eating right, yada yada, before and during that down-slope phase of life for bone density. All about reducing that 1% per year age-related bone density loss as best as we can. Level of activity is precisely like weight-bearing exercise. (Consider: no activity, bed-ridden -- say goodbye to your bones; highly active, runs every other day -- good amount of weight-bearing / stress to induce remodeling and maintain integrity of the bones.)


... monoloco made a comment on nbme20/block2/q#26 (A male newborn is found to have a decreased blood...)
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submitted by monoloco(2)

Decreased total, normal free (unbound) = Thyroid hormone-binding globulin deficiency


... monoloco made a comment on nbme20/block2/q#32 (A 12-year-old girl is brought to the physician by...)
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submitted by monoloco(2)

This is a conditional called craniocleidodysplasia. The kid on Stranger Things with the lisp has the disorder. No collar bones, too many teeth, frontal bossing => craniocleidodysplasia. CBFA1 is a gene highly implicated in osteoblast function.


... monoloco made a comment on nbme20/block2/q#11 (A female newborn delivered at 36 weeks' gestation is...)
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submitted by monoloco(2)

This is a hypoplasia of the pleuroperitoneal membrane. The guts herniate into the thorax, usually on the left side, and result in hypoplasia of the lungs (because they're horribly compressed).


... monoloco made a comment on nbme20/block2/q#19 (A 66-year-old man is brought to the emergency...)
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submitted by monoloco(2)

Is this the one with the poor kidney that was cut in half against its will and has a dilated distal ureter? If so, probably showing us transitional carcinoma with mild invasion into that distal ureter. Pathoma does a pretty awesome job of talking about GU cancers (and most cancers) ((and most medicine)) IMO.


... monoloco made a comment on nbme20/block2/q#20 (A 19-year-old man who is a college student is...)
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submitted by monoloco(2)

I have regarded crepitus as the rubbing of bone-on-bone. My study partner and I think this is a purely definitional question. Yes, crepitus could also be trapped air. Context, I guess.


... monoloco made a comment on nbme20/block3/q#36 (A 4-year-old boy has had fever, abdominal cramping,...)
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submitted by monoloco(2)

I think Shigella is the most appropriate, as it is actually regarded as highly inflammatory. Yes, E. coli can be of the EHEC/STEC variety, but E. coli could also be of the ETEC variety or whatever other strains it has. Ergo, E. coli may be plausible, but it is not the 'most likely.' Bleh to these kinds of questions.


... monoloco made a comment on nbme20/block3/q#23 (A 50-year-old woman is brought to the emergency...)
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submitted by monoloco(2)

If you want to clear a drug, it is probably best that it not be bound to proteins (so that it gets filtered) and it has a low volume of distribution (so it isn't in the deep, hard to reach tissues).


... monoloco made a comment on nbme20/block4/q#21 (A 47-year-old woman comes to the physician because...)
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submitted by monoloco(2)

This patient is experiencing hypersensitivity pneumonitis from the parakeets. I was thinking M. Avium when I selected parakeets -- I think my logic was flawed given the specifics of the patient's story.


... monoloco made a comment on nbme20/block4/q#17 (A previously healthy 55-year-old man has recently...)
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submitted by monoloco(2)

As a rule of thumb, if you give someone an ACE inhibitor and they get a problem, they had renal artery stenosis (usually bilaterally, or so we were taught at our med school). Probably has to do with decreased GFR thanks to decreased Angiotensin II–selective vasoconstriction of the efferent arteriole => decreased sodium delivery to macula densa => increased renin release.


... monoloco made a comment on nbme20/block4/q#30 (A 32-year-old woman is brought to the emergency...)
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submitted by monoloco(2)

Anytime you have a person who bumps their head, gets back up, and then has severe issues or dies like 6 hours later -- you have yourself an epidural hematoma from laceration to the middle MENINGEAL artery. (Goljan really emphasizes that you don't screw up and select middle cerebral.) You know it has to be an arterial laceration since the dura is tightly adhered to the skull's inner surface. Goljan referred to his experience with it as needing pliers to remove the dura from the skull; graphic, but it drives the point home. Tenting seen on CT is because the epidural hematoma gets stuck between the suture lines. When it manages to break past one of the suture lines, it is my understanding that then is when you get severe sequelae, like death or whatever.


... onyx made a comment on nbme20/block1/q#12 (72 yo woman with dysphagia)
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submitted by onyx(0)

Thoracic duct relations.


... onyx made a comment on nbme20/block1/q#12 (72 yo woman with dysphagia)
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submitted by onyx(0)

Thoracic duct relations.


... onyx made a comment on nbme20/block1/q#12 (72 yo woman with dysphagia)
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submitted by onyx(0)

Mediastinal relations.


... onyx made a comment on nbme20/block1/q#12 (72 yo woman with dysphagia)
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submitted by onyx(0)

The mass described is in the posterior mediastinum (see images below). The thoracic duct is damaged “near the mass”, hence drainage of organs distal to that point will be affected. The images below should clarify.


... onyx made a comment on nbme20/block1/q#31 (66 yo man, cavitary lesion in right lower lobe of lung)
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submitted by onyx(0)

A radiographically visible air-fluid level suggests a pretty large lesion (hence, “cavitary”). That's not going to become normal tissue again. Six months following resolution of symptoms you can expect healing in the form of a scar; that is, fibrosis but only in a single spot.


... radion made a comment on nbme20/block4/q#7 (33 yo woman with HIV, generalized tonic-clonic seizure)
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submitted by radion(0)

Single enhancing lesion points more towards lymphoma than toxo. Toxo is usually multi-ring enhancing lesions.


... drdoom made a comment on nbme20/block4/q#15 (45 yo man undergoing surgical procedure)
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submitted by drdoom(6)

The more general principle: endothelia vasodilate in the presence of high CO2; you gotta get rid of that acid somehow! Can’t let it accumulate, as lower pH within a “micro-environment” affects structure/efficiency of enzymes, proteins, etc. The more acidic a local environment, the more you expect nearby vasculature to dilate (as a means of increasing flow rate, thereby ferrying off accumulate acid).

The anesthesiologist can exploit this mechanism. By hyperventilating (blowing off CO2), the brain vasculature senses a low CO2 / “hunky-dory state,” which requires no vasodilation. In other words, the vasculature does not need to continue the ATP-consuming practice of synthesizing Nitric Oxide (NO).


... radion made a comment on nbme20/block4/q#15 (45 yo man undergoing surgical procedure)
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submitted by radion(0)

Hypercarbia causes cerebral vasodilation. If you have ever seen an intra- or acute post-op neurosurgical patient, or really any patient about to herniate, you can remember this because they will be hyperventilated to pCO2 around 25-30 to decrease ICP via cerebral vasoconstriction; in this case, we have the opposite. The curve of pCO2 vs cerebral blood flow is quite steep in the physiologic range meaning small changes in ventilation make a significant difference in CBF.


... metformality made a comment on nbme19/block0/q#0 (Isolated skeletal muscle contracted with electrical stimulation)
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submitted by metformality(0)

When a muscle runs out of fuel (eg, glucose) and/or producing less ATP and “increased” accumulation of metabolites (all other options besides the correct choice), it is a sign of onset of muscle fatigue. The stem is asking which of the following will “decrease?”, and it is the pH that will decrease (acidosis) due to the accumulation of lactic acid (remember glycolysis pathway where pyruvate gets converted to lactic acid).


... metformality made a comment on nbme19/block3/q#12 (23 yo woman engages in 30 minutes of strenuous exercise)
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submitted by metformality(0)

High cardiac output to the pulmonary circulation during exercise will cause the distension and recruitment of micovessels and that would cause the increase in total cross-sectional area.

Here are two images that illustrate this principle nicely:


... metformality made a comment on nbme19/block4/q#17 (60 yo man, 20-year history of hypertension; shortness of breath and fatigue for 3 months)
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submitted by metformality(0)

This patient with a history chronic hypertension is most likely suffering from left heart failure (decreased cardiac outpout), causing the blood to back up in the lungs (Crackles are heard bilaterally, shortness of breath) and that resulting into increased afterload for the right side of the heart, raising the pressure in the right heart chambers, which get transmitted back to central vein.


... drdoom made a comment on nbme19/block1/q#13 (Mechanism of action of tumor suppressor genes)
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submitted by drdoom(6)

This is essentially a formal logic question. Logically speaking, the question asks us to identify a mechanism that tumor suppressors have which proto-oncogenes do not. In other words, what is a mechanism shared by all known tumor suppressors but not shared by any known proto-oncogenes? For that reason, it can’t be phosphorylation; sure, phosphorylation is a mechanism of tumor suppressors but it’s also a mechanism of many known proto-oncogenes.


... picodemolar made a comment on nbme19/block1/q#13 (Mechanism of action of tumor suppressor genes)
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submitted by picodemolar(0)

Oncogenes with gain of function mutation lead to increased transcription, etc., whereas tumor suppressor genes block G1-->S phase. NF1 gene product has RAS GTPase activity which works by phosphorylating and activating protein (neurofibromin). So there is at least 1 tumor suppressor gene that works through phosphorylation.


... quackster made a comment on nbme19/block1/q#4 (66 yo man, 2 months no erection)
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submitted by quackster(0)

This is a controversial one, but it seems the consensus is that pt had sxs of major depression, and thus his libido was most likely down. But structurally/blood flow–wise, he was fine, so nocturnal erections were normal. So, concept NBME wants us to realize is that we should screen for depression in pts who complain of sexual dysfunction? Or ask about sex in pts who display sxs of depression, like that patient had in the stem of the Q.


... shadowbox made a comment on nbme19/block3/q#40 (25 yo woman requests prenatal diagnosis at 12 weeks gestation)
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submitted by shadowbox(0)

The stem states that the mother is 12 weeks gestation. CVS is performed 1st trimester, usually b/t 10-14 weeks gestation according to Up-to-Date. Amnio is performed after 15 weeks. From Up-to-Date: “Amniocentesis should be performed after 15 weeks of gestation because earlier procedures are less likely to be successful, are associated with higher rates of cell culture failure, and carry greater fetal risks.”


... shadowbox made a comment on nbme19/block3/q#19 (30 yo man and 24 yo woman; best estimate that child will have oculocutaneous albinism?)
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submitted by shadowbox(0)

Since the father's sibling is affected, we know that the father's parents are both carriers. That means the possible genotypes of the father are AA, Aa, aA, or aa.

We know the father is unaffected, so that means he cannot be aa, and must be either AA, Aa, or aA.

Since there are only 3 different genotypes he could have, with 2 of them being carrier genotypes, there is a 2/3 probability he is a carrier.

So we obtain the probability of the father passing on a recessive allele as 2/3 (probability of being a carrier) x 1/2 (probability of passing on a recessive allele if he is a carrier). The 2/3 is not relevant to the probability that the mother is a carrier.

We know the frequency of affected individuals in the population at large is 1/40,000 (=q^2), so q=1/200.

P+q=1, so p=199/200 and 2pq=2(199/200)(1/200).

To make multiplication easier we assume 199/200=1, so:

2pq=2*(1/200)=1/100 --> this is the carrier frequency (a.k.a., heterozygotes) in the population, which we can assume for the mother.

So, to answer the entire question we multiply the probability that father is a carrier (2/3) and passes on the allele (1/2) times the probability that mother is a carrier (1/100) and passes on the allele (1/2); putting it all together we have:

(2/3)*(1/2)*(1/100)*(1/2) = 2/1200 = 1/600


... shadowbox made a comment on nbme19/block1/q#4 (66 yo man, 2 months no erection)
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submitted by shadowbox(0)

The amount of nocturnal erections is decreased, I think (atherosclerotic problem); but I thought that it was a typical case of a patient suffering from depression after a serious illness, therefore => decreased libido.


... aliyah made a comment on nbme19/block1/q#17 (29 yo man untreated HIV)
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submitted by aliyah(3)

After the CD4+ cells become infected, the CD8+ cells kill them.


... aliyah made a comment on nbme19/block1/q#35 (5 yo boy, right eye pain 1 week)
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submitted by aliyah(3)

If a germ cell or somatic cell had the original mutation, then there's an increased risk for cancer in other parts of the body too. If only retinal cells in one eye is mutated, only that one eye is at risk for cancer.


... aliyah made a comment on nbme19/block3/q#5 (30 yo woman, 1 week of visual difficulty)
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submitted by aliyah(3)

The right eye's efferent nerves are working, as left eye stimulation causes a change in the right eye. The right eye optic n. damage causes it's afferent n. to be damaged. It can't carry info to brain, so right and left eye can't constrict to light.


... ajguard26 made a comment on nbme19/block2/q#16 (40 yo woman, chorionic villus sampling)
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submitted by ajguard26(7)

Chorionic villi sampling is the taking of genetic material within in the chorionic villi of the placenta. Chorionic sampling is done when a patient is at high risk for chromosomal abnormalities (previous pos. tests, 35yo or older, family hx.) during the 10-13 weeks of pregnancy.

Confined placental mosaicism results when the C.V.S. testing comes back back showing a trisomy, but all subsequent testing (and the fetus itself) have normal chromosomal counts. This may be due to either a trophoblastic mutation, or by "trisomic rescue," in which trisomic cells that were supposed to be in the fetus are confined to the placenta to prevent an abnormal fetus.


... ajguard26 made a comment on nbme19/block2/q#13 (25 yo man, exercise test. Most likely physiologic changes)
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submitted by ajguard26(7)

As the muscle works and breaks down ATP, adenosine is produced, leading to an increase in the tissues. This increased adenosine causes vasodilation, which in turn increases vascular conductance (the flow of a volume of blood through the vasculature).

Although you may think muscle contraction may lead to a decrease in flow through the vessel(s) by squeezing down on them, this mechanism is overcome by the increased cardiac output from the heart.


... ajguard26 made a comment on nbme19/block1/q#24 (62 yo woman sudden weakness of left leg)
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submitted by ajguard26(7)

This patient presents with classic upper motor neuron lesion symptoms: weakness, hyperreflexia, and decreased sensation. However, the question states she "cannot tell whether her left great toe is raised or depressed" when her eyes are closed, which may make you reconsider and think there may be some proprioceptive issues they are trying to hint at. This is not the case. Especially once they mention there are no other abnormalities (i.e., no upper limb abnormalities or right sided abnormalities). If this is the case, there is no damage to the tracts at all (which are still considered UMN).

Therefore, the damage is purely motor and sensory in the left leg, which is on the medial aspect of the frontal and parietal lobes respectively. This area is supplied by the anterior cerebral artery.


... ajguard26 made a comment on nbme19/block1/q#48 (62 yo man, decreased speech fluency after cerebral infarct)
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submitted by ajguard26(7)

Obviously no picture here, but "A" in the picture represents Broca's area, which would cause the expressive aphasia this patient is experiencing.

However, the question also states the patient has weakness of the lower two-thirds of his face. This may cause you to think there is maybe a lesion in the pre-central motor area (thinking humonculus), but realize that the motor area travels all the way down to the bottom of the frontal lobe, RIGHT BEHIND THE BROCA'S AREA. In fact, Broca's area encompasses that part of the humonculus. And since the upper part of the face is controlled by the upper part of the facial motor cortex, and the lower part is controlled by the lower part of the facial motor cortex, you can have paralysis of the lower part of the face and have expressive aphasia if the lesion is in that specific area (does not need to be a lower motor lesion to spare the upper face/forehead).


... ajguard26 made a comment on nbme19/block1/q#42 (Advantage of randomized controlled studies)
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submitted by ajguard26(7)

"Confounding variables" here means "confounding bias," essentially. And this is true because a prospective cohort looks at a specific exposure to a substance (environmental toxin, drug, etc.), and asks "Who will develop this disease if exposed?" PCS's look attempt to find a relative risk associated with an exposure. They do not take into account the affects other exposures. This is your confounding bias. FA gives the example of confounding bias as "Pulmonary disease is more common in workers in a coal mine; however, miners are more likely to smoke," and since smoking can also lead to pulmonary disease, you can't really say whether the smoking (first or second hand) or the coal dust causes the problem. A clinical trial, on the other hand, contains a test group and a control group, so variables such as the confounding variable mentioned above are limited.


... ajguard26 made a comment on nbme19/block1/q#1 (53 yo woman with GERD.)
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submitted by ajguard26(7)

So although Misoprostol DOES increase mucus production and is gastro-protective (and in FA does state that it decreases acid production), thereby decreasing symptoms and aiding in healing, omeprazole is the "more correct" choice. This is because omeprazole is a proton-pump inhibitor, which will act directly on the proton pumps of the stomach and decrease the offending agent more than the misoprostol will. Therefore, it is the first line drug for GERD.


... doofusmd made a comment on nbme19/block1/q#35 (5 yo boy, right eye pain 1 week)
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submitted by doofusmd(5)

This is what is known as a somatic mutation: a mutation that occurs in non-germline cells and, therefore, only effects daughter cells derived from the parent cell with the mutation. So, a mutation occurred in a differentiated parent cell that gave rise to a set of daughter cells (which, in this case, were destined to become retinal tissue).


... drdoom made a comment on nbme19/block1/q#4 (66 yo man, 2 months no erection)
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submitted by drdoom(6)

Inability to maintain an erection = erectile dysfunction. So now the question is "Why?"

Fatigue, difficulty sleeping, difficulty concentrating is starting to sound like depression. "Difficulty concentrating" might be interpreted as impaired executive function or the beginnings of vascular-related dementia (dementia related to small but numerous cerebral infarcts), but on Step 1 dementia will be blatant (i.e., "lost his way home," "wandering," etc.).

Depression is actually common after a debilitating event like stroke, as you might expect. With depression comes a loss of sexual interest and desire—that is decreased libido.

One can make the argument that a "vascular patient" might have some issues with his "pipes" (arteriosclerosis, parasympathetic/sympathetic dysfunction) and, for this reason, nocturnal erection should be decreased; but note that nothing is mentioned about long-standing vascular disease (no hx of hypertension).

As a result, the best answer choice here is C. (Libido decreased but nocturnal erections normal.) The big question I have is, how the heck does this guy know he's hard when he's asleep!!? :p