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 +0  (free120#40)

Pill-rolling resting tremor of Parkinson’s disease secondary to loss of dopamine neurons in the substantia nigra.


 +1  (free120#39)

I’m going to point out that a normal healthy kid with no cardiac history or symptoms and no family history of sudden cardiac death for a pre-sports physical is probably going to have a benign exam no matter what you think you hear.

the260guy  What a weird question. I could definitely hear a fixed split heart sound. And it was loudest over the pulmonic valve too which makes it even more of a dirty question. But I guess what I was actually hearing was an S3 heart sound.
wutuwantbruv  @the260guy I believe the splitting is being heard only during inspiration, making this normal physiologic splitting. Perhaps that's just my ears.
angelaq11  don't have adobe and couldn't download it, so I just chose whatever, but your explanation suddenly makes me feel dumb but grateful! Loving your tips! @benwhite_dotcom

 +0  (free120#38)

Classic Moro reflex, entirely expected and normal until it disappears around age 4 months.


 +0  (free120#37)

A history of volume loss (often GI 2/2 vomiting, diarrhea) resulting in shock is consistent with a hypovolemic etiology, as corroborated by the plethora of physical evidence provided. Diuretics exacerbate the situation, working against your body’s desire to retain fluid to compensate.


 +0  (free120#36)

Below the dentate line, anal cancer drainage is superficial inguinal. Above the dentate line, superior rectal (then iliac).

sugaplum  above the dentate line superior rectal drains into inferior mesenteric then goes into the portal system http://www.surgicalcore.org/popup/420229
sugaplum  my mistake, the question is asking lymphatic drainage not venous

 +0  (free120#35)

The only thing that directly raises BP of the list is increased PVR.

amedhead  would decreased cardiac output not also increase the blood pressure due to sympathetic activation of the baroreceptor reflex?
benwhite_dotcom  I think you’re ignoring a directly correct answer, increased PVR literally equals increased BP, and are instead trying to postulate an indirectly plausible answer. Decreased CO, as you just implied, means less blood pumping into the aorta and less blood pounding and stretching the arteries and thus decreased BP. Note, your original logic would apply to stroke volume just as easily. Yes, a sympathetic response could then occur as a response to mitigate this, such as in shock or heart failure, but it would misleading to suggest that decreased CO causes hypertension.

 +0  (free120#34)

p53 is an important tumor suppressor gene, particularly in its ability to cause a cell to undergo apoptosis in the event of damage. p53 protein activity also holds the cell at the G1/S regulation point (B), limiting DNA synthesis.


 +0  (free120#33)

This patient has hepatitis (elevated liver enzymes) due to active Hepatitis C infection. Hep C and HIV infection are both associated with intravenous drug use. While most patients with Hep A will clear the virus after their acute illness, Hep C causes chronic infection in 80% of patients, which may lead to cirrhosis over time (~20 years).


 +0  (free120#32)

Many oral cavity lesions, especially anteriorly such as the tip of the tongue, drain first to submental nodes (level 1). Oropharyngeal SCCs most commonly drain to level 2.


 +1  (free120#31)

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”
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.
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!
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.
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.

 +0  (free120#30)

Targetoid rash after a woodland excursion means Lyme disease, caused by Borrelia burgdorferi, carried by the Ixodes tick. Rash (erythema migrans), viral syndrome symptoms, fatigue, and polyarthritis are common. Lyme carditis typically manifests as AV block.


 +0  (free120#29)

To amplify tiny fragments of DNA in order to detect their presence, we use PCR. The question is a description of the process. Southern Blots are used to detect a specific DNA sequence within a DNA sample.


 +0  (free120#28)

(Unstable) angina. Most immediate treatment is nitro.


 +0  (free120#27)

Cystic fibrosis is an autosomal recessive disease involving CFTR (which encodes the CFTR protein), which means you need a double hit to express the disease. If the genetic test only picked up one, then it must have missed the other.

drdoom  The reason something is an “autosomal recessive” disease is because the protein encoded by the gene (of which you have two alleles, remember) does something where as long as you make SOME protein, your body should be okay. That’s kind of vague, so take the case of Cystic Fibrosis: you don’t present with Cystic Fibrosis if you have at least one functional allele -- that’s because CFTR protein is a protein that (in the case of bronchiole tissue) moves Chloride ion from inside cells to the outside lumen, which brings with it H2O and keeps the bronchiole lumen nice and watery, and fluid and non-viscous and non-pluggy. So long as you make enough of this protein, you don’t “need” both alleles to be good; the good allele can “make up for” (make enough of the protein product) to compensate for the “broken allele.” So, once again, understanding the pathophys of a disease allows you to reason through and predict things like disease penetrance and expressivity.

 +0  (free120#26)

Specificity is how often your test is right about people without the disease:

= TN / (TN + FP)
= 95 / (95+5)
= 95%

drdoom  Put another way: Of all the people who are disease-free, how many (of those people) did you catch? In this case, there are 100 people who are disease-free; our test labeled 95 of those people as “disease-free”, but our test also called 5 of those people “positive”; so our test is good (sort of) but not that good.
drdoom  Also note how specificity only answers questions about people WITHOUT THE DISEASE; it only “deals with” people who are disease-free. (Sensitivity is the opposite: it is a formula which only deals with people WITH THE DISEASE. I think understanding that is better than coming up with some crazy Snout-Spout-Spin mnemonic, which I never remember anyway.)

 +1  (free120#25)

BK virus reactivation is a cause of renal damage post-transplant in the setting of immune suppression, also known as BK nephropathy. Treatment is a reduction in immune suppression, allowing the body a chance to fight back. The virus can cause a cold-like URI syndrome with fever.

kekescc  in FA, BK = bad kidney

 +0  (free120#24)

Osgood-Schlatter is also known as apophysitis of the tibial tubercle. It’s due to chronic stress/irritation at the insertion of the patellar tendon on the tibial tubercle. It’s classically seen in teenagers doing repetitive vigorous activity (running, jumping). The radiograph demonstrates classic fragmentation of the tibial tubercle (which isn’t necessary to recognize to get the question correct).


 +1  (free120#23)

An odds ratio greater than 1 signifies increases odds, risk, likelihood -- whichever you prefer to call it. If the 95% confidence interval range does not include 1, then the difference is statistically significant (though not necessarily clinically meaningful).


 +0  (free120#22)

Just because he’s having (unprotected) sex doesn’t mean he doesn’t have simple infectious mononucleosis. The sex implies he’s also kissing someone! Pharyngitis + lymph nodes + fatigue = mono.


 +1  (free120#21)

What we have here is a congenital intolerance to breast milk: galactosemia, in which the body cannot convert galactose to glucose (resulting in an accumulation of Galactose 1-phosphate). They then list the findings and tests used to diagnose it. Lactose (the disaccharide in milk) is composed of glucose+galactose.


 +0  (free120#19)

Absolute risk reduction is the decrease in the number affected per number exposed:

(15-5)/50 = 10/50 = 0.2


 +0  (free120#18)

DMD is X-linked. We know her mom is a carrier based on family history, supported by lab testing. But her mom has 2 X chromosomes, only one of which is mutated. There is no way to know which her daughter eventually receives and expresses by her phenotype (i.e if she is a carrier or not). Just because her CK is normal doesn’t mean she isn’t a carrier–the phenotype of the X-linked carrier depends on X-inactivation.


 +0  (free120#17)

SIADH is a test favorite a very common cause of hyponatremia (after dehydration). A variety of brain and lung pathologies are possible etiologies, with lung cancer (of any type) being an important cause.


 +0  (free120#16)

If the fluid keeps coming into the glomerulus (via the afferent arteriole), but you clamp the exiting vessel (the efferent arteriole), then it’s going to build up in the glomerulus, leading to increased hydrostatic pressure.


 +0  (free120#15)

Many autoimmune/autoinflammatory conditions, including ankylosing spondylitis, are treated with DMARDs like anti-TNF-alpha medications when milder stuff doesn’t do the trick. Common examples are infliximab (Remicade) and adalimumab (Humira).


 +1  (free120#14)

Oral vesicle (hint hint). Blistering vesicular lesion on the hand. No fever, not toxic-appearing. This is Herpes (you may remember dentists getting herpetic whitlow in your studies, which is what this is). Most folks get HSV1 as children, though obviously not all are symptomatic. HSV is a large double-stranded, linear DNA virus.

jiya   why cant this be hand foot and mouth disease cause of coxsache
drachenx  Also thought it was Hand-foot-mouth an RNA virus but I did consider Herpes. Changed because I thought Hand foot and mouth would be more common.

 +0  (free120#13)

Blood at the meatus is the red flag (see what I did there?) for urethral injury, which should be evaluated for with a retrograde urethrogram. The membranous the most commonly injured by fracture. In contrast, the spongy urethra is most likely to be injured during traumatic catheter insertion or in a straddle injury.

canyon_run  Should we just assume that a pelvic fracture implies a membranous urethral injury? I was between membranous and spongy and I ended up choosing spongy because of the perineal bruising and fact that the patient was riding a motorcycle (and therefore susceptible to straddle injury).
benwhite_dotcom  Yes. You should think of spongy as the penile urethra, hence the predisposition to catheter-related trauma.

 +1  (free120#12)

Stress-related bowel issues, sometimes but not always alternatively involving both diarrhea and constipation, are a hallmark of irritable bowel syndrome (IBS). A diagnosis of exclusion, most of the stem is helping you rule out more serious issues. Lubiprostone, which is a fatty acid that induces stool-softening intestinal secretions, is approved for idiopathic constipation, most commonly in the context of IBS and or secondary to opiate use. The other drugs listed are for inflammatory bowel disease (IBD).


 +0  (free120#11)

There is an inferior orbital wall blow-out fracture. If you happen to know CT anatomy, this is actually involving the infraorbital foramen, which transmits the infraorbital artery and nerve, but really, so long as you notice the obvious fracture it’s the only choice that makes sense.


 +1  (free120#10)

This patient has chronic kidney disease, as indicated by elevated serum creatinine/BUN and evidence of anemia of chronic disease (normochromic normocytic). Poorly functioning kidneys do not hydroxylate 25-dihydroxycholecalciferol to 1,25-dihydroxycholecalciferol well nor produce adequate erythropoietin (hence the CKD-related anemia). Patient’s with CKD thus develop secondary hyperparathyroidism due to deranged phosphate excretion and inadequate Vitamin D activation resulting in hypocalcemia. Thus, we should expect to see low calcium, high phosphorus, low 1,25 vitamin D, and low Epo.

houseppary  Any guesses as to why he might have CKD at 4 y.o.?

 +1  (free120#9)

Stroke characterized by left hemiparesis and right CN12 palsy. Crossed findings mean a brainstem lesion. Right (ipsilateral) tongue, left-sided (contralateral) weakness means the exiting right hypoglossal nerve has been affected (within the right medulla). C is the pyramid where the corticospinal tract runs to control muscles (prior to the decussation). This is known as the medial medullary syndrome or Dejerine syndrome.

d_holles  It seems to me that the brain stem problems can all be answered using the Rule of 4s rather than memorizing the actual brain stem histology.

 +2  (free120#8)

The proliferative phase of the menstrual cycle is controlled by cyclin-dependent kinases. (This makes sense as cyclin-dependent kinases govern virtually all cellular division in eukaryotic cells.)


 +1  (free120#7)

They have described what you assume is a classic case of pneumonia. But, PNA isn’t an answer choice. What the next best thing? The cause! Old frail people (and alcoholics) love to get aspiration pneumonia. RLL is the most common site, which they have provided (thank you, big vertical bronchus). They even gave you the hint that the patient has “difficulty swallowing,” which is code for “aspirates when swallowing.”


 +0  (free120#6)

The main downside of live vaccines is that they can (but rarely do) cause the disease they’re designed to prevent, typically in immune-compromised individuals, who either receive the vaccine or are a close contact of someone who did.


 +0  (free120#5)

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).


 +0  (free120#4)

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.


 +0  (free120#3)

No relation between the atrium (P) waves and the QRS complex means third-degree AV block (aka “complete” heart block). Symptomatic (even fatal) bradycardia can result. “Cannon” atrial waves are prominent jugular venous pulsations that occur when the atria and ventricle contract simultaneously (which, of course, doesn’t normally happen).


 +0  (free120#2)

Timolol is a beta-blocker. Beta blockers can exacerbate asthma/COPD/reactive airway disease.


 +1  (free120#1)

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.

 +0  (free120#40)

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.


 +0  (free120#39)

Calcium oxalate stones are the most common variety of kidney stones, but uric acid stones make up 5-10% as well. None of the other choices are associated with renal calculi of any variety.

wes79  Also, the fact that hydroureter/hydronephrosis was seen in the absence of a stone on ultrasound supports that the stone was composed of UA

 +0  (free120#38)

This is a (prospective) case series. There is no control group (and certainly no blinding).


 +0  (free120#37)

The arrowed fluid is contained in a space behind the stomach but in front of the retroperitoneal structures (e.g. the pancreas), i.e. the lesser sac.


 +0  (free120#36)

The usual cold-like symptoms of runny eyes and a sore throat are common of several strains of adenovirus that are readily communicated amongst humans in close contact.


 +2  (free120#35)

An annular pancreas surrounds the duodenum and can cause intermittent duodenal obstruction. While this question theoretically requires the imaging to answer correctly, the only other choice that is feasible is Choice D, which is known as SMA syndrome. SMA syndrome is quite rare and typically seen in people who have recently had significant weight loss. On the imaging, it would be smooshing of the duodenum by a bright contrast filled artery as opposed to surrounding by soft tissue. I also think it’s highly unlikely to be tested.

houseppary  I agree except that on the imaging, if this was SMA, the artery would not be bright and filled with contrast because the problem states that these studies were taken with oral contrast. So that's not a feasible way to eliminate SMA as the correct answer. I to think the quality of the obstruction seen in the UGI series show an annular-looking obstruction rather than a focal compression as you'd see in SMA.

 +1  (free120#34)

Intermittent hyperbilirubinemia/jaundice in an otherwise healthy individual is typical of Gilbert’s syndrome, which is caused by the decreased activity of UDP glucuronosyltransferase.


 +0  (free120#33)

Androgen insensitivity is caused by a defective androgen receptor. DHT is responsible for creating male genitalia during fetal sexual development. The default human gender is female. So a genetically male patient with complete androgen insensitivity is externally phenotypically female. Lack of response to adrenal androgens prevents hair formation during puberty (adrenarche).


 +0  (free120#32)

TTP has a classic pentad: microangiopathic hemolytic anemia, thrombotic purpura, fever, renal failure, neurologic abnormalities (AMS). Whenever you see a question where the patient suddenly has a lot going on, consider TTP.


 +0  (free120#31)

A genetic variation in a particular nucleotide is by definition a polymorphism. Note that the question specifically states that the protein remains unchanged.


 +4  (free120#30)

As always, it’s almost better to ignore the pictures when possible. This gentleman has a peptic ulcer, which we know is caused predominately by H. pylori infection. H. pylori produces proteases and particularly urease, which allow it to increase the pH of its local environment by cleaving urea into ammonia, which is toxic to gastric mucosa. The picture demonstrates H pylori, which are evident with silver staining.

joonam  Hey bro, thank you so much for your contributions on these free 120 questions. Your advice on test taking strategies for step 1 have been very helpful.

 +0  (free120#29)

Catalase and coagulase-positive gram-positive cocci = staph aureus. mecA positivity means the bacteria carry the gene that confers methicillin-resistance, hence MRSA. Of the choices, MRSA is treated with vancomycin.


 +1  (free120#28)

Splitting is an immature defense mechanism often employed by patients with borderline personality disorder. When splitting, a person fails to see others as capable of having both positive and negative qualities; at any given time, it’s all or nothing.

d_holles  Got this one wrong -- thought it was acting out.

 +0  (free120#27)

The Lincoln’s beard distribution described is that of the V3 branch of the trigeminal nerve, which exits the skull base via foramen ovale. V2 exits via foramen rotundum. V1 exits via the superior orbital fissure.


 +0  (free120#26)

A new blistering disease in an older person is typically going to be a pemphigus question. Then you just have to remember the difference between bullous pemphigoid vs pemphigus vulgaris. Bullous pemphigoid is characterized by the loss of hemidesmosomes that bind keratinocytes to the basement membrane, resulting in bulla (big blisters) in areas of friction (Choice A). Patients with pemphigus vulgaris lose their desmosomes (which bind keratinocytes to each other), so that their skin is super friable, which results in ulceration. Mouth ulcers are more common in PV.


 +0  (free120#25)

Thiazides (typically used as antihypertensives) also increase calcium resorption in the distal tubule and are therefore useful in preventing calcium oxalate stone formation in patients with hypercalciuria (the mechanism is not really worth learning). Thiazides block the Na-Cl symporter, as opposed to loop diuretics, which block the triporter, and acetazolamide, which blocks carbonic anhydrase in the proximal tubule.


 +0  (free120#24)

This question is asking for the vascular supply of the parathyroid glands. That would be the inferior thyroid arteries, which arise from the thyrocervical trunk.


 +0  (free120#23)

Swallowing amniotic fluid is a critical component of lung development. Fetuses with severe oligohydramnios are plagued by pulmonary hypoplasia, which is the cause of death in fetuses born with Potter syndrome (renal agenesis).


 +0  (free120#22)

The alpha-value corresponds to the p-value we will accept as significant and reflects the likelihood of a type I error (a false positive). A lower alpha-value means a lower acceptable likelihood of obtaining the same results by chance, and thus, significant results can be reported more confidently (a 1% false positive rate instead of a 5% rate).


 +1  (free120#21)

Fear = amygdala

That is all I wanted to say but I guess that is too short to be accepted by the webform.


 +0  (free120#20)

The infraspinatus and teres minor are responsible for external rotation. Both the infraspinatus and supraspinatus muscles are innervated by a suprascapular nerve.


 +0  (free120#19)

Subacute combined degeneration (progressive peripheral sensory and motor loss) is a late sign of B12 deficiency, which is common in old people. On exams, a geriatric patient who lives alone and may have a “tea and toast” diet is likely to have vitamin deficiencies, particularly of folate and B12.


 +1  (free120#18)

Relationship with former patients are generally frowned on, but they’re especially problematic if the patient was a psychiatric patient, as the power imbalance of the practitioner-patient relationship and information the provider is privy to because of their patient care involvement preclude a healthy balanced relationship of equals.


 +0  (free120#17)

Multiple infections. Abscesses. Then you hear decreased oxidative burst and immediately think NADPH oxidase deficiency aka Chronic granulomatous disease, which causes recurrent abscess-forming infections due to the inability to kill ingested organisms because of the inability to generate superoxide radicals.

jean_young2019  Then why the choice D, “Inability of leukocytes to ingest microorganisms“, is incorrect?Moreover, Staphylococcus aureus is not an intracellular microorganism. Thank you for your help!
houseppary  Because in CGD, the macrophages are capable of taking in bacteria but aren't able to do the oxidative burst required to actually kill them. So the macrophages just house live bacteria which leads to granulomas full of walled-off but not dead bacteria. And S. aureus isn't intracellular as part of its normal life cycle, but being eaten by a macrophage isn't part of its normal life cycle. Whether an organism gets eaten by a macrophage isn't part of the consideration of whether it's intracellular.

 +0  (free120#16)

Pubertal gynecomastia in males is normal and generally goes away on its own. If “normal” is an answer choice, make really sure you don’t want to pick it.


 +0  (free120#15)

The scenario described is heart failure 2/2 mitral valve regurgitation. If we want to prove the regurg, we can confirm and grade it using an echo.


 +1  (free120#14)

This question is a little bit BS, in that there is nothing in the stem at all to make you infer this specifically. What the question is trying to ask is what factors cause malpractice suits in general. While professional incompetence is a cause, people love to discuss (and the boards love to test) poor physician communication and lack of empathy as root causes.

angelaq11  THANK YOU! here I was thinking I was the only one. I chose the incompetent physician xD

 +0  (free120#13)

Acetylcholine increases after drug X, which is the same we’d expect if drug X were a cholinesterase inhibitor.


 +0  (free120#12)

Vincristine (a mitosis inhibitor) frequently causes peripheral neuropathy, which can be severe and irreversible. Other fun associations are Bleomycin with pulmonary fibrosis, Cyclophosphamide and bladder cancer, and Doxorubicin with dilated cardiomyopathy.


 -1  (free120#11)

This is obviously a clinical trial. If you know you are getting a drug, then you are not blinded: it’s an open-label trial. There is no randomization as there is only a single treatment group.

charcot_bouchard  But they grouped them based on dosaged?
keyseph  I think the key thing here is that the participants were told what treatment they would be receiving. This is in line with an open-labeled clinical trial. Open-labeled clinical trials can still be randomized and do not need a control (as in this case).

 +0  (free120#10)

Carbamazepine is a notorious CYP450 inducer, so you should be guessing metabolism no matter what. CYP450 plays an important role in both vitamin D bioactivation and degradation in the liver.


 +0  (free120#9)

The effects of excess thyroid hormone: attempted compensatory TSH suppression, increase in both T4 and free T4, and normal TBG. Note that the question doesn’t even hinge on TBG and is also unlikely to on the real thing.

d_holles  When do we care about TBG?
zpatel  @d_holles in pregnancy.

 +1  (free120#8)

You will remember that G6PD deficiency causes red blood cells to break down in response to certain stressors, infections, and drugs. The patient’s symptoms are a manifestation of indirect hyperbilirubinemia due to hemolysis (RBC breakdown). Sulfa, fava beans, nitrofurantoin, isoniazid, and antimalarials (e.g. primaquine) are the common test favorites.

benwhite_dotcom  This question was updated. It is a now a case of bubonic plague (or possibly ulceroglandular Tularemia), both which are treated by aminoglycosides, which target the 30S ribosomal subunit.
wes79  do you happen to remmeber what the original question was? thx!
notachiropractor  treatment would be amino glycoside + tetracycline, double whammy on that 30s ribosomal subunit

 +0  (free120#7)

This is serum sickness, a type III (immune complex) hypersensitivity.


 +0  (free120#6)

Remember that transference is when the patient is transferring (redirecting) feelings about someone on to you (you remind them of their dad). Countertransference is when you do it about them (they remind you of your son). Projection is when you assign your own feelings to them (you are angry, so you think you they are angry).


 +1  (free120#5)

Codeine is a prodrug with basically no analgesic effects by itself. It instead must be metabolized (mostly by the liver via CYP2D6) into morphine in order to provide analgesia. Some folks convert more, some less.


 +0  (free120#4)

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.

 +0  (free120#3)

Diffuse low-level ST elevation means pericarditis. These patients often complain of pleuritic chest pain that is somewhat alleviated by sitting up and leaning forward and have distant heart sounds. Common test causes include viruses, uremia, and 2-3 weeks after myocardial infarction (Dressler syndrome).


 +0  (free120#2)

Androgens stimulate sebaceous glands and cause acne. In girls, this is primarily due to adrenarche (DHEA/DHEAS androgen production made by the adrenal gland the zona reticularis). Boys can also blame testosterone from gonadal puberty (pubarche).


 +0  (free120#1)

Statins raise HDL and decrease LDL and TGs. Their effect on LDL is by far the most potent, but they do a little good on everything.


 +0  (free120#40)

Anorexia leads to hypogonadotropic hypogonadism, as the body realizes that the possibility of nourishing a fetus is zero and gives up the pretense. There’s a lot of supporting data, but one should guess this answer once you read the word “gymnast” (or “dancer”).


 +0  (free120#39)

N. gonorrhea can change its pilus, which is responsible for adhesion to host cells and the main antigen to which the host mounts an immune response. Neisseria gonorrhoeae is able to switch out different pilin genes, and for this reason, prior infection does not confer long-lasting immunity.


 +0  (free120#38)

Metformin is awesome. It decreases hepatic glucose production, decreases intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization.


 +0  (free120#37)

The purpose of Rhogam is to bind to and remove the RhD antigens so that the mother does not form an immune response against the antigen in fetus’ blood. It’s given to at-risk Rh negative moms at 28 weeks and at delivery.


 +0  (free120#36)

A b2 agonist like the bronchodilator albuterol would sure help that wheezing. Note that epinephrine (such as in an epi-pen) would also achieve this but is nonselective; in this case, the patient’s symptoms would be helped most by the beta-2 component.


 +0  (free120#35)

He has (presumably RSV) bronchiolitis. RSV is an RNA virus that enters the cell via a fusion protein (which is the target of the prophylactic monoclonal antibody drug Palivizumab).


 +0  (free120#34)

Gram-positive rods in a diabetic foot wound (or a World War I soldier fighting in a trench) means Clostridium perfringens (the causative organism of gas gangrene). Crepitus means gas in the tissues, which is produced as a byproduct of its highly virulent alpha toxin.


 +1  (free120#33)

Fragile X is a CGG trinucleotide repeat expansion disorder (which like Huntington’s is a test favorite). The maternal uncle is the hint to the X-linked inheritance. Autism-like behaviors and relatively large head are common; large testicles only appear after puberty.


 +0  (free120#32)

von Willebrand disease is by far the most common inherited bleeding diathesis. Frequently, the only laboratory abnormality is increased bleeding time (literally you prick the patient and see how long it takes them to stop bleeding). On Step, bleeding women have VWD. Bleeding boys have hemophilia.


 +1  (free120#31)

Air and fluid = hydropneumothorax. If that fluid is blood (s/p stabbing), it’s a hemopneumothorax. Lack of mediastinal shift indicates that it’s not under tension.

d_holles  @benwhite_dotcom how can it not be under tension if air is entering the pleural cavity?
nwinkelmann  Because the stab wound isn't functioning like a flap, meaning the air can escape. The reason a tension pneumothorax occurs is because the wound acts as a flap, where on inspiration it is open and air enters, but on expiration is closes and traps the air.

 +0  (free120#30)

While E coli is normal gut flora, your body would prefer it stay intraluminal.


 +0  (free120#29)

The arrow is pointing to a neutrophil (multilobed nucleus): main fighter of the immune system in acute inflammation and bacterial infection (such as aspiration pneumonia). C5a is a chemotactic factor for PMNs.


 +0  (free120#28)

Approximate fasting physiology timing: the post-absorptive phase (6-24 hours after a meal) is dominated by glycogenolysis. Gluconeogenesis from 24 hours to 2 days. Then ketosis.


 +0  (free120#27)

The mom will pass on her deletion in 50%. The father will pass it on in 100% (because both of his copies are affected). Therefore, the child will automatically have at least one deletion and will have the double deletion in 50%.


 +0  (free120#26)

Crohn’s: skip lesions, fistulae, strictures (and the unnecessary transmural involvement on histology).


 +0  (free120#25)

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.


 +1  (free120#24)

p53 protein is the quintessential tumor suppressor (it activates apoptosis). HPV carcinogenesis is caused by insertion of the virus into host DNA that produces a protein which binds to an essential p53 substrate, functionally inactivating p53 and preventing its apoptotic cascade. Transactivation/TAX is how HIV and HTLV cause cancer. c-myc translocation causes Burkitt lymphoma.

claptain  Just to add to this, HPV can also inactivate Rb via E7 viral protein.

 +2  (free120#23)

Endemic Burkitt lymphoma can happen in Brazil as well as Africa (jaw lesion, puffy face). The photomicrograph is demonstrating tingible body macrophages, a type of macrophage containing many phagocytized, apoptotic cells in various states of degradation.


 +0  (free120#22)

Endothelial tight junctions’ permeability is increased in response to injury and inflammation, allowing migration of white blood cells and friends to the site of injury.


 +0  (free120#21)

Don’t let them blind you with this patient’s misery. The issue of the day is that he has a DVT. That’s why he came to the ER in the first sentence and what the ultrasound shows at the end. Patients with cancer are hypercoagulable.


 +0  (free120#20)

Note that the question is not asking what cells fight URIs. The question asks what lab finding would be consistent with decreased immune activity (and thus the only choice that matches “decreased” with an immune cell is the best answer).

sugaplum  So I read Lymphocyte as leukocyte (because cortisol probably) so that is what I put. but cortisol does increase levels of neutrophils floating around in the blood right, I was going for stress demarg. Can't tell if i am thinking too hard about this.

 +0  (free120#19)

Memorize aspirin’s unique acid-base effects: metabolic acidosis and respiratory alkalosis. Note, this is likely actual respiratory alkalosis, not simply normal respiratory compensation for metabolic acidosis.

mikerite  Based on the correct answer choice, the person is now in metabolic acidosis with respiratory compensation.
benwhite_dotcom  The correct answer choice is as listed above (all decreased). Note that whether metabolic acidosis is combined with primary respiratory alkalosis, which is an important teaching point I’ve argued the question writers are probably getting at, or even if just simple respiratory compensation for metabolic acidosis–both can have the same arrows. In this case, it’s not respiratory compensation. In ASA overdose, the respiratory alkalosis actually happens first. Ultimately, the metabolic acidosis dominates and the pH is almost always low. This mixed primary acid/base response to ASA toxicity is highly testable.
ali  How long till the respiratory alkalosis turns into a metabolic/mixed picture?
benwhite_dotcom  @ali 12 hours is a good number to memorize but it can definitely happen much earlier.
yoav  From what I understand, the metabolic acidosis only presents 12h post ingestion, while she is only 3h. What do you think?
benwhite_dotcom  @yoav, It can definitely happen earlier. It’s more of a by 12 hours (not only beginning then).
angelaq11  I'm beginning to think that they don't actually care about how many hours lapse after the ingestion, but if we actually know the unique acid-base disturbance. I chose the wrong one, again because I was foolishly thinking about those 12 hours postintoxication
charcot_bouchard  I think this is good rule of thmb in USMLE "a Right answer may or may not tick all the correct things but will NEVER have a wrong thing in it". So the ans choice we all chose has Bicarb inc. But this will never happen. at 3 hour we should have pure resp alkalosis with normal bicarb (as per uw). Or in this case decreased due to neutralization by organic salicylic acid. In Aspirin poisoning bicarb will nver increase.
elasaf@post.bgu.ac.il  Another important point- they probably gave her RR (30) to indicate that she is hyperventilating==> LOW CO2

 +0  (free120#18)

Bisphosphonates work by decreasing osteoclast activity (thereby reducing bone resorption). “Increased receptor activation of NFkB ligand (RANKL) production” is the opposite of how estrogen therapy works (RANKL is found on osteoblasts, and its activation triggers osteoclasts and stimulates bone resorption).


 +0  (free120#17)

Sensitivity rules things out. It’s TP / (TP + FN). So in order to calculate the sensitivity of this test, we need the true positives (the 90 with cancer) and the false negatives: the patients for whom the test is negative but actually do have prostate cancer.


 +0  (free120#16)

Pulmonary fibrosis (a restrictive pattern disease) is a major cause of mortality for patients with scleroderma. Logically, if the disease causes fibrosis elsewhere, it’s going to cause fibrosis in the lungs.


 +0  (free120#15)

Leydig cells make testosterone. Leydig cell tumors aren’t always physiological active, but those that are can cause masculinization. Granulosa cell tumors, on the other hand, sometimes produce estrogen (which can lead to precocious puberty in young girls but otherwise may be occult). Teratomas are oddballs that typically have fat, hair, teeth, etc. Thecomas will not be on your test. Ovarian carcinoid is highly unlikely to show up on your test, but if it did, it would likely present with a classic carcinoid syndrome.

sugaplum  FA 2019 page 632

 +0  (free120#14)

The “migratory serpiginous perianal rash” (ick) is classic for strongyloides, a parasitic roundworm acquired from larvae-contaminated soil. Strongyloides larvae can borrow (hence the rash) and can migrate to the GI tract and lay their eggs, which then hatch in the intestine and cause diarrhea. Treatment is Ivermectin (and if not, mebendazole/albendazole). Checking the stools for larvae is the most sensitive test. Parasite life cycles are gross.

benwhite_dotcom  As an addendum, I believe this is larva currens (https://en.wikipedia.org/wiki/Larva_currens) in the setting of strongyloides infection and not Cutaneous larva migrans. Strongyloides, unlike CLM, explains the diarrhea, weight loss, and not just the eosinophilia. CLM is generally limited to the skin and typically appears first in hands or feet (whatever touches soil) with perianal involvement being significantly less common. Stool studies are unnecessary in CLM, which is primarily a clinical diagnosis. The other information in the stem is there for a reason. See this nice comparison page: https://www.derm101.com/therapeutic/cutaneous-larva-migrans-larva-currens/introduction/

 +0  (free120#13)

The Pouch of Douglas is the space between the uterus and the rectum (i.e. the place where pelvic free fluid goes).


 +0  (free120#12)

PCP is a sedative-hypnotic and dissociative anesthetic that generally acts as a downer but can also cause incredible aggression coupled with pain insensitivity (the superman drug). Vertical nystagmus is a commonly mentioned physical exam finding.


 +1  (free120#11)

The baroreceptors are stretch receptors (the more fluid in the vessel, the more they fire). So a patient with hemorrhagic shock will see a decrease in the baroreceptor firing rate. Activation of RAAS will result in increased vascular resistance (vasoconstriction) in order to maintain blood pressure. And capillaries, such as those in the kidney, will be primed for resorption and not filtration (no one wants to pee out good dilute urine when they’re dehydrated). Likewise, systemic capillaries will prefer to hold onto plasma and not let it leak into the interstitium (third-spacing).


 +0  (free120#10)

Total peripheral resistance goes down during exercise as the arterioles supplying muscle and skin dilate.


 +1  (free120#9)

Southern blots are commonly used in immunological studies, as the southern blot allows for the study of DNA alterations. What is normally one gene configuration related to immune globulins in most tissues demonstrates multiple different bands in the bone marrow, indicative of gene rearrangement. This is basically how we create new antibodies. Reactive processes are polyclonal (multiple bands); leukemia, in contrast, is monoclonal (single band).

ali  I still don’t understand this one. Could you provide a better explanation?
benwhite_dotcom  The cDNA tag is tagging a constant region common to immunoglobulins, so it normally only finds the one band corresponding to that particular gene (the bands travel different amounts due to their differing size/weight). In the bone marrow sample, that gene has rearranged itself, so the cDNA clone instead tags multiple different genes that are of different sizes on the gel (each one has that same constant region the cDNA is tagging, but with different stuff around it such that the restriction enzyme has cut it up differently). I’d be happy for someone to step in and do a better job on that explanation.

 +0  (free120#8)

The left-sided system is much higher pressure than the right side, hence the aortic valve closing is usually louder than the pulmonic valve. A P2 louder than A2 means that the pulmonary arterial pressure is significantly elevated.


 +0  (free120#7)

Filgrastim is a granulocyte colony stimulating factor (GCSF), which are drugs used to increase white blood cell count in patients with leukopenia. Leucovorin (folinic acid) sounds like it would also be right, but it’s used to prevent bone marrow suppression in patients taking methotrexate. Darbepoetin (like erythropoietin) is used to stimulate red blood cell production.


 +1  (free120#6)

Pseudogout is caused by positively-birefringent rhomboid calcium pyrophosphate crystal deposition. Most commonly affected location is the knee. Contrast with gout, negatively birefringent, big toe. A differential for both to keep in mind is septic arthritis.


 +0  (free120#5)

VEGF is a major tissue growth factor activated by injury, cytokine release (infection, inflammation) and hypoxia that promotes angiogenesis and also increases vascular permeability (hence the edema). This increased permeability aids in the movement of proteins and white blood cells to the site of injury.


 +0  (free120#4)

And the answer is, acting out aka “being a teenager.”


 +0  (free120#3)

Hot tub folliculitis, it’s a thing. Classically pseudomonas.


 +1  (free120#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).





Subcomments ...

The “migratory serpiginous perianal rash” (ick) is classic for strongyloides, a parasitic roundworm acquired from larvae-contaminated soil. Strongyloides larvae can borrow (hence the rash) and can migrate to the GI tract and lay their eggs, which then hatch in the intestine and cause diarrhea. Treatment is Ivermectin (and if not, mebendazole/albendazole). Checking the stools for larvae is the most sensitive test. Parasite life cycles are gross.

benwhite_dotcom  As an addendum, I believe this is larva currens (https://en.wikipedia.org/wiki/Larva_currens) in the setting of strongyloides infection and not Cutaneous larva migrans. Strongyloides, unlike CLM, explains the diarrhea, weight loss, and not just the eosinophilia. CLM is generally limited to the skin and typically appears first in hands or feet (whatever touches soil) with perianal involvement being significantly less common. Stool studies are unnecessary in CLM, which is primarily a clinical diagnosis. The other information in the stem is there for a reason. See this nice comparison page: https://www.derm101.com/therapeutic/cutaneous-larva-migrans-larva-currens/introduction/ +  


Blood at the meatus is the red flag (see what I did there?) for urethral injury, which should be evaluated for with a retrograde urethrogram. The membranous the most commonly injured by fracture. In contrast, the spongy urethra is most likely to be injured during traumatic catheter insertion or in a straddle injury.

canyon_run  Should we just assume that a pelvic fracture implies a membranous urethral injury? I was between membranous and spongy and I ended up choosing spongy because of the perineal bruising and fact that the patient was riding a motorcycle (and therefore susceptible to straddle injury). +  
benwhite_dotcom  Yes. You should think of spongy as the penile urethra, hence the predisposition to catheter-related trauma. +2  


submitted by canyon_run(0),

I can’t seem to find a similar image online that describes exactly what the other areas are covering. Any help?

benwhite_dotcom  See this image (Fig.6) from https://teachmeanatomy.info/neuro/brainstem/medulla-oblongata/ A and D, for example, would reflect lesions that cause what is called lateral medullary syndrome (Wallenberg syndrome). +  
canyon_run  Thank you! Would E then be the inferior vestibular nucleus based on that linked image? Also, is hypoglossal involved in the stem because of damage to the nerve fibers themselves rather than the nucleus? +  
benwhite_dotcom  I think the level in the teachmeanatomy link is a bit off from the NBME image. I assume the NBME is showing E as the hypoglossal nucleus (https://en.wikipedia.org/wiki/Hypoglossal_nucleus). Yes, it’s the fibers. The nucleus is ventral. +  


submitted by canyon_run(0),

I can’t seem to find a similar image online that describes exactly what the other areas are covering. Any help?

benwhite_dotcom  See this image (Fig.6) from https://teachmeanatomy.info/neuro/brainstem/medulla-oblongata/ A and D, for example, would reflect lesions that cause what is called lateral medullary syndrome (Wallenberg syndrome). +  
canyon_run  Thank you! Would E then be the inferior vestibular nucleus based on that linked image? Also, is hypoglossal involved in the stem because of damage to the nerve fibers themselves rather than the nucleus? +  
benwhite_dotcom  I think the level in the teachmeanatomy link is a bit off from the NBME image. I assume the NBME is showing E as the hypoglossal nucleus (https://en.wikipedia.org/wiki/Hypoglossal_nucleus). Yes, it’s the fibers. The nucleus is ventral. +  


submitted by canyon_run(0),

why is the platelet aggregation test is normal in VWD? my problem is that Gp1b and VWfactor have to interact to induce a confirmational change in platelets to release ADP –> ADP binds to adp-receptor and induces Gp2b/3a which enables aggregation via fibrinogen. which would lead to abnormal aggregation? and is the ristocetin assay not a platelet aggregation test? or can it sometimes be normal and sometimes not?

benwhite_dotcom  It can be abnormal as well, depends on the subtype and severity (the wikipedia page does a decent job explaining). The most common subtype of VWD is a quantitative defect, which is often mild/nearly clinically occult and can have essentially normal laboratory testing. This is one of those questions where the labs are really there to exclude the other choices. +1  


The only thing that directly raises BP of the list is increased PVR.

amedhead  would decreased cardiac output not also increase the blood pressure due to sympathetic activation of the baroreceptor reflex? +  
benwhite_dotcom  I think you’re ignoring a directly correct answer, increased PVR literally equals increased BP, and are instead trying to postulate an indirectly plausible answer. Decreased CO, as you just implied, means less blood pumping into the aorta and less blood pounding and stretching the arteries and thus decreased BP. Note, your original logic would apply to stroke volume just as easily. Yes, a sympathetic response could then occur as a response to mitigate this, such as in shock or heart failure, but it would misleading to suggest that decreased CO causes hypertension. +  


submitted by ashmash(1),

Why can’t we assume that the patient with an elevated direct bilirubin does not have some sort of obstruction where the alkaline phosphatase would be elevated (or even dubin johnson syndrome)? I didn’t think of Gilbert disease despite the intermittent course because I tend to look at direct and total bilirubin levels first to see if the direct bilirubin is elevated which in this case was elevated.

benwhite_dotcom  Few things. History always comes first. She also has even more indirect bili than direct. There’s also no other indication of obstruction clinically (such as pruritis), and you can’t infer an elevated lab value (alk phos) and rely on that in order to have everything come together. They have to give it to you. +3  
morelife  I saw this question on Gilbert’s and also put down increased ALP. I noticed the relapsing-remitting history. However, my thoughts were that a direct bilirubinemia is a false finding in Gilberts (since it is due to lower UDP enzyme activity), and would more likely indicate obstruction. As you said, you would consciously neglect this finding in favor of the history? For these specific NBME style questions -- you know, the wishy/washy ones -- would you follow the principle of “history first”? +  
benwhite_dotcom  @morelife, Plethora of evidence first. Here everything points in one direction except one small detail. If you were to make a list of pro/cons for each diagnosis using history, physical and objective data (labs, imaging, etc), the scales usually tip firmly in one direction. +1  
wowo  also, unless I'm mistaken, it's not a direct bilirubinemia - tbili is 3 and direct is 1, so unconjugated is 2. They're both elevated. Even with a decrease in function of the enzyme, it still works, so if unconj bili increases, you'll get somewhat of an increase of conjugated bili +  


submitted by ashmash(1),

Why can’t we assume that the patient with an elevated direct bilirubin does not have some sort of obstruction where the alkaline phosphatase would be elevated (or even dubin johnson syndrome)? I didn’t think of Gilbert disease despite the intermittent course because I tend to look at direct and total bilirubin levels first to see if the direct bilirubin is elevated which in this case was elevated.

benwhite_dotcom  Few things. History always comes first. She also has even more indirect bili than direct. There’s also no other indication of obstruction clinically (such as pruritis), and you can’t infer an elevated lab value (alk phos) and rely on that in order to have everything come together. They have to give it to you. +3  
morelife  I saw this question on Gilbert’s and also put down increased ALP. I noticed the relapsing-remitting history. However, my thoughts were that a direct bilirubinemia is a false finding in Gilberts (since it is due to lower UDP enzyme activity), and would more likely indicate obstruction. As you said, you would consciously neglect this finding in favor of the history? For these specific NBME style questions -- you know, the wishy/washy ones -- would you follow the principle of “history first”? +  
benwhite_dotcom  @morelife, Plethora of evidence first. Here everything points in one direction except one small detail. If you were to make a list of pro/cons for each diagnosis using history, physical and objective data (labs, imaging, etc), the scales usually tip firmly in one direction. +1  
wowo  also, unless I'm mistaken, it's not a direct bilirubinemia - tbili is 3 and direct is 1, so unconjugated is 2. They're both elevated. Even with a decrease in function of the enzyme, it still works, so if unconj bili increases, you'll get somewhat of an increase of conjugated bili +  


Memorize aspirin’s unique acid-base effects: metabolic acidosis and respiratory alkalosis. Note, this is likely actual respiratory alkalosis, not simply normal respiratory compensation for metabolic acidosis.

mikerite  Based on the correct answer choice, the person is now in metabolic acidosis with respiratory compensation. +1  
benwhite_dotcom  The correct answer choice is as listed above (all decreased). Note that whether metabolic acidosis is combined with primary respiratory alkalosis, which is an important teaching point I’ve argued the question writers are probably getting at, or even if just simple respiratory compensation for metabolic acidosis–both can have the same arrows. In this case, it’s not respiratory compensation. In ASA overdose, the respiratory alkalosis actually happens first. Ultimately, the metabolic acidosis dominates and the pH is almost always low. This mixed primary acid/base response to ASA toxicity is highly testable. +1  
ali  How long till the respiratory alkalosis turns into a metabolic/mixed picture? +  
benwhite_dotcom  @ali 12 hours is a good number to memorize but it can definitely happen much earlier. +  
yoav  From what I understand, the metabolic acidosis only presents 12h post ingestion, while she is only 3h. What do you think? +  
benwhite_dotcom  @yoav, It can definitely happen earlier. It’s more of a by 12 hours (not only beginning then). +  
angelaq11  I'm beginning to think that they don't actually care about how many hours lapse after the ingestion, but if we actually know the unique acid-base disturbance. I chose the wrong one, again because I was foolishly thinking about those 12 hours postintoxication +  
charcot_bouchard  I think this is good rule of thmb in USMLE "a Right answer may or may not tick all the correct things but will NEVER have a wrong thing in it". So the ans choice we all chose has Bicarb inc. But this will never happen. at 3 hour we should have pure resp alkalosis with normal bicarb (as per uw). Or in this case decreased due to neutralization by organic salicylic acid. In Aspirin poisoning bicarb will nver increase. +  
elasaf@post.bgu.ac.il  Another important point- they probably gave her RR (30) to indicate that she is hyperventilating==> LOW CO2 +  


Memorize aspirin’s unique acid-base effects: metabolic acidosis and respiratory alkalosis. Note, this is likely actual respiratory alkalosis, not simply normal respiratory compensation for metabolic acidosis.

mikerite  Based on the correct answer choice, the person is now in metabolic acidosis with respiratory compensation. +1  
benwhite_dotcom  The correct answer choice is as listed above (all decreased). Note that whether metabolic acidosis is combined with primary respiratory alkalosis, which is an important teaching point I’ve argued the question writers are probably getting at, or even if just simple respiratory compensation for metabolic acidosis–both can have the same arrows. In this case, it’s not respiratory compensation. In ASA overdose, the respiratory alkalosis actually happens first. Ultimately, the metabolic acidosis dominates and the pH is almost always low. This mixed primary acid/base response to ASA toxicity is highly testable. +1  
ali  How long till the respiratory alkalosis turns into a metabolic/mixed picture? +  
benwhite_dotcom  @ali 12 hours is a good number to memorize but it can definitely happen much earlier. +  
yoav  From what I understand, the metabolic acidosis only presents 12h post ingestion, while she is only 3h. What do you think? +  
benwhite_dotcom  @yoav, It can definitely happen earlier. It’s more of a by 12 hours (not only beginning then). +  
angelaq11  I'm beginning to think that they don't actually care about how many hours lapse after the ingestion, but if we actually know the unique acid-base disturbance. I chose the wrong one, again because I was foolishly thinking about those 12 hours postintoxication +  
charcot_bouchard  I think this is good rule of thmb in USMLE "a Right answer may or may not tick all the correct things but will NEVER have a wrong thing in it". So the ans choice we all chose has Bicarb inc. But this will never happen. at 3 hour we should have pure resp alkalosis with normal bicarb (as per uw). Or in this case decreased due to neutralization by organic salicylic acid. In Aspirin poisoning bicarb will nver increase. +  
elasaf@post.bgu.ac.il  Another important point- they probably gave her RR (30) to indicate that she is hyperventilating==> LOW CO2 +  


Memorize aspirin’s unique acid-base effects: metabolic acidosis and respiratory alkalosis. Note, this is likely actual respiratory alkalosis, not simply normal respiratory compensation for metabolic acidosis.

mikerite  Based on the correct answer choice, the person is now in metabolic acidosis with respiratory compensation. +1  
benwhite_dotcom  The correct answer choice is as listed above (all decreased). Note that whether metabolic acidosis is combined with primary respiratory alkalosis, which is an important teaching point I’ve argued the question writers are probably getting at, or even if just simple respiratory compensation for metabolic acidosis–both can have the same arrows. In this case, it’s not respiratory compensation. In ASA overdose, the respiratory alkalosis actually happens first. Ultimately, the metabolic acidosis dominates and the pH is almost always low. This mixed primary acid/base response to ASA toxicity is highly testable. +1  
ali  How long till the respiratory alkalosis turns into a metabolic/mixed picture? +  
benwhite_dotcom  @ali 12 hours is a good number to memorize but it can definitely happen much earlier. +  
yoav  From what I understand, the metabolic acidosis only presents 12h post ingestion, while she is only 3h. What do you think? +  
benwhite_dotcom  @yoav, It can definitely happen earlier. It’s more of a by 12 hours (not only beginning then). +  
angelaq11  I'm beginning to think that they don't actually care about how many hours lapse after the ingestion, but if we actually know the unique acid-base disturbance. I chose the wrong one, again because I was foolishly thinking about those 12 hours postintoxication +  
charcot_bouchard  I think this is good rule of thmb in USMLE "a Right answer may or may not tick all the correct things but will NEVER have a wrong thing in it". So the ans choice we all chose has Bicarb inc. But this will never happen. at 3 hour we should have pure resp alkalosis with normal bicarb (as per uw). Or in this case decreased due to neutralization by organic salicylic acid. In Aspirin poisoning bicarb will nver increase. +  
elasaf@post.bgu.ac.il  Another important point- they probably gave her RR (30) to indicate that she is hyperventilating==> LOW CO2 +  


Southern blots are commonly used in immunological studies, as the southern blot allows for the study of DNA alterations. What is normally one gene configuration related to immune globulins in most tissues demonstrates multiple different bands in the bone marrow, indicative of gene rearrangement. This is basically how we create new antibodies. Reactive processes are polyclonal (multiple bands); leukemia, in contrast, is monoclonal (single band).

ali  I still don’t understand this one. Could you provide a better explanation? +  
benwhite_dotcom  The cDNA tag is tagging a constant region common to immunoglobulins, so it normally only finds the one band corresponding to that particular gene (the bands travel different amounts due to their differing size/weight). In the bone marrow sample, that gene has rearranged itself, so the cDNA clone instead tags multiple different genes that are of different sizes on the gel (each one has that same constant region the cDNA is tagging, but with different stuff around it such that the restriction enzyme has cut it up differently). I’d be happy for someone to step in and do a better job on that explanation. +1  


You will remember that G6PD deficiency causes red blood cells to break down in response to certain stressors, infections, and drugs. The patient’s symptoms are a manifestation of indirect hyperbilirubinemia due to hemolysis (RBC breakdown). Sulfa, fava beans, nitrofurantoin, isoniazid, and antimalarials (e.g. primaquine) are the common test favorites.

benwhite_dotcom  This question was updated. It is a now a case of bubonic plague (or possibly ulceroglandular Tularemia), both which are treated by aminoglycosides, which target the 30S ribosomal subunit. +3  
wes79  do you happen to remmeber what the original question was? thx! +  
notachiropractor  treatment would be amino glycoside + tetracycline, double whammy on that 30s ribosomal subunit +