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 +2  (familymed1#4)

Pt is an 11 yo M, 2 days of nasal congestion and sore throat. Coughing and sneezing productive of green mucus. There is postnasal drainage of copious yellow-green mucus, and enlarged tonsils.

This patient has a head cold, with postnasal drip that is causing his cough. Antiviral therapy (E) is not directed against the Rhinovirus. The patient does not show signs of bacterial infection which would require antibiotic therapy (F), namely tympanic membrane bulging and ear pain. There is no fever to indicate sever infection or sinus tenderness to indicate an X-ray of the sinuses is warranted (D), or that culture of discharge would change current treatment (C). Because this infection is self-limited and the child can blow their nose, sinus lavage in the clinic is not necessary. (B).

 +4  (nbme23#41)

Wouldn't total AV nodal ablation destroy to autorhythmicity of the pacemaker? That would mean that below the AV node the rhythm would be provided by a ventricular foci, and those usually create wide QRS complexes.

haliburton  that was my reasoning as well. guess not.
yotsubato  Shitty NBME grammar strikes again.
charcot_bouchard  No. No guys. Bundle of his located below AV node and it can generate impulse. it calls junction escape rhythm and narrow complex. Below this is purkinje, bundle branch & ventricular muscle. those are wide complex
abhishek021196  Third-degree (complete) AV block The atria and ventricles beat independently of each other. P waves and QRS complexes not rhythmically associated. Atrial rate > ventricular rate. Usually treated with pacemaker. Can be caused by Lym3 disease

 +6  (nbme23#11)

Male pattern baldness./androgenic alopecia is caused by the effects of dihydrotestosterone (DHT) on the skin of the scalp. Testosterone is converted by the enzyme 5-alpha-reductase into DHT. Finasterideis a 5-a-reductase inhibitor, and so blocks the production of DHT and can halt or even cause some reversal of make pattern baldness. However this same activity may also result in signficant sexual side effects including gynecomastia, erectile dysfunction, ejaculatory dysfunction, and decreased libido.

A) Danazol- a weak androgen with antiestrogenic effects, used in the treatment of endometriosis and fibrocystic breast disease. C) Methyltestosterone- synthetic T, it is used to supplement in testosterone deficiency, or in the treatment of some breast cancers. D) Oxandrolone- an anabolic steroid used to regain weight. E) Stanozolol- another anabolic steroid, with potential used for hereditary angioedema.

sajaqua1  I am embarrassed by these typos.
drdoom  lol

 +6  (nbme23#25)

The patient exhibits memory loss and cognitive impairment with gradual onset. Alzheimer's disease is likely. Acetylcholine activity is down in Alzheimer's, so ACh-esterase inhibitors are used to make ACh more available, stopping some of the effects of Alzheimer's. Donepezil is an ACh-esterase inhibitor.


A) Co-Q- a factor in mitochondrial OxPhos, it is also an antioxidant. It is used as a dietary supplement, and is not FDA approed for the treatment of anything. C) Riluzole- a glutamate antagonist used to prevent excitotoxicity in ALS patients. D) Selegiline- Selective MAO-B inhibitor that may be used in the treatment of Parkinson's, although I believe other treatments are preferred these days. E) Zinc- important cofactor in many reactions including transcription factors (zinc fingers) and in wound healing.

 +2  (nbme23#2)

Gynecomastia, spider angiomata, and hypogonadism (as well as palmar erythema) are all signs of excess estrogen. The liver in patients with hepatic disease is impaired and so cannot clear estrogen sufficiently. Six 12 oz beers daily (72 oz, or half a gallon) is too much, and is destroying his liver.

uslme123  No hepatosplenomegaly, ascites, or edema through me off. We that being said, I shied away from cirrhosis. I thought that he showed signed of depression, so I went with the thyroid. But who's to say he isn't injection anabolic steroids?!
catch-22  The principle is you can get liver dysfunction without having HSM, ascites, etc. Liver disease is on a progressive spectrum.
notadoctor  He likely has hepatitis B/C given his history of intravenous drug use. I believe both can have liver dysfunction but may or may not have ascites, whereas the type of damage we would expect from alcohol that would match this presentation would also show ascites.
charcot_bouchard  For Ascities u need to have portal HTN. Thats a must. (unless exudative cause like Malignancy)
paulkarr  For anyone who needs it; the FA photo is kinda burned into my mind for these questions. NBME has some weird infatuation with this clinical presentation.. FA (2019) Pg: 383 "Cirrhosis and Portal HTN".
snripper  @paulkarr the problem was that the FA image was burned into my mind so without no ascites or edema threw me off of cirrhosis.
tyrionwill  cirrhosis doesn't present hepatomegaly, instead, the liver could be shrunken.

 +11  (nbme23#38)

The marrow shows precursors to erythrocytes, as well as megakaryocytes. This is to show you that the issue isn't underproduction, which means that we are losing RBC and platelets somewhere ie destruction. That rules out D and E. There is nothing to indicate tha the child has disseminated tuberculosis (B). At this point we are left with A or C. A would indicate Disseminated Intravascular Coagulation (DIC) or something similar, which would result in low platelets and RBC but we would also see abnormal RBC like schistocytes ("helmet" cells). We are explicitly told that the erythrocytes are normochromic and normocytic. However, immune destruction of platelets explains it all- the destruction of platelets leads to some hemorrhaging and so a drop in RBC, and ITP classically arises after a recent upper respiratory tract viral infection.

meningitis  Just in case anyone is wondering like I did, the low platelet count explains thethose multinucleated cells. They are Megakaryocytes in Bone Marrow Biopsy.
nwinkelmann  Also, don't forget that autoimmune thrombocytopenia purpura has 2 demographics: young kids, which generally resolves spontaneously fairly quickly, and then young adult females which is a true autoimmune condition that doesn't resolve. Patient's age + thrombocytopenia + essentially normal rest of heme pannel = autoimmune thrombocytopenia purprua in child.
abhishek021196  That is exactly how I approached this question. Normal heme panel and a decreased Platelet count in a young boy after an infection just made me intuitively select ITP.

 +8  (nbme23#37)

A standard deviation is a measure of probability in resembling the average. One standard deviation on a bell curve distribution creates a 67% chance that the answer will lie in there. Two standard deviations will create a 95% chance. Three standard deviations creates a 99.7% chance.

This patient has an average of 113, and a 95% confidence at 110-116 means that the SD is 1.5 . So one additional SD would give us a range of 108.5-117.5, rounded to 108-118.

usmleuser007  How did you get the SD to be 1.5?
usmleuser007  NVM Got it
jesusisking  You wouldn't use Standard error with Confidence Interval? (pg. 262 FA 2019)

 +5  (nbme23#32)

The macula densa of the nephron helps maintain tubular flow by adjusting dilation of the afferent arteriole of the nephron. When salt is low, its COX enzymes synthesize PGI2 which dilate the afferent arteriole. NSAIDs inhibit COX, blocking synthesis of PGI2 and so indirectly inhibiting afferent arteriole dilation. Two weeks ago our patient was put on ibuprofen, a non-selective COX inhibitor. This lead to all these effects, shutting off blood supply to the nephrons, creating an artifically induced drop in blood flow that looks has elevated BUN and creatinine, but maintains the 15:1 ratio.


 +6  (nbme23#14)

Duodenal atresia is frequently associated with Down syndrome, and is caused when the duodenum fails to recanalize during development. The infant presents with bilious vomiting, so we know that food is at least making it down to the duodenum where the pancreatic duct empties into the duodenum. This eliminates D (would present with nonbilious vomiting, typically a few weeks after birth) and E (would present with choking and vomiting immediately on feeding).

The presence of bile tells us that bile is getting to the duodenum, so extrahepatic biliary atresia does not seem possible (B). There is nothing to indicate that the child has an omphalocele (C) since the abdomen is distended with food that isn't passing, but the guts are still inside the abdominal cavity.

 +5  (nbme23#43)

In an elderly patient with isolated elevated alkaline phosphatase (normal serum calcium and phosphate) Paget's disease of bone should be at the top of the differential. This disease is due to dysregulation of osteoclastic and osteoblastic activity; first an initial osteoclast hyperactivity phase, then increased osteoblast activity for a mixture, then osteoclasts "burnout" leading to over-mineralization and sclerotic bone plaques. In addition, this can create arteriovenous shunts in the bones which decreases resistance, leading to high output cardiac failure (a similar problem can arise in arteriovenous fistulas from blood dialysis). On histology it will have a "mosaic" pattern.

A)- Aneurysmal bone cyst- largely a product of hyperactivity of osteoclasts, this occurs more often in the limbs, and shows a cystic space with balloon-like dilation. B) Angiosarcoma- angiosarcoma of the bone is n almost purely lytic lesion. They occur more frequently in younger people. C) Niacin deficiency- I can find nothing about vitaminb B3 deficiency involving bones. B3 deficienct results in pellagra, with the classic Three D's- dermatitis (rash necklace on C3/C4 dermatome), dementia, and diarrhea. E) Osteosarcoma- Found almost exclusively in younger people, this bone growth occurs at the growth plate, particularly at the proximal end of the tibia, distal end of the femur, or proximal end of the humerus (in the long bones around your knees or at your shoulders). It shows a large, solid growing mass that may raise the periosteum in a sunburst pattern/Codman's triangle. F) Prostatic carcinoma- rare for being one of, if not the only metastatic bone cancer that is purely osteoblastic.

alexb  Great explanation, except that there was a question in NBME 22 in which the prostatic carcinoma was osteolytic. One of the commenters here looked it up and apparently it's like that 30% of the time or something. So I guess you would have to use the high output HF, normal Ca, high ALP, and mosaic pattern to "play odds" as Goljan would say.
qball  At least they were nice enough to put Paget disease because I had no idea what osteitis deformans is.
drzed  USMLE seems to be moving away from using eponymous names... so it's a good idea to see if there is a descriptive name for diseases. For example, they don't use the word "Wegener" anymore if you have noticed, since it turns out that guy was a nazi. So now they call it by what it is -- granulomatosis with polyangitis.

 +3  (nbme23#36)

Serum sickness is a Type 3 hypersensitivity reaction, in which the body responds to antigenic medical substances and produces antibodies. These antibodies in circulation then bind to the antigenic drugs and set off the complement cascade. Rheumatoid arthritis is also a Type 3 hypersensitivity reaction.

A) Apoptosis of macrophages- apoptosis is generally not a type of hypersensitivity reaction. B) Mast cel degranulation- this is part of a Type 1 hypersensitivity reaction/anaphylaxis, in which mast cells bind IgE on their surface, and IgE binding to the target antigen induces a conformational change in the IgE that sets off mast cell degranulation. C) Natural Killer Cell killing- plays a variety of roles, including cancer suppression and destruction of virally infected cells. If they play a role in hypersensitivity, it is part of Type 2 HSR in which they would respond to Ig on the cell surface. E) Wheel and flare reactions- This is also a Type 1 HSR.

meningitis  I didn't pick this one because I thought Serum sickness was too systemic and RA was a more localized Type 3. Again, im overthinking things.
youssefa  Goljan: RA is a mixed type III and type IV immune reaction
dinagohe23  I though NK cell killing was similar to T cell so and RA is also Type IV
nephcard  ,blll sdouof

 +7  (nbme24#11)

Primary prevention is an active step taken to head off or mitigate a disease- think of vaccinations. In this case, it is lifestyle modification (exercise) to help 30-40 year old women (weight bearing exercise can mitigate osteoporosis, benefits of aerobic exercise).

Seconday prevention is early detection of a disease, promoting early intervention. This could inclue things like HIV testing every 6 months, or or annual mammography.

Tertiary intervention is therapy aiming at reducing complications, allowing relapse, or improving function. Abstinence from alcohol may be here because of substance abuse problems, or because some damage previously done by alcohol cannot be prevented. Similarly for a low carbohydrate diet we may be mitigating the effects on metabolism that have already been done.

sunshinesweetheart  p 269 FA 2019

 +5  (nbme24#22)

The keys to this answer are that it is fairly sudden in onset, and migrates. None of the other answers could explain the movement of pain from flank to LLQ to scrotum. While the kidney stone does not actually enter the scrotum, the pain can be referred to the testicles.

 +13  (nbme24#20)

Vibrio cholera and V. parahaemolyticus are frequently associated with consumption of undercooked seafood like shellfish. V. vulnificus is associated with brackish water or saltwater.

A) B. cereus- vignettes tend to associate this with reheated rice at a buffet, vomiting is more common than diarrhea. B) C. jejuni- associated with undercooked food, especially chicken, or can be contracted by contact with animals. It causes inflammatory, bloody diarrhea, and may also lead to Guillan-Barre syndrome. C) C. perfringens- as a sporulator, this is associated with good that is reheated then left to germinate at room temperature for a long time before consumption. Symptoms include vomiting and diarrhea. D) S. aureus- a heat stable toxin produced by S. aureus is associated with rapid onset of vomiting, may be accompanied by diarrhea. Most often associated with dairy products and meat.

 +11  (nbme24#44)

This answer rests on the difference between Folate and Leucovorin. Intrathecal methotrexate is given to block dihydrofolate reductase (DHFR) from making folic acid into DHF, and then turning that DHF into THF. This is done to prevent the production of downstreamn products necessary for metabolism including DNA synthesis. Leucovorin (also called 5-formy-lTHF) can be used to sidestep this product by being put into play downstream. See the diagram here: https://www.emed.com.au/folic-acid-and-fertility-doing-more-harm-than-good/ Folate is listed as Folic Acid, methotrexate interferes with DHFR, and Leucovorin is 5-formyl-THF. There is also further description here: https://www.drugbank.ca/drugs/DB00158

Why does this not simply undo the action of methotrexate? This is because many cancers do not have the reduced folate carrier. So the cancers pick up folate and methotrexate, and their DNA synthesis is reduced. Meanwhile other healthy cells can pick up the Leucovorin and stave off some of the worst effects. Remember, leucovorin cannot be given intrathecally.


 +13  (nbme23#3)

Because the baby's mother has Type 1 Diabetes mellitus, it is plausible that they had elevated blood glucose levels during or shortly before birth. Insulin does not cross the placenta, but glucose does, so during birth the neonate would have been hyperglycemic. This would lead to the neonatal pancreas releasing insulin, driving glucose into cells and turning down gluconeogenesis; this is why the baby is hypoglycemic right now.

B) Decreased glycogen concentration- I don't know the glycogen concentration compared to an adult patient, but a decrease in glycogen concentration would indicate glycogen/glucose release, which would not be a hypoglycemic state. C) Decreased glycogen synthase activity- decreased glycogen synthase activity indicates energy catabolism, and would lead to higher serum glucose levels. D) Decreased serum insulin concentration- decreased serum insulin would lead to higher levels of glucose in serum. E) Increased serum insulin-like growth factor- IGF does not bind nearly as well to insulin receptors as insulin does, and so would have to be in extremely high concentrations to have this effect. IGF is associated with somatic growth and muscle development.

yotsubato  His glycogen concentration is high, since he's been hyperglycemic with lots of insulin until birth.
alexb  Also explains why he's 12 pounds.
krewfoo99  Also, think of it like this: Insulin causes hypoglycemia, thus this baby must have increased insulin. It is also an anaobolic hormone which is clear by the babys weight. Insulin increases glycogen synthase activity, and causes an increase in concentrations of glycogen. Decrease in insulin would do exactly the opposite
tyrionwill  fetus of a mom with DM will develop pancreatic beta cell hyperplasia, which leads to insulinemia trying to reduce the blood glucose. after birth, the excessive blood glucose will be automatically withdrawn while the insulin at that moment is still high, which leads to hypoglycemia.

 +3  (nbme23#7)

At week 8 in gestational development the developing gut herniates out of the embryo and undergoes significant growth. At week 10, this rotates and is reabsorbed into the abdominal cavity. Failure to completely reabsorb the gut and rotate properly can result in a number of defects. Gastroschisis is failure to completely reabsorbed the gut, leaving some outsice the abdomen, with no covering. http://perinatology.com/Reference/Fetal%20development.htm

B) Midgut volvulus- occurs as a result of malrotation as the gut is reabsorbed. Ordinarily the cecum is held to the back of the RLQ by fibrous bands. In the event of midgut volvulus, these bands (Ladd's bands) are still attached to the now displaced cecum in the RUQ; the compress on the intestines, preventing food from moving through and often causing bilious vomiting in newborns. C) Omphalocele- a defect similar to gastroschisis, but covered by the omphalocele sac. D) Umbilical hernia- the gut is entirely reabsorbed in the abdomen, but a defect in the muscular wall overlying it allows omental fat or gut to slip through and bulge out near the umbilicus, still beneath the skin. This hernia is usually reducible with pressure. E) Urachal fistula- failure of the urachus to close, resulting in the leaking of urine from an opening near the umbilicus.

 +6  (nbme23#8)

Labetalol is a nonselective alpha-1 and Beta adrenergic antagonist. In the vasculature, alpha-1 receptors are responsible for vascular constriction which increases blood pressure/systemic vascular resistance. Antagonism would decrease the BP. At the same time, Beta-1 receptors in the heart are responsible for a positive inotropic and chronotropic effects, increasing both heart rate and contractility. Antagonism at the Beta-1 receptors in the heart would decrease heart rate.

A) Albuterol- short acting Beta-2 agonist, used for bronchodilation in the lungs. There is typically no large systemic absorption. C) Phentolamine- a non-selective alpha-1 and alpha-2 reversible competitive antagonist, it can be used in hypertensive emergencies or in Raynaud phenomenon. It would not effect heart rate. D) Prazosin- an alpha-1 antagonist, it can be used to treat hypertension or to treat nightmares associated with PTSD. It would not effect heart rate E) Propanolol- a non-cardio-selective Beta antagonist, used for many cardiac issues, for anxiety, and in pheochromocytomes. This would not affect systemic vascular resistance.

 +5  (nbme23#15)

Pravastatin is the only statin drug not metabolized by the P450 system in the liver. Because of this, pravastatin is also unique in that more of it is excreted by the kidneys than any other statin, In addition to hypothyroidism this patient has mild renal failure. This will impair excretion of pravastatin, leading to increased pravastatin and its metabolites, increasing its potential for causing myopathy.

B) Nephrolithiasis- while the patient is hypercalcemic, pravastatin does not increase the incidence of kidney stones. C) Pancreatitis- I do not know of any significant interactions between the pancreas and pravastatin. D) Toxic hepatitis- while statins can cause mildly elevated liver function test scores, they are generally not associated with hepatotoxicity. E) Type 2 Diabetes mellitus- I do not know of any effect that pravastatin has on diabetes or diabetes medications.

motherfucker2  Lucid. Nice
qfever  But isn't statin associated with hepatotoxicity too? FA 2019 page 320

 +14  (nbme23#5)

This patient has widespread destruction of both adrenal glands, which means that she will lose both her mineralocorticoids and her glucocorticoids. The loss of the mineralocorticoids and the effect on the kidneys is what is being tested here. When aldosterone is functioning and abundant, it has several critical functions on the nephron. First, it upregulates Na+/K+ ATPase expression on the basolateral membrane, establishing a strong electrochemical gradient that better absorbs Na+, while the increased intracellular K+ concentration makes it easier to lose K+ from the cell into the lumen. Aldosterone also upregulates the expression of epithelial sodium channels (ENaC) on the collecting duct, reabsorbing more Na+. Finally, aldosterone increases expression of H+ ATPases on alpha-intercalated cells of the collecting duct, which are responsible for secreting H+ (this is part of contraction alkalosis).

With the loss of aldosterone, we will see a decreases Na+/K+ gradient and decreased Na+ reabsorption; this leads to decreased serum sodium and increased serum potassium. At the same time, not expressing H+ ATPases will lead to H+ not being secreted, creating a more acidic environment (pH will decrease).

abhishek021196  Very well written explanation. Bravo

 +15  (nbme23#28)

Posterior cord syndrome occurs due to infarction of the posterior half of the spinal cord, from occlusion of the posterior spinal artery. Our patient presents with decreased sensation to pinprick below the level of the knees as well as walking with a wide-based gait, likely indicating loss of proprioception. The patient is also anemic with hyper-segmented neutrophils.

Hypersegmented neutrophils are typically caused by an inability to make enough DNA, caused by a lack of necessary precursors and vitamins including B9 (folate) and B12 (cobalamin). If the patient is folate deficient, we see elevated homocysteine deficiency. If the patient is B12 deficient, we see elevated methylmalonic acid and homocysteine levels. Hyperhomocysteinemia can increase thrombosis. Thrombosis in the posterior spinal artery can cause posterior cord syndrome. In addition, lack of vitamin B12 impairs myelin formation and leads to Subacute Combined Degeneration, which affects the Spinothalamic tract (accounting for decreased pinprick sensation), Corticospinal Tract, and Dorsal Column-Medial Lemniscus Tract (accounting for the reduced proprioception.

A) Anterior cord syndrome- loss of motor command, as well as bilateral loss of heat and pain, the patient has not lost motor function, so it cannot be this. B) Central cord syndrome- presents as a combination of motor and sensory loss, usually with bladder dysfunction. This patient does not display motor loss or bladder dysfunction. C) Hemicord syndrome- Also called Brown-Sequard, this is complete injury to either the left or right side of the spinal cord. It presents with motor dysfunction and reflex dysfunction ipsilaterally at the level of the lesion; loss of upper motor command below the lesion ipsilaterally (spastic paresis); loss of dorsal column-carried sensation ipsilaterally at and below the lesion; and loss of pain and temperature sensation contralaterally 2 to 3 vertebra below the lesion. E) Segmentary syndrome- a congenital failure to develop part of the spinal cord. The new onset of symptoms at 82 years old makes this an unlikely diagnosis,.

yb_26  amazing, thank you!
aisel1787  great explanation
rockodude  sensation to pinprick is DCML tract. SCD affects spinocerebellar (not spinothalamic), corticospinal, and DCML. otherwise good explanation.

 +8  (nbme23#47)

Budd-Chiari syndrome occurs when there is occlusion of the hepatic vein or the hepatic vein fails to drain into the IVC. This can be caused by thrombosis of the hepatic vein, or by right sided heart failure (causing blood to 'back up' everywhere, but its manifestation through the hepatic vein are all the signs of Budd-Chiari syndrome). Anything that can increase the risk of thrombosis can then increase the risk of Budd-Chiari syndrome. This includes polycythemia vera, a hypercoagulable state. Our patient and PV but missed his appointment two weeks ago. He now presents with scleral icterus, an enlarged liver, and some signs of portal hypertension. Thrombosis of the only anatomical option presented that covers all of this is the hepatic vein ie our patient has Budd-Chiari. Remember that Budd-Chiari will have a "nutmeg liver" appearance on gross pathology.

B) Hepatic cirrhosis- it's entirely possible our patient does have hepatic cirrhosis for unrelated reasons, however the acute onset makes this less likely. C) Pancreatic carcinoma- pancreatic carcinoma obstruction of the common bile duct could cause a 'back up' of bile, ultimately causing some liver damage and scleral icterus. However once again the timing makes this unlikely. D) Portal vein thrombosis- portal vein thrombosis could cause some splenic enlargement and portal hypertension. However, its obstruction would not cause a tender, enlarged liver because it is upstream. E) Primary hemochromatosis- due to a defect in hepcidin production, this iron overload presents with darkened skin, insulin disregulation, hepatic damage (with the potential for hepatocellular carcinoma) and heart disease (restrictive or dilated cardiomyopathy, depending on your source). The only one of these signs that our patient has is an enlarged liver.

almondbreeze  FA 2019 pg 386

 +33  (nbme23#44)

A and J represent the gracile fasciculus, while B and I represent the cuneate fasciculus. Together they make up the dorsal column-medial lemniscal tract, responsible for pinpoint perception, proprioception, vibration, and pressure. Input is ipsilateral.

C and H make up the lateral corticospinal tract (also called the lateral cerebrospinal fasciculus), responsible for motor command of ipsilateral limbs.

D and G represent the lateral spinothalamic tract. It is responsible for pain and temperature conduction. The input arises in a limb (left lower extremity in this case), enters through the dorsal root (pictured between J and H), decussates and ascends at the anterior commissure (just behind E and F), and finally synapses on the second order neuron in the lateral spinothalamic tract. So the spinothalamic tract is responsible for contralateral pain and temperature sensation. Because our patient has lost sensation on the left, the lesion is in the right.

E and F are the anterior corticospinal tract. It is involved in motor control of proximal muscles, typically of the trunk.

nor16  good job

 +9  (nbme23#39)

First, critically, it is not described as ion radiation (alpha and beta particles) but as radiation that has an ionization effect. Our farmer has been out standing in his field, soaking up the sunlight. UV-B is wave radiation that induces the formation of free radicals. These free radicals in turn do damage to the cell, including the formation of pyrimidine dimers. This DNA damage is the bases for his squamous cell carcinoma. For more on UV-B induced free radical damage of DNA, https://www.ncbi.nlm.nih.gov/pubmed/16765564 . For more information on UV radiation from the American Cancer Society, please visit https://www.cancer.org/cancer/cancer-causes/radiation-exposure/uv-radiation/uv-radiation-what-is-uv.html

A) Decreased function of the skin as a barrier to carcinogens- the patient has no history suggest exposure to carcinogens besides UV light, and as long as the skin is intact and relatively healthy it should function as some kind of barrier. C) Increased conversion of 25-D3 to 1,25-D3 - this conversion takes place in the kidneys via 1-alpha-hydroxylase, also expressed in granulomas (and so 1,25-D3 is often elevated in sarcoidosis). This would not explain cancer. D) Increased mitotic activity through stimulation of melanocytes- our patient is diagnosed with squamous cell carcinoma, not melanoma. E) Increased susceptibility to skin trauma- while the damage from UV light to collagen does make skin thinner and more readily damaged, this would not explain squamous cell carcinoma.

 +9  (nbme23#6)

Borderline personality disorder- feelings of "emptiness," suicidality, self-mutilation, unstable relationships, and more common in women than in men. A common defense mechanism in this disorder is "splitting" in which people are seen as entirely good or entirely bad. Borderline personality disorder is also part of the Cluster B personality disorders, which are associated with substance abuse.

imnotarobotbut  Suicide attempts are also commonly seen with Borderline

 +17  (nbme23#42)

The patient has a prior history of hysterectomy with bilateral salpingo-oophorectomy, and received external beam radiation to the pelvis. The patient now displays hydronephrosis and hydroureter, with distal ureteral narrowing bilaterally. The likeliest option is that we are seeing adhesions from previous surgery constrict the ureters, causing this.

E) Urothelial carcinoma (also called transitional cell carcinoma) is also a possibility. What makes this unlikely is the location: bilateral. The prior hysterectomy and bilateral salpingo-oophorectomy would leave scar tissue on both sides of the body, but the odds of urothelial carcinoma arising bilaterally are very slim.

A) The patient had a hysterectomy, so the odds of recurrent cervical carcinoma are also incredibly low. C) and D) Urethral condyloma and urethral transitional cell papilloma are in the wrong location to account for bilateral urethral narrowing with hydroureter.

stinkysulfaeggs  Great explanation - just one addition. The retroperitoneal fibrosis could also be a direct consequence of the external beam radiation. It's linked to both causes. Either way, it's a better fit than urothelial carcinoma (in retrospect).
spow  Why would the onset be 15 years later though?
drzed  I was thinking the same thing @spow. I had put urothelial carcinoma, thinking that a field defect would result in bilateral tumor.

 +3  (nbme23#9)

From First Aid- schizotypal personalities exhibit eccentric appearance, odd beliefs or magical thinking, and interpersonal awkwardness. These describe the several layers of clothes, belief in psychic abilities and crystals, and poor eye contact.

A) Borderline- unstable moods with impulsivity, self-mutilation, suicidality, and a sense of emptiness, along with a greater likelihood in women B) Dependent- those with an excess need for support and low self-confidence C)Histrionic- excessively emotional, seeks attention, sexually provocative, concerned with appearance ("actor's disease") D) Narcissistic- grandiosity, entitled, lacks empathy, demands 'the best' E) Schizoid- voluntary social withdrawal, limited emotional expression, content to be on their own

abhishek021196  SCHIZOTYPAL = Included on the schizophrenia spectrum. Pronounce schizO-TYPE-al: Odd-TYPE thoughts.

 +10  (nbme23#22)

MHC I function is integral to cancer suppression. MHC I displays endogenously synthesized proteins and presents them to CD8+ T cells. The failure to display MHC I, or MHC I display of non-self (and by extension cancerous) proteins triggers a cellular immune response, leading to destruction of the cell.

The proteasome is used for the degradation of worn out, senescent, or malformed proteins. As cancer develops, more mutations lead to increased wrong proteins. Only by expression of the proteasome, or its over-expression, can these mutant proteins be degraded fast enough to not be displayed by MHC I and lead to the cell being killed. Bortezomib blocks the proteasome, so the mutant proteins are displayed on the surface, allowing the immune system to recognize and kill pathological cells.

catch-22  Another way to approach it is to think about MHC class I processing. Basically, if you inhibit the proteasome, peptides will not be generated and nothing is available to be loaded onto MHC I (remember MHC I has to be loaded before it's transported to the cell surface). Cells that don't express MHC I get killed by the natural killers. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2214736/
kai  "In conclusion, we have demonstrated that the proteasome inhibitor bortezomib down-regulates class I and enhances the sensitivity of myeloma to NK cell–mediated lysis" from the conclusion of the NIH paper
maddy1994  another mechanism is by blocking proteosome u even decrease degration of proapoptotic proteins...so it enchances apoptosis(from uworld)

 +6  (nbme23#40)

Plasma membranes are a lipid bilayer, typically with phosphate heads on each surface and long carbon tails on the inside. These carbons are neutral, and undergo hydrophobic interactions for an energetically favorable state.

Integral membrane proteins pass through this lipid bilayer, and so must be capable of interacting both with the polar solvents of intracellular and extracellular space, as well as the hydrophobic core of the layer. The transmembrane portion often has alpha-helical secondary conformation, with hydrophobic residues like glycine on the outside towards the carbon tails with polar amino acid residues tucked in.

makinallkindzofgainz  "high school biology" lmao we really out here

 +5  (nbme23#14)

The patient started receiving post-surgical subcutaneous anticoagulation therapy, so most likely either unfractionated heparin or low molecular weight (LMW) heparin. Unfractionated heparin's primary anticoagulation ability comes from working with antithrombin III to block coagulations factors II and X.

However, heparin can also bind to a platelet protein called Platelet Factor 4 (PF4), found in alpha-granules. When it binds PF4, the new heparin-PF4 molecule is immunogenic. The immune response to this generates anti-heparin-PF4 Ig. Platelets already have Ig receptors on their surfaces, so when these anti-heparin-Pf4 Ig trigger the receptors on the platelets, these platelets degranulate. The degranulation kicks off further clotting, leading to a drop (often more than 50%) in platelet count.


 +4  (nbme23#46)

Tetracyclines are calcium chelating agents. Because of this, in a developing fetus or child they will bind to calcium deposits, namely teeth and bones. This can cause blue-black discoloration of teeth, and is contraindicated in pregnant mothers for this reason or in children under 8 years of age. Additionally, this same chemical property of binding to calcium is why certain divalent cations (Calcium, magnesium, iron [Fe2+]) prevent absorption of tetrayclines, and so medicines with these ions (antacids, iron supplementation) should be timed not to interfere with absorption.


 +17  (nbme23#18)

Enzyme A stands in for Phospholipase A2, turning phospholipids in the cell membrane into arachidonic acids. From there, Enzyme B stands for Cyclooxygenase (COX), while Enzyme C stands for 5-Lipoxygenase (5-LO). 5-LO produces 5-HPETE, which is turned into leukotrienes. Leukotrienes play a double role in events like asthma, because they cause bronchoconstriction (seen in this patient) and by acting as chemical attractants for inflammatory cells, whose activity will close the airway further. By blocking COX (presumably with an NSAID), we leave more of the substrate arachidonic acid for 5-LOX to ultimately convert into leukotrienes. This is the basis for aspirin-intolerant-asthma, which is frequently associated with nasal polyps. (Samter's triad).


D) Prostacyclin synthase . E) Thromboxane synthase

 +7  (nbme23#30)

The patient underwent removal of a rectal tumor which had involvement with the prostate. The prostatic capsule is rich with nerves including the pelvic splanchnic nerves, a set of parasympathetic nerves responsible for PNS autonomic regulation. Erections are a parasympathetic function.

A) Gray rami from the sympathetic chain- erections are a parasympathetic function, not sympathetic. Emission of sperm is a sympathetic function, and is directed by the inferior hypogastric nerve. C) Pudendal- the pudendal nerve is a somatic nerve that receives sensation from the penis, posterior scrotum, clitoris, and labia, as well as being responsible for some movement of the pelvic floor, and ejaculation. D) Superior hypogastric nerve- a sympathetic nerve, this contributes to the hypogastric plexus and may also contribute to sympathetic control of emission. E) Ventral ramie of S2-S4- These rami contribute to the pudendal nerve.

focus  Diagrams here are pretty good too: https://obgynkey.com/introduction-of-pelvic-anatomy-2/ "Point, Squeeze, Shoot" Point- erection: pelvic splanchnic nerves (S2-4) Squeeze- emission: superior hypogastric plexus Shoot- ejaculation: pudendal nerve

 +9  (nbme23#34)

The single most important thing about this gross pathology is that the disease is multinodular. This indicates metastases from distant sites.

Liver abscesses are usualy singular, filled with creamy yellow pus, and may show a fibrous capsule. Cirrhosis often shows a yellow color due to fatty change as well as regenerative nodules, which are not present here. A focal nodular hyperplasia is a singular tumor of the liver, and this is multinodular. Hepatitis B is a little harder to distinguish because from what I can tell it can be multinodular in some cases, but this liver also shows none of the sclerosis from chronic inflammation that would likely accompany Hep B. Finally, we see no dark discoloration to indicate infarction.

monkd  It doesn't explain the sudden death, but I suppose they aren't asking for that!
charcot_bouchard  I hate this type of ques. Here it is. Tell me what it is?
divya  also, a liver infarct is unlikely due to rich dual blood supply.
drzed  @divya Rather, if there was an infarct, it will be hemorrhagic, not pale.
llamastep1  Multiple solid lesions on a healthy liver = meta. I assumed breast wouldn't meta to liver (it's usually GI cancers) but it makes sense since all the blood gets filtered by the liver at some point. TIL!

 +21  (nbme23#25)

Critical points for this question: 5 year old boy, immunosuppressed because of chemotherapy, 2 day history of fever, cough, shortness of breath, febrile (101.8 F), respirations 46/min, with cyanosis and generalized vesicular rash. Extensive nodular infiltration.

Of the options listed only measles and VZV give a rash. A rash from measles usually starts rostrally and descends caudally, and is flat and erythematous. By contrast, VZV (chickenpox) presents with generalized rash that quickly transitions from macular to papular then to vesicular.

sympathetikey  Good call.
imnotarobotbut  Also, VZV causes pneumonia (what this patient probably had) and encephalopathy in the immunocompromised.
nwinkelmann  What threw me off was that it didn't mention the synchronicity of the rash. I stupidly took failure to mention to mean that the rash was synchronous, which doesn't fit VZV because chickenpox rash is characterized as a dyssynchronous rash (i.e. all stages of the macule to papule to vesicle to ulceration are seen at the same time). MUST REMEMBER: don't add information not given!
jboud86  If anyone wants to refresh info on Vaicella-Zoster virus, page 165 in FA 2019.

Subcomments ...

Patient has a fracture to the inferior orbit. This can dmg V2 or entrap the IR muscle. Only IR entrapment would impair vision.

nlkrueger  if this isn't a globe rupture than idk what is tbh +10  
mousie  the air in the center of the globe made me think rupture too ..... +2  
sajaqua1  There may be some global rupture, but impairment of one of the ocular muscles causing diplopia would still be the best explanation for this patient's double vision. +7  
catch-22  Globe rupture leads to entrapment of the IR muscle which causes diplopia. The question is asking what is causing his visual complaints, which is diplopia, not loss of vision. +1  

submitted by sajaqua1(390),

Male pattern baldness./androgenic alopecia is caused by the effects of dihydrotestosterone (DHT) on the skin of the scalp. Testosterone is converted by the enzyme 5-alpha-reductase into DHT. Finasterideis a 5-a-reductase inhibitor, and so blocks the production of DHT and can halt or even cause some reversal of make pattern baldness. However this same activity may also result in signficant sexual side effects including gynecomastia, erectile dysfunction, ejaculatory dysfunction, and decreased libido.

A) Danazol- a weak androgen with antiestrogenic effects, used in the treatment of endometriosis and fibrocystic breast disease. C) Methyltestosterone- synthetic T, it is used to supplement in testosterone deficiency, or in the treatment of some breast cancers. D) Oxandrolone- an anabolic steroid used to regain weight. E) Stanozolol- another anabolic steroid, with potential used for hereditary angioedema.

sajaqua1  I am embarrassed by these typos. +  
drdoom  lol +  

submitted by shaydawn88(8),

Is it intra-alveolar transudates because this patient might have HF d/t a. fib and left atrial enlargement-> inc hydrostatic pressure-> transudate pleural effusion?

sajaqua1  Basically. +1  
medschul  Why can it not be arterial hypertension? +2  
meningitis  I think Arterial HTN is referring to Pulmonary Artery HTN which would be present in LT HF in the long run with RT HF and edema. Pulm HTN would cause a backflow, and doesn't really answer the question "explain the patients Dyspnea". At least, that's how I saw it. Hope this helped. +4  
sugaplum  the question has 2 murmurs, so does she have aortic stenosis too? i guess it is not relevant since it asked for what is causing her SOB +  
nukie404  I guess pulmonary HTN would happen in response to increased pressure after the edema happens, and would cause backflow (to the RV) over pulmonary edema. +  
vulcania  There's a really great diagram in UWorld (QID 234) that explains what happens as a result of mitral stenosis. Very similar sounding to the patient in this question. +  

submitted by seagull(846),

This is a panic attack. Hyperventilation drops pCO2 leading to a respiratory alkalosis. po2 is relatively unaffected (don't ask me how?)

sympathetikey  Yeah haha I had the same conundrum. +  
sajaqua1  If she's breathing deep as she breathes fast, then oxygen is still reaching the alveoli , so arterial pO2 would not be effected. +8  
imnotarobotbut  lmao i'm so freaking dumb i thought she was having alcohol withdrawals because it was relieved by alcohol +1  
soph  Maybe Po2 is unaffected bc its perfusion (blood) limited not difusion limited (under normal circumstances). +2  
charcot_bouchard  PErioral tingling- due to transient hypocalcemia induced by resp alkalosis. +1  
rainlad  I believe CO2 diffuses ~20x faster than O2, so increases in her respiratory rate have more effect on her PCO2 than her PO2 +1  

submitted by m-ice(237),

The patient seems to have an infection due to their elevated temperature and abnormal chest X-ray. However, their leukocyte count is low. In addition, the patient has hepatitis C, which is often associated with similar transmission routes to HIV, like intravenous drug use.

sajaqua1  Not only is their WBC count low, it is not uniform. If we assume a minimum normal WBC count of 5000 cells/mL^3, and a regular range of ~60% neutrophils, then normally a person should have ~3,000 neutrophils/mL^3. This patient has a total of 2000 cells/mL^3, with 1,800 neutrophils/mL^3. Their lymphocytes and macrophages have been whiped out. This is best accounted for by HIV. +20  

submitted by keycompany(218),

Can somebody who understand why PVR decreases with a Left-Sided infarct please enlighten me. I would also appreciate it if you could relate it to right sided heart failure too (i.e. how would it change).

sajaqua1  I believe that keycompany's answer comes the closest. In an MI, consider it as cardiogenic shock. The heart is a pump, and it is failing to move blood out of the heart and into vasculature. This is why PCWP increases. Because of insufficient output, the body has a sympathetic response. The catecholamines then cause vasoconstriction in peripheral vasculature to keep blood pressure up and continue flow, leading to increased SVR. Meanwhile, the sympathetic response causes vasodilation in the lungs; this would be an appropriate autoregulatory response, because the body is trying to keep up the flow of oxygen throughout the system. This decreases PVR. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5715548/ Is a pretty good article on this. Of course the binding of catetcholamines changes depending on saturation and the response is not perfectly understood. +9  
usmleuser007  My understanding is that the pulmonary circulation changes very little in terms of an acute MI. It is b/c pulmonary circulation has a lot more room to fill with blood much like the spleen in terms of blood accumulation. With higher volume of blood in pulmonary circulation, more blood vessels are able to be recruited specially the apex. With more recruited blood vessels = reduced pressure d/t circulation in parallel. +1  

submitted by seagull(846),

I have an issue with this question which also conflicts with UWorld. In order to be degraded by proteosomes the misfolded protein would need to be present in the cytosol for ubuination. It it accumulated in the RER then how does it get tagged? Honestly, so conflicted...

sajaqua1  So ordinarily a misfolded protein does undergo ubiquitination and proteolysis. It is noteable that CFTR misfolding doesn't even allow it escape the ER, so it accumulates in the ER +5  

Can anybody explain this one? I put repeated tests because I assumed an 83-year-old woman is an unusual demographic for syphilis.

m-ice  83 might seem an uncommon age, but we don't know for sure her sexual history. She only recently (8 months ago) started showing some signs of mild cognitive impairment. She has all these results implying that she has syphilis, so the most likely answer is that she has syphilis, so we should speak to her privately about her sexual history. The tests don't necessarily means she got syphilis very recently, it's possible she's had syphilis for a while and never got treated. +4  
mousie  I understand that she could possibly have syphilis but I also put repeat tests because I know there are a few things that can cause false positive VRDLs but if she also has a + RPR does this make a FP less likely? And also if she has mild cognitive impairment you still discuss with her not her daughter correct ...? +4  
m-ice  This definitely could be a false positive, but before we want to consider it to be a false positive, we should talk to the patient about it privately. Assuming that it's a false positive before asking the patient about it could delay treatment of her syphilis. There's a chance she didn't want to disclose her sexual history in front of her daughter or maybe she was embarrassed or didn't think it was important to mention. And you're absolutely right, she only has mild cognitive impairment, so we most definitely should talk to the patient alone without her daughter first. +3  
seagull  She has dementia. She doesn't have the capacity to determine her own care (23/20 MME). I feel the daughter should have the word on the care since Grandma likely doesn't have the capacity to understand her actions. +4  
sajaqua1  From what I remember, dementia is typically a combination of impaired memory *and* impaired thought processes. There is nothing to indicate that the patient has impaired thought processes, and the memory impairment is only mild. The patient can still reasonably said to be competent, and so her private information should be discussed with her alone. +8  
yotsubato  Elder care homes or elderly communities actually have a high rate of STDs. Turns out, when you put a bunch of divorced/widowed adults together in a community they have sex. +7  
yotsubato  Additionally, you should respect the privacy of a competent adult with "Mild memory" impairment. I know I could have mild memory impairment considering the crap I forget studying for step 1 +9  
drdoom  @seagull dementia ≠ absence of competence -- the two are separate concepts and have to be evaluated independently. see https://meshb.nlm.nih.gov/record/ui?ui=D003704 and https://meshb.nlm.nih.gov/record/ui?ui=D016743 +3  
wowo  also important to note, d) repeated tests is also incorrect as the microhemagglutination assay is a confirmatory treponemal test (along the same lines as FTA-ABS) https://www.uofmhealth.org/health-library/hw5839 +5  
sunshinesweetheart  also.... I think we can assume that "repeated tests" means repeat VRDL, not "additional tests to rule out false positives" +2  

submitted by neonem(452),

The patient has low cortisol, which causes body wasting. The patient is hyperpigmented since low cortisol increases ACTH secretion from the pituitary, but this shares a common precursor protein with melanocyte-stimulating hormone (MSH), so that's often a sign of either adrenal failure or an ACTH-secreting tumor. Put together, the high ACTH but low cortisol happening over a period of 6 months means that the adrenal must be getting hit by something -- only option here was autoimmune adrenalitis. Waterhouse-Friderichsen syndrome also causes adrenal insufficiency but this happens acutely, in the timeframe of hours-days.

sajaqua1  The combination of low blood pressure (from lack of mineralocorticoids) and low glucocorticoids (cortisol) indicate adrenal failure. Hyperpigmented skin is a sign of elevated ACTH, indicating that this is a failure of the adrenal gland and not the pituitary. In the industrialized western world, autoimmune destruction of adrenal glands is the leading cause of primary adrenal failure (disseminated tuberculoid destruction of the adrenal glands is significant outside of industrialized nations). It also fits the time line better than Waterhouse-Friederichsen syndrome, which is sudden in onset and associated with hemorraging. Metastases to the adrenal glands *might* be a possibility, but autoimmune destruction is simply likelier. +17  
mamorumyheart  Chronic Addisons disease. Pretty straightforward here. Decreased gland function -> decreased Cortisol, decreased Aldosterone -> hypotension (with hyponatremic volume contraction) Hyperpigmentation from increased ACTH (from POMC) making MSH. (FA) Due to adrenal atrophy or destruction by disease (autoimmune destruction most common in the Western world; TB most common in the developing world). +1  
ac3  I picked autoimmune adrenalitis but was tempted to pick Waterhouse syndrome because of the low BP (hemorrhaging). But I believe Waterhouse-Fried. syndrome is more likely associated with Neisseria infection +  

submitted by hyoid(22),

Can someone explain this one––I didn't really know what to make of the lab values. Clearly she was taking too much insulin, but how can you differentiate factitious disorder from a type 1 diabetic who takes too much of their insulin dose?

m-ice  I think the trick here is that they don't mention that the daughter has a history of Type 1 DM, so she has no reason to be taking insulin at all. She's definitely receiving insulin, but we don't have any history implying she's a type 1 diabetic. That, combined with the fact that there have been multiple episodes like this one, favors that the mother is giving the daughter insulin when she doesn't need it. +8  
sajaqua1  C-peptide is produce by endogenous insulin, but is not part of exogenous insulin. She has elevated insulin, with low C-peptide, so she is receiving too much exogenous insulin. A history of recurrent episodes this year implies a behavioral issue; Factitious disorder imposed on another (also called Munchausen syndrome by proxy). +5  

submitted by m-ice(237),

This man has pulsus paradoxus, a sign in which blood pressure decreases drastically during inspiration. Pulsus paradoxus is a classic sign of pericardial tamponade.

When fluid (often blood) has pooled around the heart, the heart struggles to expand and fill with blood. This becomes a bigger problem for the right ventricle during inspiration, because the right side of the heart receives increased venous return during inspiration. Because there is fluid preventing the right ventricle from expanding outward, the only other place it can expand to accommodate is by pushing on the septum, shrinking the size of the left ventricle. This causes decreased BP when the left ventricle contracts during that cardiac cycle.

sajaqua1  In addition to causing pulsus paradoxus, we see jugular venous distension, and muffled/distant heart sounds (hard to hear through the cardiac tamponade). https://radiopaedia.org/articles/beck-triad?lang=us +2  

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