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Comments ...

 +0  (nbme23#33)

1) know that BC>AC = conductive hearing loss 2) conductive hearing loss means issue with structure before the inner ear 3) everything else occurs in the inner ear or in the brain


 +0  (nbme22#36)

1st clue is that its a restrictive lung disease via the FEV1/FVC ratio being increased.

Next, the DLCO is decreased (normal is 80 to 120%), meaning an issue with the alveolar-pulmonary capillary barrier (a diffuse lung process).

The CT has classic findings for idiopathic pulmonary fibrosis.

The clinical picture (non-productive cough, SOB with exertion, afebrile) are consistent with idiopathic pulmonary fibrosis.

Overall a very non ambiguous question.


 +1  (nbme22#14)

This question sweet literally the definition of trigeminal neuralgia

key findings for others

a) periorbital pain, rhinorrhea, lacrimation

b) unilateral HA, aura, photophobia

c) multiple lesions in time and space

d) jaw pain, blindness, headache


 +0  (nbme22#28)

Eosiniphilia = parasite large spine + hepatosplenomegaly = schistosome mansoni


 +0  (nbme15#6)

Medullary thyroid carcinoma is defined as:

a malignant proliferation of parafollicular "C" cells that secrete calcitonin

histology shows malignant tumor cells within pink (hyalin), amyloid stroma


 +1  (nbme15#15)

Due to "contraction alkalosis" loop diuretics cause volume contraction, thats why you give them.

As a result, there is increase angiotensin II release, increase in Na+/H+ exchange in the PCT (a function of increase angiotensin II), and then increased HCO3- reabsorption, leading to alkalosis


 +0  (nbme15#36)

This question is asking what left dominant circulation means. I suppose it wants us to infer that the PDA is supplying the diaphragm surface and AV node.

It is confusing to me because normally the Right marginal artery supplies the diaphragmatic border (acute margin) of the heart. I'm not sure that it changes in left dominant circulation. Furthermore it would not branch off the PDA, although maybe parts of it are supplied by the PDA

Also the AV node is supplied by the Atrioventricular nodal artery, which can be a branch off of the LCA or the LCX but not really the PDA

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3537199/

so confusing question for me but the point is to know the course of left dominant circulation to the PDA


 +0  (nbme15#26)

Acute MI and mitral regurg (from the murmur) leads to LV failure and backflow of blood into the lungs.

This leads to increased pulmonary hydrostatic capillary pressure. This will lead to excess volume leaking from the pulmonary capillaries into the interstitial and this will manifest as pulmonary edema (crackles).

Pulmonary edema will interfere with gas exchange leading to hypoxemia.


 +0  (nbme15#40)

Classic picture for Duchenne muscular dystrophy. which is due to deleted dystrophin protein.

From FA: "Dystrophin helps anchor muscle fibers, primarily in skeletal and cardiac muscle. It connects the intracellular cytoskeleton (actin) to the transmembrane proteins α- and β-dystroglycan, which are connected to the extracellular matrix (ECM)"


 +0  (nbme15#43)

Cool and pale extremities rules out distributive causes (neurogenic, anaphylaxis, septic).

Hypovolemic would describe a process of volume loss (bleeding or dehydration) and would not explain the crackles or jugular vein distension.

don't be thrown off by the normal heart sounds.


 +1  (nbme15#45)

This question describes I-cell disease (inclusion cell disease/mucolipidosis type II). You can tell because there is mixed accumulation of junk forming the inclusion bodies. Other lysosomal storage diseases have accumulation of one type of substance.

Essentially, there is a defect in defect in the enzyme N-acetylglucosaminyl-1-phosphotransferase.

This means the mannose-6-phosphate tag cannot be added to proteins. Without this tag, proteins are incorrectly sent to the extracellular space rather than delivered to lysosomes.

ergogenic22  ^^correction. You can tell because there are elevated lysosomal enzymes in the plasma. This is because the proteins are not tagged with M6P and thus are excreted to the extracellular space.

 +0  (nbme15#49)

A cohort study compares a group with a given exposure (cigarette smoking) to a group without such exposure. It then looks to see if exposure or risk factor is associated with later development of disease. "does smoking lead to COPD"

on the other hand, a case-control study looks at those with the disease vs without to see if there is a difference between prior exposure or risk factor "Did people with COPD smoke"


 +0  (nbme15#15)

TLC decreased suggests restrictive disease. Reticular pattern suggests pulmonary fibrosis


 +0  (nbme15#21)

She has motor and sensory symptoms. This r/o both kinds of simple. Her seizures are not described as tonic/clonic movements, and include periods of impaired consciousness. This rules out generalized tonic/clonic. There is a post-ictal state, that rules out absence.

Also the lip smacking is characteristic of automatism, which is found in complex partial seiuzres


 +0  (nbme15#28)

classic myasthenia gravis picture. Worsens with use. Sx include diplopia. Improvement with AChE.

Also side note, don't focus on the pregnancy status, but women who are in the postpartum eriod are at particularly high risk of developing myasthenia gravis


 +0  (nbme15#47)

blood count shows elevated neutrophils, Neutrophil chemotactants include bacterial products, IL-8, C5a, kallikreinm platelet-activating factor and LTB4


 +0  (nbme15#14)

Strep Viridans is oral flora, causes subacute endocarditis affecting previously damaged valves, and is often associated with sequelae of dental procedure.

A) enterococci can also cause subacute endocarditis but they are gamma hemolysis and follow GI/GU procedure B) beta hemolysis and causes acute c) beta hemolysis and causes acute e) alpha hemolysis but unlikely to cause endocarditis, causes meningitis, otitis, pneumonia, sinusitis - (MOPS)


 +0  (nbme15#3)

vitals and need to be treated first, so atropine and then pralidoxime.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493390/

important to note that organophosphates become irreversible at a certain point so pralidoxime does still need to be given early


 +0  (nbme15#39)

NAPQI is a toxic intermediate is formed by in small amounts by metabolism of acetaminophen. Depletion of hepatic glutathione stores by NAPQI leads to acute APAP toxicity and acute liver injury.


 +0  (nbme15#6)

mass in the esophagus with solid/liquid dysphagia. I'm not sure what the histo shows but on the bottom there are more flat cells and the top there are wider spaces within the cells with some fat, so I think it maybe a healing ulcer leading to a stricture.

anways other pathogens are more associated with other infections

A) gallstones and cholangiocarcinoma B) esophagitis c) liver abscess E) i think miliary TB can present in the liver


 +0  (nbme15#6)

mass in the esophagus with solid/liquid dysphagia. I'm not sure what the histo shows but on the bottom there are more flat cells and the top there are wider spaces within the cells with some fat, so I think it maybe a healing ulcer leading to a stricture.

anways other pathogens are more associated with other infections

A) gallstones and cholangiocarcinoma B) esophagitis c) liver abscess E) i think miliary TB can present in the liver


 +0  (nbme15#9)

He has a down and out pupil, caused by CN III palsy. His gaze is due to unopposed action of the lateral rectus and superior oblique; ptosis due to denervation of levator palpebrae superiosis.

The only injury listed that could cause a CN III palsy is aneurysm of the PCA compressing the ocularmotor nucleus.


 +0  (nbme13#20)

I believe that the question is suggesting the patient has a methanol overdose.

First Aid 2018 page 72: "FOMEpizole—inhibits alcohol dehydrogenase and is an antidote For Overdoses of Methanol or Ethylene glycol."

The reason I am unsure is that wikipedia states most paint thinners are ketones or hydrocarbons

lae  that's correct, I don't know about what the thinner has but the clinics is methanol toxicity for sure

 +0  (nbme21#6)

chromatin negative = no barr bodies = person with XY genotype or XO because anytime you have more than one X chromosome you have a barr body (chromatin positive)


 +2  (nbme21#10)

Na-(Cl-+HCO3-)=anion gap = 140-(105+10) = 25 mEq/L

normal range for anion gap is 8 to 16 mEq/L...Therefore, positive anion gap.

pH = 7.25, normal range 7.35-7.45... Therefore acidosis

Normal bicarbonate 22-28, questions shows bicarb of 10. Therefore metabolic acidosis

Additionally PCO2 normally 33-45 mm Hg, question shows PCO2 of 23 with normal PO2, therefore respiratory compensation


 +2  (nbme21#18)

elderly lady with slow, progressive memory loss, normal physical exam, no signs of depression, this is most likely Alzheimer disease.

AChE inhibitors are used for treatment because Alzheimer's is associated with low ACh. Also used are NMDA receptor antagonist (memantine)


 +0  (nbme21#33)

why is protection of the choroid plexus, from intraventricular rupture secondary to germinal matrix hemorrhage not a possible answer?

whoissaad  yes same question, both retinopathy and intraventricular hemmorage can occur due to high oxygen levels..
cienfuegos  I mistakenly chose choroid plexus too, based on wiki seems this is most common cause of IVH in term infants: IVH in the preterm brain usually arises from the germinal matrix whereas IVH in the term infants originates from the choroid plexus. However, it is particularly common in premature infants or those of very low birth weight... Most intraventricular hemorrhages occur in the first 72 hours after birth. The risk is increased with use of extracorporeal membrane oxygenation in preterm infants. https://en.wikipedia.org/wiki/Intraventricular_hemorrhage#Babies
burak  choroid plexus is different than germinal amtrix

 +0  (nbme21#10)

why is hyperlipidemia secondary to cushing syndrome not a possibility?

hello  SIADH = MC paraneoplastic syndrome of small oat cell lung cancer. Also, Cushing syndrome would cause would weight gain, skin hyperpigmentation, and hypokalemia. Not, lyperlipidemia.
charmrooftops  You do get hyperlipidemia in cushing though? https://www.amboss.com/us/knowledge/Cushing_syndrome So still unsure why this is not a possibility. Is it just a "more common" thing for SIADH?

 +3  (nbme20#9)

Pt has signs and Sx of hypercortisol. Low/normal ACTH favors elevated cortisol independent of ACTH, confirmed by lack of response to dexamethasone suppression. Zona fasciculata is origin of cortisol production.

champagnesupernova3  They tried to confuse us saying both low dose and high dose dexamethasone didnt suppress it. But when ACTH is low you dont even need to do high dose dexamethasone test. The high dose is only to differentiate between Pituitary adenoma and ectopic ACTH production

 +0  (nbme20#2)

CRP is an acute phase reactant, these are synthesized primarily by the liver


 +1  (nbme20#16)

See the first aid entry on Tuberous sclerosis. It is associated with increased incidence of subependymal giant cell astrocytoma and many other conditions.


 +1  (nbme20#5)

A stretch injury during childbirth will result in damage to the external uretheral and anal sphincters and damage to the pudendal nerve (S2-S4). This can lead to decreased sensation in the perineal and genital area and fecal or urinary incontinence

thepacksurvives  I think that there can also be a direct tear to the anal sphincter muscles
sympathetikey  A better answer choice would have been "damage to the nerves innervating the anal sphincter" but eh, ok.

 +0  (nbme20#4)

classic for Syringomyelia - results in bi-lateral loss of pain and temperature sensation in a "cape-like" distribution


 +0  (nbme20#23)

aging results in increased arterial stiffness (change in Extra Ccellular Mmatrix composition - decreased elastin, increased collagen deposition); ISH is responsible for 60-80% of HTN cases in patients > 60. Also, decreased compliance as a result of aging causes increased pulse pressure

rio19111  why not dev. of coronary atherosclerosis?
pakimd  @rio19111 i think the Q stem is asking in absence of any lesions of blood vessels; the number and severity of which increase with age. So with normal aging SBP should increase in isolation which may then result in the development of coronary atherosclerosis- if that makes sense
chandlerbas  aging causes decreased compliance in large arteries: (1) accumulation of collagen and calcium (2) degraded elastin and large arteries accumulation and it also may have something to do with lipofuschin




Subcomments ...

submitted by krewfoo99(4),

Why would perforins be the wrong answer? Wouldnt accumulation of toxic proteins cause the cell to undergo apoptosis ?

ergogenic22  Bortezomib does not directly activate perforin. It directly inhibits the proteasome which → enables CD8+ T cells to initiate apoptosis → via perforin release (in essence a downstream effect). +  


submitted by krewfoo99(4),

In what situations will HbH be formed (3 alpha chain deletions)?

ergogenic22  one parent has 2 deletions on the same gene, the other parent has 1 deletion, and the offspring receives all three. In this question, both parents have alpha 1 deletion +  
ergogenic22  actually its possible that they both have 2 gene deletions, but regardless, a-thalassemia trait is more likely +  
ergogenic22  and someone above said Asian people are cis-2 deletion so the offspring will not receive two deletion from one parent +  


submitted by krewfoo99(4),

In what situations will HbH be formed (3 alpha chain deletions)?

ergogenic22  one parent has 2 deletions on the same gene, the other parent has 1 deletion, and the offspring receives all three. In this question, both parents have alpha 1 deletion +  
ergogenic22  actually its possible that they both have 2 gene deletions, but regardless, a-thalassemia trait is more likely +  
ergogenic22  and someone above said Asian people are cis-2 deletion so the offspring will not receive two deletion from one parent +  


submitted by krewfoo99(4),

In what situations will HbH be formed (3 alpha chain deletions)?

ergogenic22  one parent has 2 deletions on the same gene, the other parent has 1 deletion, and the offspring receives all three. In this question, both parents have alpha 1 deletion +  
ergogenic22  actually its possible that they both have 2 gene deletions, but regardless, a-thalassemia trait is more likely +  
ergogenic22  and someone above said Asian people are cis-2 deletion so the offspring will not receive two deletion from one parent +  


submitted by cat5280(1),

Could someone please explain why you were able to eliminate the spinocerebellar tracts?

ergogenic22  Spinocerebellar is only responsible for Proprioception (unconscious). This patient also has reduced vibration sensation, which the dorsal column tracts are responsible for. +  


submitted by mousie(84),

Can someone please explain this to me? I don't understand why starting the other drug would not count as exclusion criteria?

seagull  This has to do with Intention-to-treat analysis. Essentially, when participants are non-adherent but the data shouldn't be lost. They just undergo another statistical model to account for their changes. Here is a nice video https://www.youtube.com/watch?v=Kps3VzbykFQ&t=7s +7  
dr.xx  Where does the question mention "intention-to-treat"? +  
notadoctor  They seem to be pretty obsessed with "intention-to-treat" it's been asked in one way or another in all the new NBMEs that I've done. (Haven't done 24 as yet) +4  
wutuwantbruv  They don't, intention-to-treat is just the best way to go about it @dr.xx +  
smc213  Great for ITT: https://www.youtube.com/watch?v=Kps3VzbykFQ +  
yex  I agree with @notadoctor !! +  
ergogenic22  i think if it were per protocol, both groups would be excluded, the ones that were inconsistent, the ones that dropped out, and the ones that switched. But answer choices only allow ITT or exclusion of one group. +  


submitted by titanesxvi(2),

why not decrease CA activity in the proximal tubule? this also could lead to metabolic acidosis.

ergogenic22  carbonic anhydrase inhibitors can cause Type 2 RTA but it is not the cause here (cystinosis) +  


submitted by seagull(437),

Splenectomy patients are vulnerable against encapsulated organisms. Which commonly include Strep Pneumo, Niesseria, H. Influenza.

ergogenic22  although Pseudomonas, Klebsiella are also encapsulated, strep pneumo is more common for pneumonia in a 25 year old F without other comorbidities +  


submitted by sunny(0),

WHY NOT YES,and then share the money with the patieny so he doesn't doubt your motives.

ergogenic22  because then it is as if you are paying the patient to enroll in the experimental treatment +  
ergogenic22  because then it is as if you are paying the patient to enroll in the experimental treatment, which I don't know why that would be wrong +  
dubywow  Bribery is only good for doctors. Can't bribe patients. That's illegal. Kind of like how NCAA gets paid a lot, but student athletes get nadda. Still the TLDR is it always ethical to disclose financial incentives when they relate to anything that may affect your decision on how to treat a patient. +  


submitted by sunny(0),

WHY NOT YES,and then share the money with the patieny so he doesn't doubt your motives.

ergogenic22  because then it is as if you are paying the patient to enroll in the experimental treatment +  
ergogenic22  because then it is as if you are paying the patient to enroll in the experimental treatment, which I don't know why that would be wrong +  
dubywow  Bribery is only good for doctors. Can't bribe patients. That's illegal. Kind of like how NCAA gets paid a lot, but student athletes get nadda. Still the TLDR is it always ethical to disclose financial incentives when they relate to anything that may affect your decision on how to treat a patient. +  


submitted by ergogenic22(47),

This question describes I-cell disease (inclusion cell disease/mucolipidosis type II). You can tell because there is mixed accumulation of junk forming the inclusion bodies. Other lysosomal storage diseases have accumulation of one type of substance.

Essentially, there is a defect in defect in the enzyme N-acetylglucosaminyl-1-phosphotransferase.

This means the mannose-6-phosphate tag cannot be added to proteins. Without this tag, proteins are incorrectly sent to the extracellular space rather than delivered to lysosomes.

ergogenic22  ^^correction. You can tell because there are elevated lysosomal enzymes in the plasma. This is because the proteins are not tagged with M6P and thus are excreted to the extracellular space. +  


submitted by mcl(220),

Patient may have hereditary angioedema, which is associated with "recurrent attacks of intense, massive, localized subcutaneous edema involving the extremities, genitalia, face, or trunk, or submucosal edema of upper airway or bowels". The article goes on to say "C1-esterase inhibitor works directly on the complement and contact plasma cascades to reduce bradykinin release" which is also probably good to know.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3666183/

notadoctor  Thought this was a trick question as C1 esterase deficiency also results in a decrease in C4. However, the second answer choice was not referring to C4 but to C4 binding protein, which I now know is different. I also didn't realize C1 esterase was technically a complement protein. +3  
youssefa  Based on many sources hereditary angioedema does NOT cause a rash (urticaria) which is a main differentiating point between angioedema and allergy. This mislead me in this question. Any clarification? +3  
ergogenic22  +1 on the above because uptodate states that c1 esterase inhibitor deficiency, both acquired and nonhereditary, are both non-urticarial, non-pruritic, and that is confirmed by the above linked article +1  
sahusema  Question writer probably didn't know the difference between cutaneous urticaria and subcutaneous edema. +  


submitted by temmy(27),

please help according to winters equation the patient has a normal anion gap

ergogenic22  winter's formula is to look at the compensation to see if it is appropriate. PCO2 = 1.5[HCO3-] + 8 +/- 2 In this case, 1.5* 10 (Pt's bicarb) +8 +/-2 = 21 to 25 Pt's PO2 is 23, so compensation is appropriate. If PCO2 was below 21, it would be concomitant respiratory alkalosis +1  
ergogenic22  in other words, winter's formula is not necessary for this question +1  
the_sacramento_kings  lol unless you want to make sure its not A. +1  
hello  @ergogenic22 Someone might use Winter's formula to rule out choice A. +  
maxillarythirdmolar  respiratory depression of alcohol should rule out "A" +  


submitted by temmy(27),

please help according to winters equation the patient has a normal anion gap

ergogenic22  winter's formula is to look at the compensation to see if it is appropriate. PCO2 = 1.5[HCO3-] + 8 +/- 2 In this case, 1.5* 10 (Pt's bicarb) +8 +/-2 = 21 to 25 Pt's PO2 is 23, so compensation is appropriate. If PCO2 was below 21, it would be concomitant respiratory alkalosis +1  
ergogenic22  in other words, winter's formula is not necessary for this question +1  
the_sacramento_kings  lol unless you want to make sure its not A. +1  
hello  @ergogenic22 Someone might use Winter's formula to rule out choice A. +  
maxillarythirdmolar  respiratory depression of alcohol should rule out "A" +  


submitted by hayayah(418),

the majority of carbon dioxide molecules are carried as part of the bicarbonate buffer system. In this system, carbon dioxide diffuses into the RBCs. Carbonic anhydrase (CA) within RBCs quickly converts the carbon dioxide into carbonic acid (H2CO3). Carbonic acid is an unstable intermediate molecule that immediately dissociates into bicarbonate ions (HCO3-) and hydrogen (H+) ions.

The newly synthesized bicarbonate ion is transported out of the RBC into the plasma in exchange for a chloride ion (Cl−); this is called the chloride shift. When the blood reaches the lungs, the bicarbonate ion is transported back into the RBC in exchange for the chloride ion. The H+ ion dissociates from the hemoglobin and binds to the bicarbonate ion. This produces the carbonic acid intermediate, which is converted back into carbon dioxide through the enzymatic action of CA. The carbon dioxide produced is expelled through the lungs during exhalation.

hungrybox  Amazing explanation. Thank you!! +  
namira  in case anyone wants to visualize things... https://o.quizlet.com/V6hf-2fgWeaWYu1u23fryQ.png +3  
ergogenic22  CO2 is carried in the blood is bound to hemoglobin, known as carbaminohemoglobin (HbCO2) (5%), dissolved CO2 (5%), bicarb is 90% +  


The patient suffered from Immune Thrombocytopenia. autoantibodies against the glycoproteins GP2B/3A.

On labs, you’ll see: increase in megakaryocytes; on the question stem they’re described as “rare but large.” Megakaryocytes are not suppressed.

ergogenic22  isolated thrombocytopenia (low platelets) should be highly suggestive of ITP https://www.aafp.org/afp/2012/0315/p612.html +  


submitted by hungrybox(245),

This video explains genital embryology extremely well.

If you felt totally lost like me, watch the video first at 2x, then check out the bottom figure on pg. 608 in FA 2019.

Relevant to this question:

  1. SRY proteins stimulate development of testes
  2. This pt has testes => he must have the SRY gene on the Y chromosome
  3. MIF degrades the Mullerian duct, which would otherwise become the internal female genitalia
  4. This pt has internal female genitalia => didn't make enough MIF

Quiz yourself (answers in a separate post):

  1. This patient's disorder can be traced back to which cells?
  2. This patient had normal genitalia. If this patient had smaller genitalia than normal, that would be a defect in what enzyme?
ergogenic22  I like to work backwards. 1) patient has normal testicles on histology, normal appearing penis this must mean a Y chromosome is present, as testis determining factor is on the y chromosome (see above post point #2). I.e. you can eliminate choice A and B. Theoretically, 47XY and 47XYY could also present with female genitalia due to lack of MIF, but normal 46XY is more common +1  


submitted by usmleuser007(127),

Vitamin E deficiency is known to cause similar spinal defects as Vitamin B12 deficiency. However, anemia is not seen.

ergogenic22  Also corticalspinal tract symptoms are not seen, but dorsal column and spinocerebellar tracts are seen +1  
sinforslide  In this case, patient's CF also predisposes fat-soluble vitamin deficiency. +3  
breis  FA pg 70 +  
usmleuser007  Correction: Read more on this Vitamin-E deficiency can in fact cause anemia - hemolytic anemia. This is b/c VitE work as an anti-oxidant; and therefore with reduced anti-oxidation RBCs are more prone to oxidative injuries. +3  


submitted by xxabi(98),

I was under the impression that this was an aortic dissection, due to "severe chest pain" as well as the false lumen in the aorta. And HTN is the #1 risk factor for aortic dissection. Someone correct me if i'm wrong, but I think this is aortic dissection rather than aortic aneurysm.

chefcurry  I believe so, FA 2018 pg 299 +2  
ergogenic22  It is dissection "extra lumen in the media of the proximal aorta" = "a longitudinal intimal (tunica intima) tear with dissection of blood through the media of the aortic wall" ... answer is still hypertension +  
breis  FA 2019: 301 +  


submitted by sympathetikey(317),

Direct Antiglobulin = Direct Coombs Test

Detects antibodies bound directly to RBCs. Hemolysis most likely due to something in the transfused blood (not sure why it took 4 weeks when Type 2 HS is supposed to be quicker but w/e).

ergogenic22  there is a delayed onset hemolytic transfusion reaction which should be evaluated with direct cooms test. https://www.ncbi.nlm.nih.gov/books/NBK448158/ +1  
hungrybox  such a dumb question wtf +8  


submitted by hayayah(418),

Glucagonoma: Tumor of pancreatic α cells Žcausing an overproduction of glucagon.

Presents with 5D’s:

  • Dermatitis(necrolytic migratory erythema)
  • Diabetes (hyperglycemia)
  • DVT
  • Declining weight
  • Depression
killme  And the sixth D: Diarrhea +1  
ergogenic22  a) CAT1 and CAT2 are important enzymes of fatty acid beta oxidation. Glucagon upregulates this process b) glycogen formation is inhibited by glucagon, so that glucose can be used by cells c) acetyl CoA carboxylase is used for fatty acid synthesis and thus decreased by increased glucagon d) glucagon increases ketogenesis +20  


submitted by hayayah(418),

Rhabdomyolysis can present looking like a kidney injury (it can lead to acute tubular necrosis as well). The electrolyte findings are just like renal failure (Inc. K+, inc. PO4-, dec. Ca)

To differentiate between rhabdomyolysis and kidney injury, you check the urine to see if there are any RBCs. In rhabdomyolysis there are no free RBCs in the urine.

ergogenic22  "Crush injury" is a buzz word for rhabdo +1  


submitted by ark110(1),

But what is the difference between option A and option C (132; 4.9; 90; 35)

sympathetikey  K+ shouldn't increase. It's moving into cells due to metabolic alkalosis. +  
home_run_ball  In the parietal cell of the stomach Hydrogen ions are formed from the dissociation of carbonic acid. Water is a very minor source of hydrogen ions in comparison to carbonic acid. Carbonic acid is formed from carbon dioxide and water by carbonic anhydrase. The bicarbonate ion (HCO3−) is exchanged for a chloride ion (Cl−) on the basal side of the cell and the bicarbonate diffuses into the venous blood, leading to an alkaline tide phenomenon. +  
ergogenic22  RAAS increases from volume loss, and thus more aldosterone leads to low K+ +  
sinforslide  Three reasons for hypokalemia. First, some K+ is lost in gastric fluids. Second, H+ shifts out of cells and K+ shifts into cells in metabolic alkalosis. Third, ECF volume contraction has caused increased secretion of aldosterone. +2  


submitted by hayayah(418),

With chronic vomiting, you lose electrolytes and a lot of acid. It triggers metabolic alkalosis which is why all the serum values are low (or on the lower end of the normal range) except for bicarbonate.

ergogenic22  decreased K+ (from increased RAAS due to volume loss) and decreased Cl- (loss of HCl from the stomach), Alkalosis from loss of HCl and thus high bicarb. For this reason high to mid range K is wrong +3  
sbryant6  Wouldn't increased RAAS lead to increased Na+? The answer shows decreased Na+. +1  
sbryant6  Also, remember Bulimia Nervosa is associated with hypokalemia. +  
sugaplum  so the range they gave for K is 3-6? so 3.2 is WNL then? or are we just operating on "it is on the lower end of normal in peds" +1  
dbg  sodium levels in pyloric stenosis vary, nothing really classic, can be high as in this case simply due to hydration, can low in other cases if aldosterone managed to reverse that to the other extreme +  


submitted by hayayah(418),

This is an example of Shingles. Herpes simplex and herpes zoster viruses cause abnormal cell division in epidermal cells, and this creates multinucleated giant cells.

A Tzank smear showing multinucleated giant cells is characteristic of Varicella Zoster Virus infections. (HSV will have similar findings).

ergogenic22  other identifying terms for herpes: Single dermatome (does not cross the midline), painful (burning and itching),and lesions in multiple stages. +1  
redvelvet  and why neutrophile infiltration, is it a thing? or just a distracting thing? +  
charcot_bouchard  Neutrophil comes into party always first. but it was distracting for me too. +  


submitted by hayayah(418),

Prostatitis is characterized by dysuria, frequency, urgency, low back pain. Warm, tender, enlarged prostate.

Acute bacterial prostatitis—in older men most common bacterium is E. coli.

ergogenic22  In young men it could be chlamydia but the question stem makes no mention of sexual activity, so it is e. coli +3  
charcot_bouchard  First this guy isnt older! He may incite Daddy issue but not older. At this age people tend to be more monogamous so E Coli the more likely answer. But again cont NBME 20 trend this one was pretty vague too. +  
monkey  They classify at 35 year old (<35 = Chlamydia or Neisseria and > 35 = E.coli) +1  


submitted by monoloco(57),

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

ergogenic22  Meckel diverticulum also occurs distal to the CBD but less likely to be associated with bilious vomiting +  
sympathetikey  Correct. Might cause pain due to ectopic gastic tissue. +