Official NBME 19 Discussions Thread - Answers with Explanations (No Questions)

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GunnerLifeGuy

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Hey guys,
So NBME 19 just came out a month back or so and I still don't see 1 firm thread on SDN (yo, where my fellow gunners at ?).. So i thought it might be a wise idea to create just 1 thread where people can discuss and solve each other queries by confirmed correct answers to NBME 19.

I did this and score a 260+ (wont divulge the exact score).. just port the questions you have a query about below and i will try to help if i got it correct. I will post my doubts here too..

Let's do this !

Disclaimer: I am not gonna respond to "Bro, hit me up with a download link to NBME 19" or " Can i get a NBME 19 pdf ?" or "I want a download link with all the screenshots of NBME 19".. I dont want trouble form the NBME so don't ask me to share that.. We are here just to discuss like every year SDNers get together to dissect a new NBME..

Also form @Ismet :
You may ask a question about an NBME question, but in no way should your post resemble or reproduce the actual question. Simply abbreviating words and taking out a few filler words doesn't count as paraphrasing. Please note that the companies that own the rights to these questions often come to SDN and may pursue legal action against the user if there is copyrighted material posted here.

So all in all.. You can ask things like "That question asking about the type of cancer that had mets in the vertebrae.. what was the answer" is OK.. and someone can say it was lytic and the only lytic mets in the options was RCC.. I picked that and it was correct.

But it is not Ok to write " A 65 year old male patient.... bla bla bla"

Got it ?

(Btw that example was made up and is not a NBME question)

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We had a thread like this with 10+ pages of posts but it was removed due to copyright violations.

edit: Sorry, I should have read your entire post first. Yes, that is exactly why that thread was removed... people were posting the exact questions and answer choices.
 
So I'll go first.
Obviously it's a spoiler
1) Does seborrheic keratosis has the same chance to appear on non sun-exposed areas as sun exposed areas?
2) Is acetaminophen indicated in patients with gastric ulcers.
3) Without any referral to any NBME question, would someone be so kind to explain the mechanism by which oral fluid therapy is useful in vibrio cholerae diarrhea
4) If a 2 week old newborn has difficulty excreting bile what's the most likely pathologic condition?
5) How can fibrates cause renal failure?
6) HCV expresses antigens in which liver cells?
7) a woman has arthritis and she has a blood uric acid level of 9. Is it likely that she has a disease characterized by negatively birefringent crystals
8) what do you think it's happening if you find trisomy on amniotic fluid and then you repeat it and there's no trisomy?
9) Your girlfriend wants to have unprotected sex with you but you'are scared that she might get pregnant. What do you measure to know if ovulation has occured or not?
10) there is a few months child with congenital HIV with a diaper rash. You take a biopsy and it resembles more or less aspergillus or maybe malassezia. Where did you think she get the infection from?
11) trendelenburg gait: which muscles compensate for the nerve damage
12) Complications associated with bulimia?
13) Doesn't nieman pick result in decreased synthesis of ceramide or what
14) Your preadolescent cousin cannot walk anymore and she is not worried about it. No neurological abnormalities, what do you suspect
15) name me the first drug that comes in your mind when you think about a drug against ulcers which decrease symptoms and helps healing the ulcers
16) that one about erectile dysfunction
17) an immigrant from zimbawe has slimy stools and abnormal findings on colonoscopy which agent do u suspect
18) How to ask sex-related questions to adolescents?
 
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So I'll go first.
Obviously it's a spoiler
1) Does seborrheic keratosis has the same chance to appear on non sun-exposed areas as sun exposed areas?
Don't remember the question
2) Is acetaminophen indicated in patients with gastric ulcers.
All the other options in that question were NSAIDs and would exacerbate the ulcer. I didn't know people used acetaminophen for ulcers, but that one made the most sense (probably to relieve the pain).
3) Without any referral to any NBME question, would someone be so kind to explain the mechanism by which oral fluid therapy is useful in vibrio cholerae diarrhea
Oral fluid therapy contains glucose. This provides a stronger gradient favoring Na and glucose symporter transport into the cell.
4) If a 2 week old newborn has difficulty excreting bile what's the most likely pathologic condition?
I forget how this question went exactly, but I believe it was decreased glucuronic acid conjugation to bilirubin. Neonatal jaundice starts ~2 days after birth, and can last ~1-2 weeks since the conjugating enzymes don't work as efficiently that early in life.
5) How can fibrates cause renal failure?
Myopathy --> myoglobin in kidneys --> tubular necrosis
6) HCV expresses antigens in which liver cells?
HCV antigens are released by the hepatocytes
7) a woman has arthritis and she has a blood uric acid level of 9. Is it likely that she has a disease characterized by negatively birefringent crystals
The answer is indeed gout.
8) what do you think it's happening if you find trisomy on amniotic fluid and then you repeat it and there's no trisomy?
Can you confirm whether they used just amniotic fluid or chorionic villus sampling followed by amniotic fluid? I believe I picked confined placental mosaicism.
EDIT: I can confirm that it is confined placental mosaicism. They did CVS initially, which looks at the chorionic villus. In some cases, the placental villi can have a trisomy due to some division error. But they did an amniocentesis afterwards, which was normal, suggesting that the fetus itself does not have a trisomy. These results are consistent w/ CPM.
9) Your girlfriend wants to have unprotected sex with you but you'are scared that she might get pregnant. What do you measure to know if ovulation has occured or not?
Progesterone will increase after ovulation (released by corpus luteum to maintain endometrium)
10) there is a few months child with congenital HIV with a diaper rash. You take a biopsy and it resembles more or less aspergillus or maybe malassezia. Where did you think she get the infection from?
It was a Candida infection; Candida makes up normal flora of vagina, skin, oral cavity.
11) trendelenburg gait: which muscles compensate for the nerve damage
I think the patient had something else wrong with their gait, not trendelenburg gait. Was it the one where the obturator nerve was injured? The answer was train the adductors since that's what the obturator innervates.
12) Complications associated with bulimia?
Don't remember the answer choices.. was parotid gland enlargement one of them? FA lists a bunch.
13) Doesn't nieman pick result in decreased synthesis of ceramide or what
There are 2 other enzymes that produce ceramide, so I think they would just compensate. All the sphingolipidoses/mucopolysacchardioses are problems w/ lysosomal enzymes i.e. hydrolases, so that one is the answer.
14) Your preadolescent cousin cannot walk anymore and she is not worried about it. No neurological abnormalities, what do you suspect
Conversion disorder
15) name me the first drug that comes in your mind when you think about a drug against ulcers which decrease symptoms and helps healing the ulcers
Omeprazole. I think the help healing w/ ulcers made people pick misoprostol (including myself), but reducing acid secretion via PPI would help with ulcer healing. Not the best wording here, more of a test-taking problem.
16) that one about erectile dysfunction
Was this the one with the picture? The answer is corpus cavernosa (look up a picture online).
17) an immigrant from zimbawe has slimy stools and abnormal findings on colonoscopy which agent do u suspect
Don't remember the vignette.
18) How to ask sex-related questions to adolescents?
Ask the mother to leave the room and then talk to the kid.
 
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thanks man! The question about erectile dysfunction is about a old man who had a cerebral infarction and difficulty sleeping/concentrating. the amount of nocturnal erections is decreased I think (atherosclerotic problem) but I thought that it was a typical case of a patient suffering of depression after a serious illness so I put decreased libido.

What an idiot I was in that question about Candida, I don't know why I kept thinking it was disseminated aspergillus but it didn't make any sense at all
 
Hi guys, I have a question about the aphasia question that asked us to ID where on the brain the stroke happened.
How can you tell whether a stroke has damaged Broca's area or if it has damaged the facial muscles in the PMC (so the patient can't talk because they can't move their muscles). The question stem said the patient has weakness on the lower 2/3 of the face so I assumed it was a stroke to the facial area of PMC rather than Broca's area... (but obviously, this was wrong haha)

Sorry if this is a dumb question, it has tripped me up so many times now! Thanks for your help!
 
1) pathophysio of decling CD4 cells in AIDS/HIV???
2) why inactivating Na+ channels decrease amplitude and not frequency? Isn't action potential all or nothing?
3) soft, mobile cyst lateral to midline that moves with tongue protrusion? I put lymph node cause thyroglossal cyst is midline, persistent cervical sinus is lateral but doesn't move w/ tongue protrusion
4) dry skin, keratoses and freckling on exposure to sunlight -> what is the disease and mechanism?
5) what is unique about tumor suppresor gene that differentiates it from proto-oncogene? I put phosphorylation of gene product cause I thought tumor suppresor p53 phosphorylates Rb (i know Rb phosphorylation inactivates Rb but none of the other answer choices made sense)
6) neimann pick pathophysio, is decreased lysosomal hydrolase? why?
7) primary syphilis ulcer histology description?
8) definiton of in situ cervical carcinoma? I think I misread the question as what is invasive cervical carcinoma (which is invasion into cervical stroma) so the answer for insitu just superficial to basement membrane?
9) older lady w/ jerky movements, ring enhancing lesion on MRI near central sulcus. positive babinksi, is it astrocytoma?
10) SCC of the skin pathophysio? Is it single strand breaks by UV?
11) loss of micturition reflex after hip trauma 2wks status post pelvic fracture, what nerve injured? Is it pudental or pelvic nerve injury, I am confused don't injury to either cause urinary retention (and loss of hypogastric would cause incontinence vs retention)
12) tibia fracture in young male playing sport leading to significant blood loss, what is the initial mechanism of compensation for decreased blood volume?
13) what causes skeletal muscle action potential to travel deep within skeletal muscle fiber? Is it transmission along T tubule?
14) granuloma or granulation in a young girl 2 weeks after stitches for a cut on face? I get difference between granulation (normal wound healing) vs granuloma (infection), do we assume it is infected cause it is slightly tender and raised? I felt like it wasn't enough info to say for sure it was infected
15) exercising muscle do all go up, tissue adenosine, arteriolar diameter and vascular conductance?
16) girl grows 3 inches taller over a summer, what causes increased Ca2+ abs in this circumstance?
17) male chromosome fetus but born with female external genitalia and absent internal genitalia = decreased response to which hormone? is it defect in testosterone sensing of androgen insensitivity syndrome?
18) was it tubocurarine that paralyze phrenic nerve and decrease abdominal muscle pressure (2/2 diaphragm paralysis).
 
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Hi guys, I have a question about the aphasia question that asked us to ID where on the brain the stroke happened.
How can you tell whether a stroke has damaged Broca's area or if it has damaged the facial muscles in the PMC (so the patient can't talk because they can't move their muscles). The question stem said the patient has weakness on the lower 2/3 of the face so I assumed it was a stroke to the facial area of PMC rather than Broca's area... (but obviously, this was wrong haha)

Sorry if this is a dumb question, it has tripped me up so many times now! Thanks for your help!

there was 2 questions like this. For the facial weakness i just chose frontal motor cortex (muscle weakness = motor problem) so assumed a MCA stroke.

For the aphasia one I think it said comprehension intact = wernicke intact, so i picked broca area lesion leading to inability to produce speech. I got both right. hope this helps
 
Woman with Marfan Syndrome and signs of Cardiac Tamponade. What findings would be on cardiac catheterization?
Cardiac index, RA pressure, PCWP, Pulmonary diastolic arterial pressure, Systemic Vascular Resistance?
 
Woman with Marfan Syndrome and signs of Cardiac Tamponade. What findings would be on cardiac catheterization?
Cardiac index, RA pressure, PCWP, Pulmonary diastolic arterial pressure, Systemic Vascular Resistance?
decreased cardiac index, increased RA pressure. there was only one answer choice that fit this parameter. i think it also had increased systemic vascular resistance, but I can't remember what it was for PCWP or pulmonary diastolic arterial pressure.
 
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decreased cardiac index, increased RA pressure. there was only one answer choice that fit this parameter. i think it also had increased systemic vascular resistance, but I can't remember what it was for PCWP or pulmonary diastolic arterial pressure.
thank you, one more question please?) Man with disinhibition syndrome, emotional outbursts, inapropriate use of language, socially inaproptriate behavior. Which brain structure lesion? and why? sounds like amygdala lesion but its not an option(
 
thank you, one more question please?) Man with disinhibition syndrome, emotional outbursts, inapropriate use of language, socially inaproptriate behavior. Which brain structure lesion? and why? sounds like amygdala lesion but its not an option(
frontal lobe. i don't know exactly why, but frontal lobe lesions are associated w/ social disinhibition.
 
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If a 2-wk old infant is jaundiced w/ pale stools, not secreting bile, has portal fibrosis, and is negative for a1-antitrypsin deficiency - what condition does that point too?

That's not what the question actually asked. I was able to weed through the answer choices, but I don't know what the underlying condition was that pointed to the correct answer.
 
If a 2-wk old infant is jaundiced w/ pale stools, not secreting bile, has portal fibrosis, and is negative for a1-antitrypsin deficiency - what condition does that point too?

That's not what the question actually asked. I was able to weed through the answer choices, but I don't know what the underlying condition was that pointed to the correct answer.
Biliary atresia
 
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thank you, one more question please?) Man with disinhibition syndrome, emotional outbursts, inapropriate use of language, socially inaproptriate behavior. Which brain structure lesion? and why? sounds like amygdala lesion but its not an option(

frontal lobe. i don't know exactly why, but frontal lobe lesions are associated w/ social disinhibition.

I remember the story of Phineas Gage anytime I see a question like that. He had an iron rod driven through his head while working. It resulted in dynamic personality changes and he became socially disinhibited. It's a cool story to read about if you're unfamiliar with it.

CosmicDoc - is biliary atresia anywhere in Pathoma? I didn't see it in FA. I feel like I've read about it before, but I couldn't locate my source last night.
 
Hey guys regarding the couple who wants to know if their child would be affected with occulocutaneous albinism, could someone just be so kind as to expond why do i have to multiply 2/3 (chance of being a carrier) to the allele freq? 1/200? Like whats the principle behid that? i answered 1/4K thinking that its the disease freq in the population and granting that the woman is unaffected the child would not manifest regardless of the carrier status of the father. Thanks in advance
 
Hey guys regarding the couple who wants to know if their child would be affected with occulocutaneous albinism, could someone just be so kind as to expond why do i have to multiply 2/3 (chance of being a carrier) to the allele freq? 1/200? Like whats the principle behid that? i answered 1/4K thinking that its the disease freq in the population and granting that the woman is unaffected the child would not manifest regardless of the carrier status of the father. Thanks in advance
Since the father's sibling is affected, we know that the father's parents are both carriers. That means the possible genetypes of the father are AA, Aa, aA, or aa. We know the father is unaffected, so that means he cannot be aa, and must be either AA, Aa, or aA. Since There are only 3 different genotypes he could have, with 2 of them being carrier genotypes, there is a 2/3 probability he is a carrier. So we obtain the probability of the father passing on a recessive allele as 2/3 (probability of being a carrier) x 1/2 (probability of passing on a recessive allele if he is a carrier). The 2/3 is not relevant to the probability that the mother is a carrier. We know the frequency of affected individuals is 1/40000 (=q^2), so q=1/200. P+q=1, so p=199/200 and 2pq=2(199/200)(1/200). To make multiplication easier we assume 199/200=1, so 2pq=2*(1/200)=1/100 --> this is the carrier frequency in the population, which we can assume for the mother.

So to answer the entire question we multiply the probability that father is a carrier and passes on the allele is 2/3*1/2 times the probability that mother is a carrier and passes on the allele is (1/100)*1/2

So we have (2/3)*(1/2)*(1/100)*(1/2) = 2/1200=1/600

(Edited for clarity)
 
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Since the father's sibling is affected, we know that the father's parents are both carriers. That means the possible genetypes of the father are AA, Aa, aA, or aa. We know the father is unaffected, so that means he cannot be aa, and must be either AA, Aa, or aA. There are only 3 different genotypes he could have, with 2 of them being carried genotypes, thus there is a 2/3 probability he is a carrier. So we obtain the probability of the father passing a recessive allele as 2/3 (probability of being a carrier) x 1/2 (probability of passing on a recessive allele if he is a carrier). The 2/3 is not relevant to the probability that the mother is a carrier. We know the frequency of affected individuals is 1/40000 (=q^2), so q=1/200. P+q=1, so p=199/200 and 2pq=2(199/200)(1/200). To make multiplication easier we assume 199/200=1, so 2pq=2*(1/200)=1/100

So to answer the entire question we multiply the probability that father is a carrier and passes on the allele is 2/3*1/2 times the probability that mother is a carrier and passes on the allele is (1/100)*1/2

So we have (2/3)*(1/2)*(1/100)*(1/2) = 2/1200=1/600

I see so its a probabilitty question also, after all... Thank you so much :D
 
Yeah I don't get the one about erectile dysfunction in a post stroke victim.. does libido stay the same or does nocturnal erections stay the same... or do both decrease? Thanks!

Also is it crypt cells responsible for intestinal epithelial cell turnover?
 
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So I'll go first.
Obviously it's a spoiler
1) Does seborrheic keratosis has the same chance to appear on non sun-exposed areas as sun exposed areas?
2) Is acetaminophen indicated in patients with gastric ulcers.
3) Without any referral to any NBME question, would someone be so kind to explain the mechanism by which oral fluid therapy is useful in vibrio cholerae diarrhea
4) If a 2 week old newborn has difficulty excreting bile what's the most likely pathologic condition?
5) How can fibrates cause renal failure?
6) HCV expresses antigens in which liver cells?
7) a woman has arthritis and she has a blood uric acid level of 9. Is it likely that she has a disease characterized by negatively birefringent crystals
8) what do you think it's happening if you find trisomy on amniotic fluid and then you repeat it and there's no trisomy?
9) Your girlfriend wants to have unprotected sex with you but you'are scared that she might get pregnant. What do you measure to know if ovulation has occured or not?
10) there is a few months child with congenital HIV with a diaper rash. You take a biopsy and it resembles more or less aspergillus or maybe malassezia. Where did you think she get the infection from?
11) trendelenburg gait: which muscles compensate for the nerve damage
12) Complications associated with bulimia? dental caries i believe... but im still going through my incorrects so ill let you know if i got it wrong
13) Doesn't nieman pick result in decreased synthesis of ceramide or what
14) Your preadolescent cousin cannot walk anymore and she is not worried about it. No neurological abnormalities, what do you suspect
15) name me the first drug that comes in your mind when you think about a drug against ulcers which decrease symptoms and helps healing the ulcers
16) that one about erectile dysfunction
17) an immigrant from zimbawe has slimy stools and abnormal findings on colonoscopy which agent do u suspect
18) How to ask sex-related questions to adolescents?
 
Could someone explain how water is reabsorbed in the PCT? I though it was paracellular, and maybe via the CA enzyme and that is another way H2O is reabsorbed into the blood.
 
Hi, I am wondering in what way Cardiac Output and Central Venous Pressure Change in a patient with leg swelling, peripheral cyanosis, S3, hypertension, and shortness of breath. Also, why they go in the direction the do would be super helpful. Thank you in advance!
 
Why is amniotic fluid sampling wrong for the Down Syndrome Q? Can someone please explain why it is chorionic villi sampling?
 
Hi, I am wondering in what way Cardiac Output and Central Venous Pressure Change in a patient with leg swelling, peripheral cyanosis, S3, hypertension, and shortness of breath. Also, why they go in the direction the do would be super helpful. Thank you in advance!

Symptoms led me to diagnose pt with CHF/ pulmonary edema given edema and SOB with fluid backup in lungs. Basically I think of this as over congestion of fluid in the central (i.e heart/lungs) venous system. Heart is failing so fluid backs up from left atrium, back to pulm veins, back into lungs. So, CVP is up, and bc heart is failing, Cardiac output is down (systolic failure, ejection fraction is down)
 
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Anyone know the correct answer to the post stroke erection question?

This has been debated, but it seems consenses is that pt had sxs of major depression, and thus his libido was most likely down. But structurally/blood flow wise, he was fine, so nocturnal erections were normal.
 
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Why is amniotic fluid sampling wrong for the Down Syndrome Q? Can someone please explain why it is chorionic villi sampling?

Stem said mom was 12 weeks gestation. CVS is performed 1st trimester, usually b/t 10-14 weeks gestation according to Up to Date. Amnio is performed after 15 weeks. From UTD. "Amniocentesis should be performed after 15 weeks of gestation because earlier procedures are less likely to be successful, are associated with higher rates of cell culture failure, and carry greater fetal risks."
 
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hi guys: would you plz explain these questions for me?
thx
block1:

During a period of 24 hrs, a 25yo man has an upper respiratory infection with features of the common cold, which of the following viral or host factor is most critical in the initial establishment of the infection?

presence of viral receptor molecules on epithelial cells?





62 yo woman abdominal cramping, pain and constipation. Tx w/ simethicone provided some relief. 20lb weight loss, increasing fatigue, and need more sleep. Endoscopy, colonoscopy, Abdomen CT normal. Pt believes insomnia due to worries about her son who’s been using drugs. She worry cancer will never get better. Vitals stable. Not anemic, all labs WNL. Next?

evaluate for Major Depressive Disorder? fatigue, insomnia, sleep disturbance……. just 3 items





45 yo man gradually worsening heartburn. Physical exam unremarkable. Endoscopy shows stomach with thickened nodular mucosa w/ no discrete ulcerations. Steiner silver stained gastric biopsy shown. Abnormality commonly associated w/ what disease?

don’t know how to read the histologic pic

Peptic ulcer Disease?


Diagram of proximal renal tubular epithelium. Which is pathway for transepithelial transport of water?

C?

by the transporter D’s help?



12 yo boy asthma and wheezing. Tx w/ inhaled bronchodilator did not resolve symptoms. What part of airway most susceptible to flow limitation due to smooth muscle contraction?

Bronchiole

Found in the trachea and along the bronchial tree, is that bc the bronchiole smaller than trachea, so it is more susceptible to flow limitation?



70 year old man develops a progressive disinhibition syndrome characterized by episodes of emotional outburst…,which of the following labeled structure is most likely damaged

is it I?

cause disinhibition syndrome can happened in frontal lobe or basal of temperal lobe
 
Anyone want to help figure out the answer to the erectile dysfunction (libido) question through process of elimination?

I can confirm that decreased libido, decreased nocturnal erections is not the correct answer. Anyone else miss it with a different answer, or get it correct and remember for sure what their answer was?

I'm not even sure what concept that question was testing haha...
 
Did anyone have the answer to the hemorrhagic shock question? I put increased renal blood Q because of sympathetics but that was wrong.
 
Did anyone have the answer to the hemorrhagic shock question? I put increased renal blood Q because of sympathetics but that was wrong.
Anyone want to help figure out the answer to the erectile dysfunction (libido) question through process of elimination?

I can confirm that decreased libido, decreased nocturnal erections is not the correct answer. Anyone else miss it with a different answer, or get it correct and remember for sure what their answer was?

I'm not even sure what concept that question was testing haha...

Answer has been debated, but it seems consenses is that pt had sxs of major depression, and thus his libido was most likely down. But structurally/blood flow wise, he was fine, so nocturnal erections were normal. So, concept NBME wants us to realize is that we should screen for depression in pts who complain of sexual dysfunction? Or ask about sex in pts who display sxs of depression, like that patient had in the stem of the Q.
 
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Did anyone have the answer to the hemorrhagic shock question? I put increased renal blood Q because of sympathetics but that was wrong.

Shock from massive fluid/blood loss will most likely result in low BP and thus weak pulse. Cool extremities, etc. I put same thing as you and got wrong. Thinking more about it, renal perfusion will go DOWN. Once of major causes of ATN is hypovolemic shock. Epi/Norepi will clamp down vessels trying to maintain central fluid/BP, so kidneys get screwed.
 
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Shock from massive fluid/blood loss will most likely result in low BP and thus weak pulse. Cool extremities, etc. I put same thing as you and got wrong. Thinking more about it, renal perfusion will go DOWN. Once of major causes of ATN is hypovolemic shock. Epi/Norepi will clamp down vessels trying to maintain central fluid/BP, so kidneys get screwed.
Thanks so much! I found this on Medscape (Hemorrhagic Shock: Background, Pathophysiology, Epidemiology) as well: Acute hemorrhage causes a decreased cardiac output and decreased pulse pressure. ... The response is an increase in heart rate, vasoconstriction, and redistribution of blood flow away from certain nonvital organs, such as the skin, gastrointestinal tract, and kidneys.

In retrospect the correct answer seems obvious, but I think I went with the knee-jerk decreased blood flow activates RAAS idea without actually thinking about what makes logical sense. I think that might have been their intention with this question.

Do you (or anyone else) have an idea about the correct answer to the water reabsorption at the PCT question?
 
hi guys: would you plz explain these questions for me?
thx
block1:

During a period of 24 hrs, a 25yo man has an upper respiratory infection with features of the common cold, which of the following viral or host factor is most critical in the initial establishment of the infection?

presence of viral receptor molecules on epithelial cells?





62 yo woman abdominal cramping, pain and constipation. Tx w/ simethicone provided some relief. 20lb weight loss, increasing fatigue, and need more sleep. Endoscopy, colonoscopy, Abdomen CT normal. Pt believes insomnia due to worries about her son who’s been using drugs. She worry cancer will never get better. Vitals stable. Not anemic, all labs WNL. Next?

evaluate for Major Depressive Disorder? fatigue, insomnia, sleep disturbance……. just 3 items





45 yo man gradually worsening heartburn. Physical exam unremarkable. Endoscopy shows stomach with thickened nodular mucosa w/ no discrete ulcerations. Steiner silver stained gastric biopsy shown. Abnormality commonly associated w/ what disease?

don’t know how to read the histologic pic

Peptic ulcer Disease?


Diagram of proximal renal tubular epithelium. Which is pathway for transepithelial transport of water?

C?

by the transporter D’s help?



12 yo boy asthma and wheezing. Tx w/ inhaled bronchodilator did not resolve symptoms. What part of airway most susceptible to flow limitation due to smooth muscle contraction?

Bronchiole

Found in the trachea and along the bronchial tree, is that bc the bronchiole smaller than trachea, so it is more susceptible to flow limitation?



70 year old man develops a progressive disinhibition syndrome characterized by episodes of emotional outburst…,which of the following labeled structure is most likely damaged

is it I?

cause disinhibition syndrome can happened in frontal lobe or basal of temperal lobe

I think the viral receptor for rhinovirus is ICAM-1 on epithelial cells.
I think that's why it says to evaluate for (not diagnose) MDD. He has some of the characteristics, so you should delve into it further. That was my rationale, anyway.
The pic shows H. pylori. Silver stain is used for it.
Transport of water question, I just chose the arrow that went from lumen to blood that didn't require the use of any transporters since water is reabsorbed by passive diffusion in the PCT.
Trachea has cartilage to keep the airway patent. Bronchioles do not.
With disinhibition, I just generally assume frontal lobe unless they include hypersexuality and hyperorality in the vignette --> amygdala.
 
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Anyone want to help figure out the answer to the erectile dysfunction (libido) question through process of elimination?

I can confirm that decreased libido, decreased nocturnal erections is not the correct answer. Anyone else miss it with a different answer, or get it correct and remember for sure what their answer was?

I'm not even sure what concept that question was testing haha...
I can confirm that the answer isn't normal libido and decreased nocturnal erections. I was thinking along the line of atherosclerosis leading to a blood flow problem, and he came in with inability to maintain an erection without mention of a change in desire, so that led me away from a decreased libido.

I agree though now that I'm reading the question again that depression should be on the radar since it talked about fatigue, difficulty sleeping, and difficulty concentrating.
 
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I can confirm that the answer isn't normal libido and decreased nocturnal erections. I was thinking along the line of atherosclerosis leading to a blood flow problem, and he came in with inability to maintain an erection without mention of a change in desire, so that led me away from a decreased libido.

I agree though now that I'm reading the question again that depression should be on the radar since it talked about fatigue, difficulty sleeping, and difficulty concentrating.

Hey, so from some research it looks like the answer they wanted was decreased libido and normal nocturnal erections. I think the idea was supposed to be that cerebral infarctions are associated with depression in the elderly. I think the nocturnal erections part was indicating that he doesn't have any problems with his autonomic nerves down there. This is not definitive, but I think I'll be choosing this answer if it shows up on my exam unless someone can confirm they chose it and it was wrong. Best of luck!
 
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Hi! Could somebody please help clarify how tumor supressors are diff from Proto oncogenes? More importantly, why isn't it the choice that says "phosphorylation of gene product?"
 
Hi! Could somebody please help clarify how tumor supressors are diff from Proto oncogenes? More importantly, why isn't it the choice that says "phosphorylation of gene product?"
Hey,

I had the same thought when I faced this question. I changed my answer to the correct one --> A (inhibition cell cycle). I changed my answer because they ask about the mechanism of actions. Oncogenes with gain of function mutation lead to increased transcription etc whereas tumor suppresor genes block G1-->S phase. NF1 gene product has RAS GTPase activity which works by phosphorylating and activating protein (neurofibromin). So there is at least 1 tumor suppresor gene that works through phosphorylation.
Hope that helps.
 
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Thanks so much! I found this on Medscape (Hemorrhagic Shock: Background, Pathophysiology, Epidemiology) as well: Acute hemorrhage causes a decreased cardiac output and decreased pulse pressure. ... The response is an increase in heart rate, vasoconstriction, and redistribution of blood flow away from certain nonvital organs, such as the skin, gastrointestinal tract, and kidneys.

In retrospect the correct answer seems obvious, but I think I went with the knee-jerk decreased blood flow activates RAAS idea without actually thinking about what makes logical sense. I think that might have been their intention with this question.

Do you (or anyone else) have an idea about the correct answer to the water reabsorption at the PCT question?

Sympathetic activation does a few things at the kidneys:
1. Constrict afferent and efferent arteriole (this maintains filtration fraction, but RPF goes down).
2. Increase renin release (B1 mediated). This increases RAAS system, leading to aldosterone-mediated Na uptake at collecting duct.
3. RELEVANT HERE: DIRECT increase in sodium reabsorption at the PCT. I didn't know this, though it rings a bell from renal block.

Source; SNS - Renal Effects | Pathway Medicine
 
Hi! Could somebody please help clarify how tumor supressors are diff from Proto oncogenes? More importantly, why isn't it the choice that says "phosphorylation of gene product?"

This is a fun "one of these things are not like the other" questions. If you read carefully it's asking "what DISTINGUISHES tumor suppressors FROM oncogenes." So you will either be looking for: something that ONLY tumor suppressors do that no oncogenes do, or something that ONLY oncogenes do that tumor suppressors do not.

Picking apart the answers you have:
G protein mutations- this is RAS, oncogene
mutations of gene activation- MYC, oncogene
phosphorylation of gene product- any tyrosine kinase
Trans factor blah blah- sounds like a fancy way of saying gene activation, again this is oncogene

So really the ONLY thing that is SPECIFIC to oncogenes is inhibition of cell cycle regulation.

Hope this helps, and is correct. I got this wrong and this is how I worked it out.
 
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This is a fun "one of these things are not like the other" questions. If you read carefully it's asking "what DISTINGUISHES tumor suppressors FROM oncogenes." So you will either be looking for: something that ONLY tumor suppressors do that no oncogenes do, or something that ONLY oncogenes do that tumor suppressors do not.

Picking apart the answers you have:
G protein mutations- this is RAS, oncogene
mutations of gene activation- MYC, oncogene
phosphorylation of gene product- any tyrosine kinase
Trans factor blah blah- sounds like a fancy way of saying gene activation, again this is oncogene

So really the ONLY thing that is SPECIFIC to oncogenes is inhibition of cell cycle regulation.

Hope this helps, and is correct. I got this wrong and this is how I worked it out.

Hey! Thanks for your explanation. Yes, hate how I sometimes get a question wrong purely due to the misunderstanding the stem. You make perfect sense, but! If you see page 42 in 2017 FA- you'll see that the Rb gene, for instance, needs to be phosphorylated before it can be active or inactive ( hypo and hyper) . This was the logic behind me choosing phosphorylation of gene product. Because essentially, if an Rb gene is hyperphosphorylated, it allows G1 to S phase transition. So, a forever hyperphosphorylated Rb gene is technically a tumor suppressor devoid of its "suppression" function. Not sure if I'm making sense. I see your point though, but just pondering over this phosphorylation logic.
 
Hey! Thanks for your explanation. Yes, hate how I sometimes get a question wrong purely due to the misunderstanding the stem. You make perfect sense, but! If you see page 42 in 2017 FA- you'll see that the Rb gene, for instance, needs to be phosphorylated before it can be active or inactive ( hypo and hyper) . This was the logic behind me choosing phosphorylation of gene product. Because essentially, if an Rb gene is hyperphosphorylated, it allows G1 to S phase transition. So, a forever hyperphosphorylated Rb gene is technically a tumor suppressor devoid of its "suppression" function. Not sure if I'm making sense. I see your point though, but just pondering over this phosphorylation logic.

I could be mistaken, but I still don't think that would qualify as a tumor suppressor mutation. If the Rb gene is being inappropriately hyperphosphorylated, I would think that would likely be a problem with the Cyclin-CDK system. The Rb gene product itself is not the problem. That's an oncogene issue, not a problem with the tumor suppressor. If Rb was not functioning, then even in its hypophosphorylated state it would be unable to prevent cell cycle progression, and that would be a tumor suppressor mutation.
 
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Hey! Thanks for your explanation. Yes, hate how I sometimes get a question wrong purely due to the misunderstanding the stem. You make perfect sense, but! If you see page 42 in 2017 FA- you'll see that the Rb gene, for instance, needs to be phosphorylated before it can be active or inactive ( hypo and hyper) . This was the logic behind me choosing phosphorylation of gene product. Because essentially, if an Rb gene is hyperphosphorylated, it allows G1 to S phase transition. So, a forever hyperphosphorylated Rb gene is technically a tumor suppressor devoid of its "suppression" function. Not sure if I'm making sense. I see your point though, but just pondering over this phosphorylation logic.

You are correct there is a tumor suppressor that has a similar mechanism as an oncogene, but remember the question we are dissecting. We are asked what is something that differentiates them, not something that is similar to both classes. Are there any oncogenes that can regulate G1-S?
 
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I could be mistaken, but I still don't think that would qualify as a tumor suppressor mutation. If the Rb gene is being inappropriately hyperphosphorylated, I would think that would likely be a problem with the Cyclin-CDK system. The Rb gene product itself is not the problem. That's an oncogene issue, not a problem with the tumor suppressor. If Rb was not functioning, then even in its hypophosphorylated state it would be unable to prevent cell cycle progression, and that would be a tumor suppressor mutation.
You are correct there is a tumor suppressor that has a similar mechanism as an oncogene, but remember the question we are dissecting. We are asked what is something that differentiates them, not something that is similar to both classes. Are there any oncogenes that can regulate G1-S?

Makes so much sense!!! Thanks a tonne.
 
Does anyone know the answer for the question about the man with rib fractures, no pneumothorax and it asked about respiratory rate, tidal volume and airway resistance? Thanks!
 
Does anyone know the answer for the question about the man with rib fractures, no pneumothorax and it asked about respiratory rate, tidal volume and airway resistance? Thanks!

I believe it is

RR- increase ( to get rid of accumulated CO2 due to inefficient breathing secondary to fractured chest wall)
TV: Decrease (because of reduced chest wall expansion you can't breath in as much)
airway resistance: no change

This was my logic and I haven't gotten it in my list of wrong ones on expanded feedback.
 
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hi guys: would you plz explain these questions for me?
thx
block1:

During a period of 24 hrs, a 25yo man has an upper respiratory infection with features of the common cold, which of the following viral or host factor is most critical in the initial establishment of the infection?

presence of viral receptor molecules on epithelial cells?
Yes they need to bind receptors on epithelial cells to start to invade.




62 yo woman abdominal cramping, pain and constipation. Tx w/ simethicone provided some relief. 20lb weight loss, increasing fatigue, and need more sleep. Endoscopy, colonoscopy, Abdomen CT normal. Pt believes insomnia due to worries about her son who’s been using drugs. She worry cancer will never get better. Vitals stable. Not anemic, all labs WNL. Next?

evaluate for Major Depressive Disorder? fatigue, insomnia, sleep disturbance……. just 3 items
We haven't evaluated her yet, so there are probably more than 3 symptoms. Also weight loss, worrying.




45 yo man gradually worsening heartburn. Physical exam unremarkable. Endoscopy shows stomach with thickened nodular mucosa w/ no discrete ulcerations. Steiner silver stained gastric biopsy shown. Abnormality commonly associated w/ what disease?

don’t know how to read the histologic pic

The little black spots are gram negative comma shaped rods (urease positive), I'll let you figure out the rest there.

Diagram of proximal renal tubular epithelium. Which is pathway for transepithelial transport of water?

C?

by the transporter D’s help?



12 yo boy asthma and wheezing. Tx w/ inhaled bronchodilator did not resolve symptoms. What part of airway most susceptible to flow limitation due to smooth muscle contraction?
Bronchioles have smooth muscle and no cartilage so they are most prone to closing up.
Bronchiole

Found in the trachea and along the bronchial tree, is that bc the bronchiole smaller than trachea, so it is more susceptible to flow limitation?



70 year old man develops a progressive disinhibition syndrome characterized by episodes of emotional outburst…,which of the following labeled structure is most likely damaged
Frontal lobe, think of phineas gage or frontotemporal dementia. Your frontal lobe = your personality.
is it I?

cause disinhibition syndrome can happened in frontal lobe or basal of temperal lobe

Does anyone know the answer for the question about the man with rib fractures, no pneumothorax and it asked about respiratory rate, tidal volume and airway resistance? Thanks!
 
Does anyone know the answer for the question about the man with rib fractures, no pneumothorax and it asked about respiratory rate, tidal volume and airway resistance? Thanks!

The guy is in pain, chest wall pain specifically. He doesnt want to expand his chest much or it will hurt. So he compensates by decreasing his tidal volume and increasing his respiratory rate.
 
First of all thanks for the topic and thanks for the explanations, I will try to talk about some confusing questions for me without writing the question itself

1- why does a karyotyping change from xx to xy for a girl after transplantation from nonautologous donor?
2- Propranolol decreases blood pressure and decreases renin secretion on the other hand it antagonize B2 receptors which causes vasodilatation, right ? why should i choose it increases total peripheral resistance based on the 2nd part when it treats HTN?
3- I see an image with continuous phrenic nerve depolarization after administration of drug X so it should be Succinylcholine not Tubocurarine but the only explanation for me is that black line means no depolarization
4- Renal O2 consumption is maximum at tubular reabsorbtion, explain please..
5- PPD should be negative in immunocompromised pts like HIV for example, so it shouldn't give response either it is 5 mm or 10 mm !
6- Injecting bcl-2 (oncogene that cause B cell lymphoma) into mice should affect B cells not T cells but they chose it will cause decreased cell death in the thymic cortex , any explanation.
7- Why should HLA matching possibility be 1:4 between a women and her brother , do they mean person gets an allele from each parent and possibility brother and sister have the same 2 alleles is 25%.
8- I dont know what is the lysosomal hydrolase , is it the same Sphingomyelinase?
9- so Crypt cells are responsible for epithelial regeneration, new info for me ..
 
First of all thanks for the topic and thanks for the explanations, I will try to talk about some confusing questions for me without writing the question itself

1- why does a karyotyping change from xx to xy for a girl after transplantation from nonautologous donor?
2- Propranolol decreases blood pressure and decreases renin secretion on the other hand it antagonize B2 receptors which causes vasodilatation, right ? why should i choose it increases total peripheral resistance based on the 2nd part when it treats HTN?
3- I see an image with continuous phrenic nerve depolarization after administration of drug X so it should be Succinylcholine not Tubocurarine but the only explanation for me is that black line means no depolarization
4- Renal O2 consumption is maximum at tubular reabsorbtion, explain please..
5- PPD should be negative in immunocompromised pts like HIV for example, so it shouldn't give response either it is 5 mm or 10 mm !
6- Injecting bcl-2 (oncogene that cause B cell lymphoma) into mice should affect B cells not T cells but they chose it will cause decreased cell death in the thymic cortex , any explanation.
7- Why should HLA matching possibility be 1:4 between a women and her brother , do they mean person gets an allele from each parent and possibility brother and sister have the same 2 alleles is 25%.
8- I dont know what is the lysosomal hydrolase , is it the same Sphingomyelinase?
9- so Crypt cells are responsible for epithelial regeneration, new info for me ..

1 - Boy's bone marrow produces XY cells
2 - B2 blockade don't overthink it.
3 - Nerve is okay but no muscle contraction
4 - PCT - max reabsorption through secondary active transport
5 - PPD cutoff is lowered, so there are now less negatives and more positives
6 - Bcl2 antiapoptotic - don't overthink it
7 - same genotype
8- hydrolase splits molecules with the addition of water.
 
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