Official nbme 15 discussion

[abelabbot]

A new NBME 15 is out! Here is the official discussion page. How did you guys feel about this nbme?

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[smith283]

The question of esophageal atresia asks what is the cell origin that fills the lumen. Also the question states it's fibrotic, does that mean that fibroblasts filled the lumen? I guess not since the answer was endoderm

 

[D0CYAN]

Couple questions for you guys!

1. The old woman with the Ca around 8 and really really high PTH-muscle pain exacrbated by activity-any idea. I put primary hyperPTH but that was wrong.

2. Vignette of a albino (white skin, hair, blue eyes) child-asks what the number of melanocytes and melanin would be, I assume its decreased melanocytes and normal melanin?

3. Right wrist injury, not a fracture in 15 y/o. Point tenderness to palpation of radial aspect between abductor pollicis longus and extensor brevis tendons-asks for sequelae. Put subluxation of trapezium, wrong. Could it be damage to median N.?

4. 18 y/o trys suicide w/ 100 ASA tablets-two days later you find blood in stool, her Hb conc is 12, what else would you expect to find abnormal?
I put platelet count, but that was incorrect.

5. newborn with esophagela atresia, what germ layer is the origin of the cells filling the lumen? Endoderm? I suck at embryo

Thanks guys

The aspirin question was increased bleeding time, because aspirin blocks TXA2 synthesis -> abnormal platelet function.

 

[Msoliman]

Hey guys did anyone get the question of influenza A virus SF and NY ?!!!!

any help please i've been trying but don't know if i'm trying right or imagining stuff,,,

 

[as90]

Regarding the patient who had cardiac failure, it would be prrenal azotemia, but what should his urine show? would it be the dirty brown casts?

 

[VCorp]

Regarding the patient who had cardiac failure, it would be prrenal azotemia, but what should his urine show? would it be the dirty brown casts?

Prerenal eventually progresses to intrarenal... And that causes ATN. In ATN you'd see the muddy brown casts, which is pathognomonic for ATN.

 

[as90]

thanks

 

[as90]

there was a q that talked about someone taking a loop diuretic and what disturbance it what cause?

i knew it would be hypokalemia so I thought cells in body will try and push out potassium to compensate for the loss of K+ and then take up Hydrogen. Then the alkalosis will happen. but the second part asks for volume contraction?

can someone explain the way to think behind this one? thanks so much guys

 

[MDSlacker]

Hey guys, just finished going over this exam. Overall I thought it was relatively difficult and a lot of WTF questions. The stems seemed pretty long and I basically had 5 minutes or less left in each block. I've been hearing that the real exam has super long stems so hopefully I'll have enough time on test day. Ended up getting a 252 (19 missed) which I was a little upset with considering the fact that I got a 252 on 13 and 12 (taken 1 and 3 weeks ago respectively). Hopefully I can go up a couple more points by test day, have little less than a week left.

I was able to find answers to all of the questions I missed but still had a couple questions on some that I don't quite understand if someone could explain. Thanks

How does smoking decrease the recurrence of a duodenal ulcer and why would decreasing caffeine and fatty foods not decrease the recurrence of either H. pylori or the ulcer.

Question about the kid who has down syndrome and now has pancytopenia, lethargy, bruising, fever, etc. Answer was ALL so he would have increased lymphoblasts but why could it not be aplastic crisis caused by parvovirus?

Question about organophosphate poisoning I understand that atropine is important and the problems it causes can be really bad but why wouldn't you want to give pralidoximine right away considering the fact that it only works prior to aging and that's a time sensitive thing?

How is H. pylori associated with esophageal adenocarcinoma? I didn't see any mention of that in First Aid, Pathoma, or Uptodate.

For the girl who has somatization disorder (I think) do you not try and confront them about this issue or do you just keep running tests, etc. Seems very against the whole idea of decreasing costs in medicine.

Alright that's it. I would appreciate it if someone could clarify any of these. Thanks.

 

[as90]

Hi guys, was wondering if I could get some help on some of the questions. A brief EXPLANATION would be great too if you have one.

Before I post though, I briefly read some of the above posts and thought I'd contribute:
- I got the Down Syndrome with ALL wrong too. I put MEGALOBLASTOSIS because of pathoma. But note that Megaloblastosis DOES NOT refer to Megakaryoblastic Leukemia, it refers to large RBC's (MCV>100). So I guess pathoma isn't wrong in this case.

- saw someone post that the anal lesion with a picture was SCC of the anus, but its actually external hemorrhoids (painful and doesn't bleed). Maybe someone already corrected this.

My questions:

Lymphocyte neoplasm DOES NOT express: CD4, CD8, surface igM, surface IgG, cytoplasmic IgM and mu-heavy chains, cytoplasmic IgG, and gamma-heavy chains. It DOES express class I MHC and show rearrangement of the T-lymphocyte receptor beta-chain gene D and J segments. Which is the normal counterpart?
a. Activated cytolytic effector T lymphocytes in circulation
b. Mature IgM-secreting B lympchotes in LN
c. Mature Immunoglovulin secreting plasma cells in LN
d. Pre-B lymphocyte progenitor of mature B lymphobytes in the BM
e. T-lymphocyte thyocytes localized to the thymic cortex

Kid presents with congestive heart failure due to a VSD. After fixing the VSD, what changes will be seen in the following:
- Left Ventricular P
- Right Ventricular P
- Left Atrial P
I though the Right ventricular P would obviously go down since the Left -> Right shunt will be closed off. What happens to LV and LA pressure and Why?? This one drove me nuts! (I put increased LA pressure because the Right ventricle wont be as overloaded from the shunt, and will be able to pump blood out more effectively, but that was wrong)

4. Woman has history of altered consciousness. She stops talking in mid-sentence, turns her head to the right, and extends and stiffens her right upper extremity. She has a blank look and does not respond to any questions. She then has some repetitive lip smacking and picking movement of the hands. Episodes lasts 30secs. She slowly returns to he normal state during the next 4-5min. What type of seizure is it?
- Absence
- Complex partial
- Generalized tonic clonic
- Simple partial motor
- Simple partial sensory
Put Tonic clonic just cause I saw the stiffness, followed by a repetitive movement. Is this wrong because its not the entire body/extremities? Is the answer Complex partial? Didn't know it would switch from stiffness to clonus like that.

67 year old man comes to the physician because of a 2 month history of pain in his feet. It is more severe at night and is relieved by taking a hot bath. He has DM2. Strength is normal and symmetric in the distal and proximal upper and lower extremities. Achilles deep tendon reflexes are decreased and quadricept deep tendon reflexes are normal. Sensation to pinprick and vibration is decreased from just above the ankles distally. This patients pain is most likely described as?
- Aching, Burning, Colicky, Cramping, Sharp, Squeezing
Put sharp thinking it was neuropathy induced pain, but I'm guessing its Cramping due to peripheral vascular disease?? Does DM neuropathy not present with sharp pain (Probably made that up during the exam haha)?

Thanks in advance guys! Again, explanations would be greatly appreciated!

Regarding the VSD, can someone explain what happens to the left atrium and left ventricle after correction? I see the RVH being corrected so the right ventricle has less pressure, not really understanding the correct answer for that one.

Thanks so much

 

[DeutscheJasmin]

In the question about the defect in renal ammoniagenesis, what is the source of ammonia production?

Hi, I just took the form 15 online and bought the expanded pack. How can you know which questions you got wrong or right? It only tells me how many questions I got wrong in each discipline. Thanks a lot!

 

[Kovach]

Hey, guys, what was answer to that question about cocaine effect on fetus?

 

[addo]

Hey, guys, what was answer to that question about cocaine effect on fetus?

Most often cocaine exposure causes IUGR... so small baby. Dont remember what the answer was worded exactly, but something to the effect of growth restriction.

 

[startswithb]

Most often cocaine exposure causes IUGR... so small baby. Dont remember what the answer was worded exactly, but something to the effect of growth restriction.

I took it yesterday, and it was prematurity. Perhaps due to the cocaine connection to placental abruption.

 

[SLC]

Hi, I just took the form 15 online and bought the expanded pack. How can you know which questions you got wrong or right? It only tells me how many questions I got wrong in each discipline. Thanks a lot!

On your score report, bottom left corner, there's a "next" button that lets you see the ones you missed.

 

[startswithb]

Regarding the VSD, can someone explain what happens to the left atrium and left ventricle after correction? I see the RVH being corrected so the right ventricle has less pressure, not really understanding the correct answer for that one.

Thanks so much

Correcting the VSD would decrease the extra blood going into the RV, so RV pressure decreases like you said, but that extra blood has to go back to the LV, so LV pressure increases. There was only one answer choice that had this combination, and it included LA pressure being decreased. My best guess is that since LA pressure is most closely related to pulmonary venous pressure, that the decrease in blood from the right side of the heart and then through the lungs would decrease pressure in the LA.

 

[startswithb]

there was a q that talked about someone taking a loop diuretic and what disturbance it what cause?

i knew it would be hypokalemia so I thought cells in body will try and push out potassium to compensate for the loss of K+ and then take up Hydrogen. Then the alkalosis will happen. but the second part asks for volume contraction?

can someone explain the way to think behind this one? thanks so much guys

Diuretics...diuresis...volume contraction.

 

[startswithb]

For the girl who has somatization disorder (I think) do you not try and confront them about this issue or do you just keep running tests, etc. Seems very against the whole idea of decreasing costs in medicine.

Alright that's it. I would appreciate it if someone could clarify any of these. Thanks.

My friend showed me in a Step 2 book that the treatment for somatization disorder is to schedule regular follow-ups. It would theoretically decrease the number of appointments that the patient may be making with multiple other doctors.

 

[Kovach]

Most often cocaine exposure causes IUGR... so small baby. Dont remember what the answer was worded exactly, but something to the effect of growth restriction.

Cocaine doesn't cause IUGR

 

[DrTica]

- sexually active 26 y/o w/ lump on rectal area...severe pain, no bleeding, inconsistently uses condoms (anal carcinoma, anal fissure, external hemorrhoid, HPV, skin tag)

This one I missed too .
The correct one is HPV which causes the SCC of the anus ( ectoderm Ca , this is the reason for pain ) .
The general rule in this type of question where you see also pictures should be HPV .
The picture was not the best one and confusing ... .

-why deoxygenated blood can carry more CO2 than oxygenated blood.
This is Halden effect . Correct answer is buffering better .. .

this one isn't HPV because I said that and got it wrong, I read on another board that it was external hemorrhoids

 

[Kovach]

this one isn't HPV because I said that and got it wrong, I read on another board that it was external hemorrhoids

External hemorroids! Not just that I had that answer right, I also have them

 

[DrTica]

1. If the patient has high PTH and low Ca then it cannot be primary hyperparathyroidism. It has to be secondary to something. I do not remember the question to tell what was the cause.

2. In albinos there are normal melanocytes and decreased production of melanin. As opposed to vitiligo where there is destruction of melanocytes.

3. Cannot remember, but I think it was median nerve dmg.

4. cannot remember the other answer choices.

5. Yes, endoderm is the right answer.

I put median nerve and it was wrong anyone else have more luck?

 

[Kovach]

Aseptic necrosis of the scaphoid bone, due to its poor vascularization

 

[Jamiu22]

experimental question about H pylori stains which shows. Which of the following mechanisms best explains this genetic change?

Original isolate:
... ACC CCC CCC ACT CAA ATT GAA CCT AGC ....
... Thr Pro Pro Thr Gln lle Glu Pro Ser .....

Subsequent isolates:
... ACC CCC CCC CAC TCA AAT TGA ACC TAG ...
... Thr Pro Pro His Ser Asn STOP

C) Slipped-strand mispairing

E) Transposon insertion (chose this and I got it wrong)

Anyone have a clue on this one?

 

[blaqmamba]

go a few pages back, someone answered my question on that and it helped me understand it better

 

[aidama]

Anyone have a clue on this one?

pretty sure it's C, but i'm not sure why. i eliminated E because i didn't think h. pylori had anything to do with transposons.. got the q right

 

[Jamiu22]

Thanks blaqmamba & aidama, i see it now!!

 

[JuliaJulia]

I just went through the whole thead but I am still unsure about these ones I missed:

72 year old man w COPD - slow the rate of decline in this pt's pulmonary function?
I put corticosteriord therapy -- is the answer smoking cessation? ( I thought smoking cessation would IMPROVE his pulmonary function)

22 year old college student who is anxious and drinks 2 cups of coffee every morning?
I put substance-induced anxiety disorder --- is the answer general anxiety disorder?

Find the Km -- I took the Vmax (2) and divided it by 2 = 1 but answer choices were
<.06
.2-.5
.5-1
1-2
8-20

If half of Vmax is 1 --how do you decided between .5-1 and 1-2?

Pt w a teratoma (cystic lesion w hair, oily substance) what is the source of the neoplasm?
germ cells
granulosa cells
sex cord cells
stromal cells
surface epithelial cells (I put this because the neoplastic part usually comes from skin)

Thanks a ton. I take the exam in 6 days.

 

[FIREitUP]

I just went through the whole thead but I am still unsure about these ones I missed:

72 year old man w COPD - slow the rate of decline in this pt's pulmonary function?
I put corticosteriord therapy -- is the answer smoking cessation? ( I thought smoking cessation would IMPROVE his pulmonary function)

22 year old college student who is anxious and drinks 2 cups of coffee every morning?
I put substance-induced anxiety disorder --- is the answer general anxiety disorder?

Find the Km -- I took the Vmax (2) and divided it by 2 = 1 but answer choices were
<.06
.2-.5
.5-1
1-2
8-20

If half of Vmax is 1 --how do you decided between .5-1 and 1-2?

Pt w a teratoma (cystic lesion w hair, oily substance) what is the source of the neoplasm?
germ cells
granulosa cells
sex cord cells
stromal cells
surface epithelial cells (I put this because the neoplastic part usually comes from skin)

Thanks a ton. I take the exam in 6 days.

teratoma is a germ cell tumor, smoking would slow the progression of disease--corticosteroids would probably help to an extent of decreasing cytokine release and whatnot, but smoking directly activates macrophages/neutrophils to release elastases and destroy the lung parenchyma (cigarettes also inactivate a1antitrypsin)

 

[wanderer]

I just went through the whole thead but I am still unsure about these ones I missed:

72 year old man w COPD - slow the rate of decline in this pt's pulmonary function?
I put corticosteriord therapy -- is the answer smoking cessation? ( I thought smoking cessation would IMPROVE his pulmonary function)

22 year old college student who is anxious and drinks 2 cups of coffee every morning?
I put substance-induced anxiety disorder --- is the answer general anxiety disorder?

Find the Km -- I took the Vmax (2) and divided it by 2 = 1 but answer choices were
<.06
.2-.5
.5-1
1-2
8-20

If half of Vmax is 1 --how do you decided between .5-1 and 1-2?

Pt w a teratoma (cystic lesion w hair, oily substance) what is the source of the neoplasm?
germ cells
granulosa cells
sex cord cells
stromal cells
surface epithelial cells (I put this because the neoplastic part usually comes from skin)

Thanks a ton. I take the exam in 6 days.

Caffeine does't really cause anxiety and if it did it would be only right around when the person drank coffee. GAD is more likely but need to see the stem.

Km is the substrate concentration at half of vmax, not vmax/2.

 

[Tamt]

this thread was really helpful

also: i dont get q about Km in lesch-n. can anyone explain it simply.

 

[JuliaJulia]

What is Vmax? So then what is half of Vmax? THANK UU!!

 

[JuliaJulia]

Is the answer .2 - .5?

 

[Tamt]

so i looked up in kap notes or i felt dumber

Vmax for this Pt is 2,0. half V/max is 1. substrate conc that gives this half.Vmax ( i.e. 1,1 in these choices) is 0.5. i got this Q wrong. so i hope i get it right now.

 

[JuliaJulia]

.5 is included in 2 answer choices

 

[Tamt]

.5 is included in 2 answer choices

feel dumb again

 

[VCorp]

The answer is .2 - .5. 1/2Vmax, so what's the maximum Vmax? 2. What is half of that, that equals 1. Go up to 1 and now go to the left, it's found between .2-.5.

 

[Tamt]

yeahhhh exactly 1,1 is at .5, so 1 is between .2 and .5 thanks

 

[Tamt]

The answer is .2 - .5. 1/2Vmax, so what's the maximum Vmax? 2. What is half of that, that equals 1. Go up to 1 and now go to the left, it's found between .2-.5.

yeaah exactly, 1.1 is found at .5, so 1 will be between .2 and .5 thanks

 

[Kovach]

Km is a concentration of a substrate needed to achieve half of the Vmax. Simple as that!

 

[patientcare]

There were a few questions asked in this thread that have not yet received a response, I think. If they have, I apologize. I only briefly reviewed the posts. I've included them below with my responses. Hopefully, they help.

Essentially getting at precocious puberty (dont give a cause) just want you to know that initially the height will be above normal (75th percentile) and there growth plates will fuse earlier leading to a shorter person than normal (25th percentile) as an adult.



Couple questions for you guys!

1. The old woman with the Ca around 8 and really really high PTH-muscle pain exacrbated by activity-any idea. I put primary hyperPTH but that was wrong.

2. Vignette of a albino (white skin, hair, blue eyes) child-asks what the number of melanocytes and melanin would be, I assume its decreased melanocytes and normal melanin?

3. Right wrist injury, not a fracture in 15 y/o. Point tenderness to palpation of radial aspect between abductor pollicis longus and extensor brevis tendons-asks for sequelae. Put subluxation of trapezium, wrong. Could it be damage to median N.?

4. 18 y/o trys suicide w/ 100 ASA tablets-two days later you find blood in stool, her Hb conc is 12, what else would you expect to find abnormal?
I put platelet count, but that was incorrect.

5. newborn with esophagela atresia, what germ layer is the origin of the cells filling the lumen? Endoderm? I suck at embryo

Thanks guys

I believe all questions here were addressed. However, I think it is worth mentioning that for number 3, the response is avascular necrosis of the proximal scaphoid because the questions stem describes the two tendons that form the borders of the anatomical snuffbox. Point tenderness in the snuffbox will always be a scaphoid fracture. The scaphoid receives blood from the dorsal scapular artery, which perfuses the scaphoid beginning from its distal end. Hence, avascular necrosis of the PROXIMAL scaphoid.

Hey guys did anyone get the question of influenza A virus SF and NY ?!!!!

any help please i've been trying but don't know if i'm trying right or imagining stuff,,,

The objective is to determine which gene (let's call it X) segregates with the resistance gene (R). You know that the SF virus carries R somewhere. If there is a gene X that segregates with R, any virus progeny strain that inherits R from SF must also inherit that gene X from SF. Knowing that, look through the progeny viruses that demonstrate resistance (there were several of them, ranging from 1.0 to 0.4 growth). Next, look through there genes to see which gene column is consistently inherited from SF (I believe it was HA). Next, double-check to make sure that those viruses that inherited the HA gene from NY lost their resistance.

I apologize if this explanation is confusing. Unfortunately, it is difficult to describe the question without having it in front of me.

Hey guys, just finished going over this exam. Overall I thought it was relatively difficult and a lot of WTF questions. The stems seemed pretty long and I basically had 5 minutes or less left in each block. I've been hearing that the real exam has super long stems so hopefully I'll have enough time on test day. Ended up getting a 252 (19 missed) which I was a little upset with considering the fact that I got a 252 on 13 and 12 (taken 1 and 3 weeks ago respectively). Hopefully I can go up a couple more points by test day, have little less than a week left.

I was able to find answers to all of the questions I missed but still had a couple questions on some that I don't quite understand if someone could explain. Thanks

How does smoking decrease the recurrence of a duodenal ulcer and why would decreasing caffeine and fatty foods not decrease the recurrence of either H. pylori or the ulcer.

Question about the kid who has down syndrome and now has pancytopenia, lethargy, bruising, fever, etc. Answer was ALL so he would have increased lymphoblasts but why could it not be aplastic crisis caused by parvovirus?

Question about organophosphate poisoning I understand that atropine is important and the problems it causes can be really bad but why wouldn't you want to give pralidoximine right away considering the fact that it only works prior to aging and that's a time sensitive thing?

How is H. pylori associated with esophageal adenocarcinoma? I didn't see any mention of that in First Aid, Pathoma, or Uptodate.

For the girl who has somatization disorder (I think) do you not try and confront them about this issue or do you just keep running tests, etc. Seems very against the whole idea of decreasing costs in medicine.

Alright that's it. I would appreciate it if someone could clarify any of these. Thanks.

Down syndrome is classically associated with ALL, and the sx fit. If it were parvo, I don't think they would mention down syndrome. Moreover, any mention of parvo is associated with either the slapped-cheek rash with circumoral pallor, arthritis-like sx in an adult, or aplastic crisis in a sickle cell or thal pt.

Organophosphate poisoning: Need to give atropine first to block the receptors being overstimulated by the acetylcholine, which is responsible for the sx. Pralidoxime regenerates the AchE, which takes longer to act. An analogous situation is the treatment of warfarin OD. You initially treat with FFP rather than vitamin K due to the urgency of the situation.

Which question was asking about H pylori and esophageal adenoCA? I don't remember one like this.

 

[VCorp]

I thought that the organophosphate question wasn't a good question. Even Kaplan emphasizes that to use 2-PAM asap, to prevent it from becoming too late, to the point you can't use it anymore.

The h.pylori question you're asking about, it was a picture question showing a H&E stain of the esophagus.

 

[patientcare]

Apologies for the delayed reply, VCorp. Unfortunately, I do not have any recollection of that question =/, but I do agree that there is no mention of H pylori being assoc with esophageal CA in First Aid or Pathoma. According to many a research article, though, H pylori is protective against esophageal adenoCA. I don't know if this helps or confuses the matter ...

 

[knowledgeispowr]

heyy.. need help on these:

1. Male newborn with right-sided aortic arch, full cheeks, low-set ears, small chin, low Calcium. defect in?? I chose 3rd & 4th branchial arches.. [wrong] Is it the 3rd & 4th pouches?? and what abt the facial anomalies?? someone kindly explain.. (options were 1st & 2nd arches/grooves/pouches/ 3rd & 4th arches/grooves/pouches)


2. In a series of skeletal muscle twitches, ATP conc. doesn't fall appreciably coz??
i saw that someone answered ATP is quickly regenerated from creatine phosphate but can onyone explain the details??


3. 72 yo woman with secondary hyperparathyroidism.. cause?? osteomalacia?? osteoporosis??


4. 72 yo man with past h/o poorly controlled HTN presents with severe pain abd, tachycardia, hypotension, S4, pulsatile periumbilical mass & guarding. what additional findings would be seen?? is it dec femoral pulses?? [i'm thinking ruptured abd aortic aneurysm].


any help would be appreciated.. thank you..

 

[shootme]

.

 

[iheartperfume]

During an experiment of muscle contraction, intracellular contraction is decreased after a substance is administered to a muscle preparation obtained from an experimental animal. which of the following explains why contraction is inhibited in this case?
1)ach release is increased
2) depolarization along t tubules is enhanced
3) myosin binding sites on on actin remain covered by troponin c
4) sodium influx is increased
5) tropomyosin is detached from actin (wrong)

 

[knowledgeispowr]

During an experiment of muscle contraction, intracellular contraction is decreased after a substance is administered to a muscle preparation obtained from an experimental animal. which of the following explains why contraction is inhibited in this case?
1)ach release is increased
2) depolarization along t tubules is enhanced
3) myosin binding sites on on actin remain covered by troponin c(correct)
4) sodium influx is increased
5) tropomyosin is detached from actin (wrong)

option 5) is wrong because tropomyosin detachment from actin would expose the myosin binding site on actin and would thus help in promoting contraction, not inhibiting it. Options 1), 2) & 4) would also help to enhance contraction.

 

[iheartperfume]

option 5) is wrong because tropomyosin detachment from actin would expose the myosin binding site on actin and would thus help in promoting contraction, not inhibiting it. Options 1), 2) & 4) would also help to enhance contraction.

the only reason why i was unsure about 3 was because i thought calcium binds tropininc c...which then removes tropomyosin...not tropnin c from the binding sites

 

[thawunandonly]

Is anyone's NBME15 score out of whack with how they've been doing on previous tests? Granted, I've only taken the UWSAs right now and I expected to dip (since everyone says the UWSAs overshoot), but I went from 244, 262, on the UWSAs then 238 here. I look at my performance and most of the bars are above the average and then I look here and lots of the questions I had trouble with I seem to have gotten right (according to discussion in this thread). Should have bought the expanded pack or whatever, because now I have no clue what I did wrong.

This one was crap. Should have bought 12 or 13 or something. Plan to take one more in about 3 days or so... any recommendations? Hoping not to deflate my morale by taking it, lol... test in 7 days.

 

[thawunandonly]

option 5) is wrong because tropomyosin detachment from actin would expose the myosin binding site on actin and would thus help in promoting contraction, not inhibiting it. Options 1), 2) & 4) would also help to enhance contraction.

Clarify please.

Not sure if I read it right or if it was how they phrased it or maybe I straight up confused myself... but I thought what they meant was actually increasing the INFLUX of sodium. I was thinking that driving more sodium into the cell would work the Na+/Ca2+ exchanger and force Ca2+ out (like a normal elimination of Ca2+) -> inhibiting contraction. As opposed to thinking of it like digoxin and letting Na+ ACCUMULATE inside.

If that even makes sense...

Also, 3) by itself doesn't make sense. The question referred to "a substance". Myosin binding sites being covered.... so what? How does that relate to the problem?

 

[knowledgeispowr]

the only reason why i was unsure about 3 was because i thought calcium binds tropininc c...which then removes tropomyosin...not tropnin c from the binding sites

That's exactly what i thought while i was picking 3) but i still went with it anyway coz the others seemed to do the opposite of what they r asking.. i got it right.. hope this link helps.. http://www.pansportmedical.ro/english/sports_medicine/articles/attach/muscle_fiber_bi_3.gif