Questions

[bigfrank]

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I just came across some questions. What do you guys/gals think?

1. A 55 year-old man has hyponatremia. What part of his nephron is involved?
- PT
- Loop of Henle
- DCT
- Collecting Ducts

2. An elderly patient has a leg wound in which the epidermis & dermis has eroded away, leaving a firm, white, avascular structure below. NO blood vessels are seen. What is it?
- Fascia
- Tendon
- Cartilage

 

[FoxyDoc]

My guesses are collecting ducts and cartilage.

 

[nuclearrabbit77]

i believe its:

1)if SIADH, water channels are put in at collecting duct

2)fascia, covering the muscles

 

[DRealDrZ]

collecting duct and fascia
???

 

[Idiopathic]

I believe the rabbit has it.

 

[Willamette]

The thing that makes the first Q tough is the fact that ADH inserts at the Late Distal Tubule & the Collecting Duct. For consistency (since the early DT is impermeable to Water) I'd go with CD.

The second one I would totally have to guess on. To round out the trifecta, I guess tendon


Willamette

 

[sunmoon]

I think it is Loop of Henle ( In particular, the ascending LoH with Na/K/2Cl pump).

The question doesn't say anything other than the age of the patient and that means the patient most likely has atherosclerosis and this leads to ischemia. The most susceptible regions in the nephron are PCT (lot of ATPase activity) followed by the Ascending limb of LoH.

Cartilage is blue in color, so I think it is tendon.

 

[Willamette]

I think it is Loop of Henle ( In particular, the ascending LoH with Na/K/2Cl pump).

The question doesn't say anything other than the age of the patient and that means the patient most likely has atherosclerosis and this leads to ischemia. The most susceptible regions in the nephron are PCT (lot of ATPase activity) followed by the Ascending limb of LoH.

Cartilage is blue in color, so I think it is tendon.

I think your ischemia logic works, to a point. Increased sodium content of the Loop would just increase the tubular concentration further along, and thus you'd end up increasing sodium resorption further along. Furosemide(mimicking ischemia in the LOH) can cause hypokalemia, but I don't ever recall reading that they cause hyponatremia...


Willamette

 

[sunmoon]

Loops and Thiazide Diuretics, for some unknown reason, increase the proximal absorption of Na and water. Hence their use, esp of Thiazides as they are weaker diuretics than loops, in Diabetes Insipidis. I think that is the reason why they dont cause hyponatremia. In this case, with hypoxia, activity across all pumps will be decreased leading to lower Na reabsorption.

I could also be a total idiot and reading too much into the question...

 

[Willamette]

Loops and Thiazide Diuretics, for some unknown reason, increase the proximal absorption of Na and water. Hence their use, esp of Thiazides as they are weaker diuretics than loops, in Diabetes Insipidis. I think that is the reason why they dont cause hyponatremia. In this case, with hypoxia, activity across all pumps will be decreased leading to lower Na reabsorption.

I could also be a total idiot and reading too much into the question...

I don't think you're an idiot at all. Your logic still seems sound. Another reason that I think CT is the answer is the fact that most of the filtered sodium is reabsorbed in the proximal tubule (something like 67% I think), and this leads me believe that most cases of sodium imbalance are actually water issues instead...I'm sure that Harrison's or Cecil's has the answer to that, but I don't feel like looking it up. Anyway, I think this question just goes to show that as bright and educated as we all are, the Step 1 can still throw lots of curves our way, making it tough to judge how we did...and since none of us know how it's scored either, even when we get our exams back we still don't KNOW .

Willamette

 

[Idiopathic]

Loops and Thiazide Diuretics, for some unknown reason, increase the proximal absorption of Na and water. Hence their use, esp of Thiazides as they are weaker diuretics than loops, in Diabetes Insipidis. I think that is the reason why they dont cause hyponatremia. In this case, with hypoxia, activity across all pumps will be decreased leading to lower Na reabsorption.

I could also be a total idiot and reading too much into the question...

Not an idiot, no...but maybe reading too much into it. Lets put it this way. All of the listed segments could contribute in some way to hyponatremia, but the only one whose job it is specifically is the collecting duct.

As far as the second question, it should have to be fascia, I believe. I would give a distant second to tendon, but not ligament ever. Technically, every structure in th ebody is covered by fascia. After you get through dermis, whaddaya have? Fascia...

 

[FoxyDoc]

How about the avascular part of the Q, doesn't fascia have blood vessels?

 

[Idiopathic]

I didnt think so...I know it surrounds them, but I dont believe fascia in and of itself is vascular. I could be wrong...it happened about 100 times this week 😉

 

[sunmoon]

"All of the listed segments could contribute in some way to hyponatremia, but the only one whose job it is specifically is the collecting duct."

Thinking more and deeper (hehe) ....

You are right that there could be many reasons/cause of hyponatremia. The question just says the pt is 55 y/o and has hyponatremia. If it said dilutional hyponatremia, yes it would definitely be collecting ducts.

Three reasons of Hyponatremia could be Hypertonic loss of water (diuretics may be for HT/CHF for his age), hypotonic gain of water (RAA system in CHF which is possible at this age) or gain of only free water (SIADH, possibly due to sulfonylureas for diabetes at his age).

In this patient, the last two involve the CT but the first one may necessarily not involve the CT. So, most likely it will involve the CT.

So, unless the original poster has some explanation from where he got the answer, we will not know for sure. In any case, I am definitely reading too much in to it which I do all the time.

I was wrong about the ligament. I just dont know what I was thinking. After the dermis, the next layer is fascia. If it is too thin, may be a tendon. I dont know where I got the ligament from as it was not even one of the choices. I must have been thinking tendon but wrote down ligament.

Anyways, good luck on your exam...

 

[bigfrank]

Hi,

On #1, that was honestly all the information that I was given -- a 55 y/o man. NOTHING else except for the hyponatremia. I thought it was either the Collecting Duct (SIADH) or the Loop of Henle (diluting segment). Poor question. I put Collecting Duct, however, don't know the correct answer

#2, it was extremely vague and said "lower leg" in terms of location. I put tendon because I felt the question stressed Avascular and I thought that fascia may have had capillarity. Is fascia felt to be "firm?" I don't know the answer to that either. Is fascie considered "white?" Again, no clue. But I put tendon and feel pretty ??? about that.

Thanks for your input.

 

[Idiopathic]

Fascia may not be inherently firm, but it is tight and the structures underneath it usually contribute to the 'firmness'.

 

[nuclearrabbit77]

i got this lame qbank question that essentially says that you should do a heimlich manevuer on a choking patient who just had colon tumor resection with complications of post-operative bleeding.... wouldn't the heimlich manuver be bad and aggrevate his abdominal condition? they chose this over trying to dislodge it by hitting his upper back.

 

[kedhegard]

Yeah I got a qbank question that said breathing in and out of a PLASTIC BAG would be a good way to stop hyperventilation. I guess it would, in the long run.

 

[nuclearrabbit77]

that's funny

 

[DRealDrZ]

I think the reason the paper bag thing works is because of acid/base control. I honestly think I heard that in school (but don't know for sure) and was thinking "so it really works?" I actually put that answer on QBank and got it right only because of that reason...

 

[DRealDrZ]

OH...plastic bag...I'm a *****...I should read better!!! Hope I read better for the USMLE, holy crap.

 

[nuclearrabbit77]

BRS path error? pg. 227
they say:
"infection with nontuberculous mycobacteria........mycobacterium avium-intracellulare...is often manifest by non pulmonary involvement"

this is wrong,isn't it?


pg. 147, lange medical microbio/immunology on MAC:

"...they cause pulmonary disease clinically indistinguishable from tuberculosis, primarily in immunocomprimised patients such as AIDS..."

 

[Idiopathic]

I think it is a catch-22. You probably wont see MAI in anyone who isnt an AIDS patient, and if you see it in an AIDS patient, it will be disseminated. Assuming intact cell-mediated immunity (i.e. CD4 > 400), then it would be contained in the lung, but then you wouldnt get infected with it anyway.

Always look for MAI when you see a sick AIDS patient and a CD4 count < 50. It is the most common cause of death I believe.

 

[nuclearrabbit77]

my main complaint with it is that they say there is no pulmonary involvement. regardless if it's disseminated, milliary, granulomatous... or not, there will be pulmonary involvement....

 

[nuclearrabbit77]

i had an interesting question that i came up with while reviewing immuno today. if NK cells kill cells that lack MHC I expression....and if MHC I is expressed on all nucleated cells....why don't NK cells kill RBC's?

is there a super-duper immuno-buff in the hiz'zouse?

 

[Idiopathic]

i had an interesting question that i came up with while reviewing immuno today. if NK cells kill cells that lack MHC I expression....and if MHC I is expressed on all nucleated cells....why don't NK cells kill RBC's?

is there a super-duper immuno-buff in the hiz'zouse?

I think it is because they are selected, just like T cells, for cross-reactivity with host cells. Cells still have to present antigen to be recognized by NK cells, to the best of my understanding. It is when those antigens change (cancer) or when they are exogenous (viral) that NK cells are most efficacious.

Someone correct me if this is wrong.

 

[nuclearrabbit77]

NK cells (hence their name, natural killer) have the ability to kill cells that have no (or very low MHC I expression). This is advantageous in certain circumstances, i.e., virally induced inhibition of MHC I expression of viral epitopes, the NK cells will blast them.

NK cells do not go through the same maturation process as t-cells.

 

[Heather Noelle]

Yeah I got a qbank question that said breathing in and out of a PLASTIC BAG would be a good way to stop hyperventilation. I guess it would, in the long run.

I just got that question, too! Plastic?? 🙄

 

[sunmoon]

NK Cells do recognize the MHC-1 on Cells. They only kill cells that have modified MHC-1 or that do not display sufficient MHC-1 molecules.

NK Cells also recognize some protein called MICA expressed on cancer cells and kills them.

Why don't they kill RBCs?
Not sure but I think just like other cells that kill, they need to be activated too and IL-12 and Gamma-Interferon are needed to activate the NK Cells. IL-12 is released by Macrophages and Gamma-interferon by TH-1 cells. These would be lacking as RBCs dont generate an immune response.