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Retired NBME 22 Answers

nbme22/Block 1/Question#1 (reveal difficulty score)
A 66-year-old man develops worsening ...
Dilution of serum sodium due to ADH (vasopressin) secretion ๐Ÿ” / ๐Ÿ“บ / ๐ŸŒณ / ๐Ÿ“–
tags: RAAS

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 +23  upvote downvote
submitted by โˆ—imgdoc(183)
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I think alot of people might have over emphasized how important ANP and BNP really are, yes it is important to know these peptides get secreted by the atrial/ventricular myocardium during heart failure. However their overall effectiveness in treating heart failure is zilch, a preceptor told me that if ANP and BNP were so useful in natriuresis then why do we give diuretics? It's because RAAS overpowers this system hence causing negative effects and the endless loop of heart failure. AKA why we give ACE inhibitors.

Knowing that ANP gets neutralized by the RAAS system, we can shift our focus back to heart failure in this patient, where cardiac output is decreased, leading to ADH secretion and finally dilutional hyponatremia.

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almondbreeze  a concept continuously emphasized by uw, but I get always wrong :'( +4
almondbreeze  good work done! +1
raffff  why does the body make anp at all since its so useless +4
makinallkindzofgainz  @raffff - at least BNP gives us a good marker for heart failure exacerbations :) thanks body! +1
mannan  Yeah it's important clinically because it has a high sensitivity (if negative, rule out) for Heart failure. +1
alimd  At the same time ANP inhibits renin release? +1
freemanpeng  If it is High RAAS, Aldo must be High as well(AngII induce Aldo more than ADH). Then that would be SALT-WATER retention rather than PURE WATER retention. NO hyponatremia +
plaguedbyspleen  This patient is third-spacing and therefore has low effective circulating volume. I like to think that given his CV history, he is probably on an ACE inhibitor or something similar. So that leaves ADH to do its thing. Also high aldosterone saving salt isn't something we need to consider given the stem and answer choices. +



 +12  upvote downvote
submitted by โˆ—meningitis(643)
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I also thought the same as @bubbles, but now trying to "justify" this tricky NBME question: I think this revolves on the fact that the patient has a HIGH blood pressure meaning we should focus on an answer that explains both increased BP and Hypovolemia (i.e: increased ADH which vasoconstricts and also absorbs free-water, both of which increase BP and cause hypovolemia).

Maybe if this patient were decompensated with LOW BP, one could think more about ANP.

I still think this question is TOO tricky.

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meningitis  Sorry, hyponatremia* right? +1
mantarayray  I think that it's not ANP because ANP will cause a loss of Na but water will follow (they usually go together), whereas ADH will cause absorption of only water and will cause hyponatremia except only thought this post getting the question wrong :") +5
mantarayray  Oops sorry the formatting is confusing: I think that it's not ANP because ANP will cause a loss of Na but water will follow (they usually go together), whereas ADH will cause absorption of only water and will cause hyponatremia. +4
pg32  @mantaray pretty sure you are right and that is the only way to get this question correct. Remembering that Na concentration really is a measure of water balance is key. If the pt is hyponatremic, that just means they have too much water in the blood, which is caused by ADH. If the patient was hypoVOLEMIC, that might mean they are losing too much Na. This is illustrated by pts with SIADH. They are hyponatremic, but euvolemic, meaning that they have too much water (hyponatremia from the ADH) but their Na balance is ok (due to excretion of Na via ANP/BNP) +1
avocadotoast  We need to be thinking about how heart failure is a condition with a low effective circulating volume. Our patient had an MI and now his heart cant keep up with the volume (low CO), leading to congestion. When congestion occurs, water is pushed into the interstitial spaces and isn't circulating in the arterial system. For that reason, the body ramps up the RAAS and ADH despite an actual increase in body water. This is a non-osmotic release of ADH. At this point plasma sodium levels are determined by relative intake and losses and hyponatremia is common in these patients because of that. Also, ANP and BNP don't hold a candle to the RAAS. +1



 +5  upvote downvote
submitted by โˆ—nwinkelmann(366)
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From UpToDate: PATHOGENESIS

Like most other causes of hyponatremia, heart failure impairs the ability to excrete ingested water by increasing antidiuretic hormone levels. When cardiac output and systemic blood pressure are reduced, "hypovolemic" hormones, such as renin (with a subsequent increase in angiotensin II formation), antidiuretic hormone (ADH), and norepinephrine, respond [1-3]. Although edematous patients with heart failure have increased plasma and extracellular fluid volumes, the body perceives volume depletion (reduced effective arterial blood volume) since the low cardiac output decreases the pressure perfusing the baroreceptors in the carotid sinus and the renal afferent arteriole. The degree of neurohumoral activation is generally related to the severity of cardiac dysfunction, as assessed by left ventricular ejection fraction or functional class [2]. The neurohumoral changes limit both sodium and water excretion in an attempt to return perfusion pressure to normal. ADH release directly enhances water reabsorption in the collecting tubules, whereas angiotensin II and norepinephrine limit distal water delivery (and thereby water excretion) by lowering the glomerular filtration rate (due to a marked reduction in renal perfusion) and by increasing proximal sodium and water reabsorption [4]. In addition, both the low cardiac output and high angiotensin II levels are potent stimuli to thirst, leading to enhanced water intake.

https://www.uptodate.com/contents/hyponatremia-in-patients-with-heart-failure#H2

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 +3  upvote downvote
submitted by โˆ—bubbles(79)
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This question confused me a lot because so many questions have drilled me on the importance of the ANP escape mechanism in times of fluid overload (as in CHF).

I thought ANP was a huge player in the loss of Na in circumstances of volume overload as in this patient (which is why you see euvolemic hypOnatremia in patients with SIADH or overactivity of the RAAS as in CHF).

Why is ADH now being named as the responsible agent?

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jooceman739  My thinking is that ANP causes natriuresis, so you're losing salt and water at the same time (isoosmotic fluid?). Meanwhile, ADH absorbs only free water, so it would dilute the serum. Correct me if i'm wrong. +13
bubbles  Ohhh you are right. Thank you for the explanation! I got so fixated on that one mechanism haha. +4



 +2  upvote downvote
submitted by โˆ—dr.xx(176)
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CHF patients often display signs and symptoms of increased vasopressin secretion.

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hyperfukus  if all else fails i hope i just drill this one statement in my brain and it comes out in the right way on test day thank u!!! +1



 +2  upvote downvote
submitted by โˆ—drmohandes(193)
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Here we go:

  • decreased LV contractility (bilateral crackles)
  • decreased cardiac output
  • activate RAAS โ†’ ADH
  • increase sympathetic activity โ†’ more RAAS โ†’ more ADH
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 +1  upvote downvote
submitted by โˆ—moloko270(77)
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https://www.ncbi.nlm.nih.gov/pubmed/7058822

"syndrome of "dilutional hypo-osmolality" in severe congestive heart failure may be caused by an inappropriately high ADH secretion in which the osmoreceptor system is dominated by nonosmolar stimuli"

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hayayah  Apparently, in chronic CHF you see hyponatremia. Because CHF causes a decrease in cardiac output and circulating blood volume, which in turn triggers a compensatory response aimed at preserving blood pressure. This stimulates the body to retain both water and sodium. +10
seagull  i agree with Hayayah... the RAAS system is activated due to poor perfusion to the kidney due to decomp heart failure. +6



 +0  upvote downvote
submitted by nicsar(1)
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Hyponatremia from Heartfailure pt.

It should be approached from Heart faiure.

HF-> RAAs -> excessive Aldosterone, ADH; ANP escape faiure, like secondary hyperaldosteronism; Hyponatremia

https://www.wjgnet.com/1949-8462/full/v5/i9/WJC-5-317-g001.htm

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 +0  upvote downvote
submitted by โˆ—dubywow(23)
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Decompensated HF. Lack of blood flow due to failing heart -> lower BP -> increased ADH to increase blood pressure back to stable level. In DHF, ADH outpaces homeostasis of counteracting ANP & BNP. Thus, the term "decompensated". Associated with shortness of breath, edema (often of lungs).

This vicious cycle continues as body prioritizes adequate BP for survival, but it comes at the expense of overworked heart that must work harder and harder, ultimately exacerbating the heart failure condition.

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 +0  upvote downvote
submitted by โˆ—asharm10(37)
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Always know this Hypo or hypernatremia is because of change in the volume, this patient is going through heart failure, renal perfusion has gone down that leads to release of ADH cos of osmoreceptors stimulation. Now high ADH will reabsorb more free water that will lead to hyponatremia. So hyponatremia is almost always related to high ADH. I know few of you will think but RAAS system is activated too but that abosrb Na along with water but ADH just free water.

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 +0  upvote downvote
submitted by โˆ—hello(429)
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There has to be a better explanation for why ANP is wrong?

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waterloo  If this pt's ANP/BNP were causing him to become hyponatremic, why does he have fluid overload symptoms (bilateral crackles, JVD, high BP)? There has to be something else overcoming the ANP system. +1



 +0  upvote downvote
submitted by โˆ—happysingh(57)
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i kinda of feel "odd" asking this question : but the patient had an MI 6 months ago, so why would it be unlikely that he was told to "restrict salt, restrict fluids (water) " ??

Guess what i'm asking is : what makes choice E such an unlikely choice (JVD, bi-basilar crackles, peripheral edema) ?

& @meningitis : his bp is 135/82 mmHg ... why is that "HIGH" ??

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 +0  upvote downvote
submitted by โˆ—freemanpeng(7)
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Firstly, I chose ADH. When I thought twice in review, I picked crossed ADH and picked ANP. My logic to cross ADH: 1. The main inducer of ADH are Osm and BP/vlomue. THis pt, Osm obviously not high, Bp obviously not low. So, nonsense in increased ADH. 2.You may see AngII also induces ADH. But it seems to be a minor inducer. Meanwhile, if it is exactly high AngIIโ†’ high ADH. Then, Aldo must be high as well, and High Aldo โ†’Salt preservingโ†’ HOW CAN serum Sodium be LOW? "Low Cardiac outputโ†’ High RASS (AngII Aldo ADH)" pathway is WATER-SODIUM retention. NOT pure WATER retention Please correct me

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