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NBME 20 Answers

nbme20/Block 1/Question#37

A 1-month-old male newborn is brought to the ...

Na+: 132; K+: 3.2; Cl: 90; HCO3: 37

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In metabolic alkalosis, potassium moves into the cells

The loss in volume through emesis triggers RAAS resulting in increased Aldosterone release and further potassium excretion


 +2  upvote downvote
submitted by hayayah(503),

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

ergogenic22  decreased K+ (from increased RAAS due to volume loss) and decreased Cl- (loss of HCl from the stomach), Alkalosis from loss of HCl and thus high bicarb. For this reason high to mid range K is wrong +3  
sbryant6  Wouldn't increased RAAS lead to increased Na+? The answer shows decreased Na+. +1  
sbryant6  Also, remember Bulimia Nervosa is associated with hypokalemia. +1  
sugaplum  so the range they gave for K is 3-6? so 3.2 is WNL then? or are we just operating on "it is on the lower end of normal in peds" +2  
dbg  sodium levels in pyloric stenosis vary, nothing really classic, can be high as in this case simply due to hydration, can low in other cases if aldosterone managed to reverse that to the other extreme +  

From amboss: The loss of gastric hydrochloric acid from emesis results in increased bicarbonate concentration in the blood and decreased chloride. Some potassium is also lost through vomiting. Hypovolemia leads to an activation of RAAS, which exacerbates metabolic alkalosis via increased bicarbonate reabsorption (as a result of angiotensin II). Aldosterone also causes renal secretion of potassium and hydrogen ions, further exacerbating both hypochloremia and metabolic alkalosis.

+1/- smpate(2),

No one here bothered to actually discuss what's going on. This is a 1-month old newborn.

He vomits after feedings, 5-day history.

At 1 month old, with vomiting after feedings, it is most likely a case of PYLORIC STENOSIS due to hypertrophy of the pyloric sphincter (usually occurs 6 weeks later).

Due to him vomiting stomach contents, he will LOSE Cl-, K+, and Na+.

He will ALSO lose H+. This is why you go into the metabolic alkalosis with a resultant increase in the HCO3-.

kamilia20  sketchy:: vomiting causes loss of WATER greater than sodium→ increased serum sodium→ INCREASED serum osmolality, So NA will decrease too, but no that far +  

 +1  upvote downvote
submitted by ark110(1),

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

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

 +0  upvote downvote
submitted by apop(0),

These explanations arent great. It doesnt really have much to do with RAAS activation. It has almost everything to do with a phenomenon called the alkaline tide. In chronic vomitting, you would expect Cl- to be low and K= to be low (similar to lab results in someone with bullemia). To compensate for the low Cl-, the stomach has an antiporter which exchanges Cl- for HCO3-. Therefore, Cl- will be replenished in the stomach, while HCO3- will increase in the blood, causing an alkalosis. In alkalotic states, the H+/K+ antiporter will begin to activate, shifting K+ INTO cells (hypokalemia) and increasing pH. RAAS probably plays a role in making the hypokalemia worse but the alkaline tide is more important here.

 +0  upvote downvote
submitted by rainlad(1),

Hypochloremic, hypokalemic metabolic alkalosis is the classic electrolyte and acid-base imbalance of pyloric stenosis.

Persistent vomiting results in loss of HCl. The chloride loss results in a low blood chloride level which impairs the kidney's ability to excrete bicarbonate. This is the factor that prevents correction of the alkalosis leading to metabolic alkalosis.

A secondary hyperaldosteronism develops due to the decreased blood volume. The high aldosterone levels causes the kidneys to retain Na+ (to correct the intravascular volume depletion), and excrete increased amounts of K+ into the urine (resulting in a low blood level of potassium).

I don't get this. Shouldn't the kidneys start correcting the bicarb levels afer 5 days? The delayed phase of the correction since they take time... and in the question they're asking "now". We have metabolic alkalosis since HCL is lost, so the body will try to correct it first by hyperventilation and later by increased excretion of bicarb. Bicarb should be low... (unless I'm missing something due to being exhausted)

thefoggymist  Nevermind, I think I got it. Beta intercalated cells cannot function and excrete bicarb because we don't have chloride. Yea apparently I was exhausted. +  

Very easy question. Nonbilious vomit. 1 month age. Most likely scenario is pyloric stenosis.

The vomiting causes loss of HCl so we have the hypochloremia, and renal compensation for this H loss is by preserving protons at the expense of K so that gives hypokalemia. As the disease is named, the red arrow in the image of the stomach is smooth muscle hypertrophy of the pyloric muscularis mucosae, forming the olive-shaped mass felt on palpation. This is a metabolic alkalosis because without Cl-, the basolateral HCO3/Cl exchanger will not work, so you retain HCO3.