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.
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.
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
http://www.labpedia.net/test/116
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-.
But what is the difference between option A and option C (132; 4.9; 90; 35)
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)
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.
submitted by apop(8)
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.