Y ringer lactate is not preffered in met alkalosis
Reading File
Finding Sources
Searching PubMed
metabolic alkalosis AND fluids
Searching the Web
Ringer lactate metabolic alkalosis chloride treatment normal saline
Ringer lactate (RL) is generally not preferred for chloride-responsive metabolic alkalosis, especially from vomiting or nasogastric suction, because:
- It contains lactate (28 mmol/L). The liver metabolizes lactate mainly to bicarbonate, which can add alkali and may sustain the alkalosis.
- Its chloride content is relatively low (109 mmol/L) compared with 0.9% saline (154 mmol/L). In volume-depleted metabolic alkalosis, chloride depletion prevents the kidney from excreting excess bicarbonate. Giving chloride is part of the treatment.
- It has less sodium than normal saline (130 vs 154 mmol/L), so it is less effective for restoring extracellular volume in this setting.
Therefore, the usual fluid is 0.9% normal saline plus potassium chloride as needed, provided the patient is volume depleted and has no contraindication. Restoring volume and chloride lets the kidney excrete bicarbonate and corrects the alkalosis.
Small nuance: RL is not universally forbidden. It can be reasonable for resuscitation when other priorities dominate, but it is not the targeted replacement fluid for chloride-depletion metabolic alkalosis. StatPearls notes that normal saline is suitable for gastric losses, whereas RL is more suited to replacing alkaline biliary or pancreatic losses.
Y there is extensive fibrosis in liver in case of ehba
Reading File
Finding Sources
Searching PubMed
biliary atresia AND fibrosis
Searching the Web
biliary atresia progressive cholestasis portal fibrosis mechanism
In extrahepatic biliary atresia (EHBA), fibrosis becomes extensive because the bile ducts are progressively destroyed and obstructed, so bile cannot drain from the liver.
This causes a chain reaction:
- Persistent cholestasis: bile, bile acids, bilirubin, and other toxic substances are retained within the liver.
- Cholangiocyte and hepatocyte injury: retained bile acids damage bile duct cells and liver cells.
- Inflammation and ductular proliferation: portal tracts develop inflammation and many proliferating small bile ductules.
- Activation of hepatic stellate cells: inflammatory signals activate these collagen-producing cells, which deposit extracellular matrix in portal areas.
- Portal fibrosis progresses quickly to bridging fibrosis and then secondary biliary cirrhosis.
EHBA is not merely a mechanical blockage outside the liver. It is a progressive fibro-obliterative cholangiopathy that often extends into intrahepatic ducts too. Therefore, the liver is exposed to ongoing cholestatic injury from early infancy, explaining the unusually rapid and marked fibrosis. The pathology classically shows portal expansion/fibrosis, bile ductular proliferation, bile plugs, and canalicular cholestasis. StatPearls review describes progression to bridging fibrosis and biliary cirrhosis; Yamada's Textbook of Gastroenterology notes that EHBA can extend intrahepatically and lead to secondary biliary cirrhosis.
One-line exam answer:
EHBA causes severe portal fibrosis because persistent obstruction to bile flow produces cholestatic bile-acid injury, inflammation, ductular reaction, and stellate-cell-mediated collagen deposition, rapidly progressing to secondary biliary cirrhosis.
EHBA causes severe portal fibrosis because persistent obstruction to bile flow produces cholestatic bile-acid injury, inflammation, ductular reaction, and stellate-cell-mediated collagen deposition, rapidly progressing to secondary biliary cirrhosis.
This is a shared conversation. Sign in to Orris to start your own chat.