Metabolic alkalosis pathophysiology
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The exact pathogenesis of [disease name] is not fully understood.
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
The progression to [disease name] usually involves the [molecular pathway].
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Loss of hydrogen ions
- Hyperaldosteronism causing retention of sodium followed with compensatory excretion of hydrogen
- Administration of non-resorbable anions such as, penicillin, carbenicillin, which complexs with positively-charged hydrogen ions in the renal tubules.
Increase in the serum bicarbonate
- Ingestion of sodium bicarbonate, baking soda, citrate, lactate, or acetate.
Shift of hydrogen ions into intracellular space
- Seen in hypokalemia. Due to a low extracellular potassium concentration, potassium shifts out of the cells, and in order to maintain electrical neutrality, hydrogen shifts into the cells, leaving behind bicarbonate.
- This results from a loss of water in the extracellular space which is poor in bicarbonate, typically from diuretic use. Since water is lost while bicarbonate is retained, the concentration of bicarbonate increases.
Compensation for Metabolic Alkalosis
- The body attempts to compensate for the increase in pH by retaining carbon dioxide (CO2) through hypoventilation (respiratory compensation). CO2 combines with elements in the bloodstream to form carbonic acid, thus decreasing pH.
- The pCO2 rises 0.5 - 1 for every 1 unit increase in serum HCO3 from a baseline of 24.
- The maximum pCO2 in compensation is 55-60.
- Renal compensation for metabolic alkalosis consists of increased excretion of HCO3- (bicarbonate), because the filtered load of HCO3- exceeds the ability of the renal tubule to reabsorb it.
- [Disease name] is transmitted in [mode of genetic transmission] pattern.
- Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
- The development of [disease name] is the result of multiple genetic mutations.
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].