Flashcards for:
Fluid, Electrolyte, and Acid-Base Balance (Part 2)

Aldosterone increases sodium reabsorption, and water follows sodium via osmosis, leading to increased blood volume and pressure.

It stabilizes pH by converting CO₂ and water into bicarbonate and hydrogen ions, responding to changes in CO₂ levels.

ADH inserts aquaporins in the kidney collecting duct and distal tubule, facilitating water reabsorption into the blood.

Respiratory acidosis is due to inadequate CO₂ elimination, while metabolic acidosis results from non-respiratory factors like diabetic ketoacidosis.

The renal system controls H⁺ secretion and HCO₃⁻ reabsorption, responding to plasma pH and aldosterone levels.

The phosphate buffer system, involving H₂PO₄⁻ and HPO₄²⁻, plays a key role in intracellular pH regulation.

Amino acids in proteins have groups that can release or absorb H⁺, with hemoglobin acting as a buffer in red blood cells.

The respiratory system adjusts pH by changing the rate and depth of respiration to manage CO₂ levels.

Low blood pressure triggers the release of renin from the kidney in the RAAS.

ANP interferes with aldosterone, leading to increased sodium and water excretion via urine, thereby reducing blood volume.

Compensatory mechanisms include buffers releasing H⁺, slowed breathing to retain CO₂, and kidneys decreasing H⁺ excretion and HCO₃⁻ reabsorption.

Metabolic alkalosis can result from excessive antacid use or severe vomiting, which cause a loss of acid.

Angiotensin II acts as a vasoconstrictor, stimulates thirst, and promotes the release of aldosterone from the adrenal cortex.

ANP is released when the right atrium is overstretched due to high venous return.

Enzymes function optimally within a narrow pH range, so maintaining pH balance is crucial for metabolic processes.