Fluid and Electrolyte Homeostasis Quiz

Fluid and Electrolyte Homeostasis

• Renal, respiratory, and cardiovascular systems control fluid and electrolyte balance.
• Renal compensation is slower than respiratory and cardiovascular compensation.
• Renal/kidney function is under endocrine/neuroendocrine control.
• Respiratory and cardiovascular systems are under neural control.
• High osmolarity leads to low water volume, resulting in less urine.
• Low osmolarity leads to high water volume, resulting in more urine.
• The kidney is the primary route for ion and water excretion.

Countercurrent Multiplier in the Loop of Henle

• The countercurrent multiplier establishes high osmolarity in the medulla's interstitial fluid.
• Active transport of sodium (Na+), chloride (Cl-), and potassium (K+) out of the nephron occurs in the thick ascending limb of the loop of Henle.
• This process is necessary for creating concentrated urine as filtrate flows through the collecting duct.
• Pumping ions creates a gradient, allowing other substances to passively follow.
• The vasa recta capillaries act as a countercurrent exchanger, removing water leaving the nephron to prevent the medulla's interstitial fluid from becoming diluted.
• Urea plays a significant role in increasing interstitial osmolarity.

Water Balance and Vasopressin

• Vasopressin/arginine vasopressin (AVP)/antidiuretic hormone (ADH) controls water permeability in the collecting duct.
• ADH increases aquaporins on the collecting duct's apical membrane.
• The effect of ADH is graded, matching urine concentration to the body's water needs.
• Increased plasma osmolarity triggers more vasopressin release to retain water.
• Absence of vasopressin results in nearly zero water permeability.
• Changes in blood volume or pressure affect vasopressin release, affecting water reabsorption.

Renin-Angiotensin-Aldosterone System (RAAS)

• Aldosterone secretion is often stimulated by angiotensin II.
• Reduced blood pressure triggers renin release from granular cells in the kidneys.
• Renin converts angiotensinogen to angiotensin I.
• Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II.
• Angiotensin II ultimately stimulates aldosterone release.
• Renin release is either directly or indirectly related to low blood pressure.

Natriuretic Peptides

• Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are released in response to increased blood volume.
• Natriuretic peptides increase sodium excretion and water loss by increasing glomerular filtration rate (GFR).
• They also inhibit tubular sodium reabsorption, renin release, aldosterone secretion, and vasopressin release.

Potassium Balance

• Potassium homeostasis maintains narrow plasma potassium (K+) concentrations.
• Hyperkalemia (excess K+) can cause cardiac arrhythmias.
• Hypokalemia (low K+) can cause muscle weakness and respiratory muscle dysfunction.

Acid-Base Balance

• Carbon dioxide (CO2) from respiration is a major source of acid.
• CO2 combines with water to form H+ and bicarbonate (HCO3-) with the help of carbonic anhydrase.
• The body utilizes buffers (proteins, phosphate, and HCO3) to control pH changes.
• The respiratory system and kidneys also help regulate pH.
• Acidosis and alkalosis lead to disturbances in nervous system functioning.

Respiratory Compensation of pH Changes

• Respiratory compensation involves changes in ventilation rate and depth.
• Increased ventilation reduces CO2 levels, lessening H+ levels.
• Decreased ventilation increases CO2 levels.

Kidney Compensation of pH Changes

• Kidneys compensate for pH changes through intercalated cells in the collecting ducts.
• Type A intercalated cells help correct acidosis by secreting H+ and reabsorbing HCO3- and K+.
• Type B intercalated cells help correct alkalosis by secreting HCO3- and K+ and reabsorbing H+.

Salt Appetite and Thirst

• Thirst is triggered by hypothalamic osmoreceptors.
• Aldosterone and angiotensin stimulate salt appetite.