Water Balance and Regulation Quiz

Water Balance and Regulation

• The urinary system is the primary route for water loss from the body.
• Cell volume and function depend on carefully regulating extracellular fluid osmolarity.
• The urinary and cardiovascular systems work together to control water balance.
• Kidney response to changes in blood volume is relatively slow.
• Hepatocyte shrinkage in the liver triggers glycogen breakdown.
• Most body water is intracellular.
• Kidneys regulate water output, not just water loss.
• Dehydration causes urinary bladder water to be expelled.
• Water reabsorption in the kidney occurs via osmosis.
• Antidiuretic hormone (ADH) directly controls kidney water excretion.
• ADH increases water permeability in specific kidney tubules.
• Loop diuretics inhibit potassium reabsorption along with sodium, necessitating potassium supplementation.
• Osmoreceptors in the hypothalamus detect changes in plasma osmolarity.
• Osmoreceptor shrinkage, due to increased plasma osmolarity, leads to depolarization.
• ADH stimulates water conservation by the kidneys.
• Increased venous return activates atrial stretch receptors, inhibiting ADH secretion.
• Increased blood pressure, detected by carotid and aortic baroreceptors, inhibits ADH secretion.

Hormonal Regulation

• Sodium is actively reabsorbed in the nephron to promote passive water reabsorption.
• Juxtaglomerular cells secrete renin.
• Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II.
• Angiotensin II elevates blood pressure, stimulates thirst, causes vasoconstriction, and triggers aldosterone release.
• Atrial natriuretic peptide (ANP) increases glomerular filtration rate (GFR) and inhibits renin release.
• Hyperkalemia is high plasma potassium.
• Kidneys excrete excess potassium.
• Thirst is regulated by hypothalamic centers, triggered by increased osmolarity.
• Aldosterone regulates blood sodium concentration.
• ANP promotes sodium loss at the kidneys, reduces thirst, is produced in the heart, and suppresses ADH.
• Renin activates angiotensin.
• Angiotensin I is converted to angiotensin II by enzymes in blood vessels.
• Osmolarity in the deepest part of the loop of Henle is 1200 mOsM.

Fluid Volume Regulation and Blood Pressure

• Reduced ECF volume increases sympathetic output from the cardiovascular control center..
• Low plasma pH symptoms involve CNS depression and confusion/disorientation.
• Carbon dioxide concentration significantly influences plasma pH.
• The carbonic acid-bicarbonate buffer system prevents pH changes from organic and fixed acids.
• Respiratory alkalosis features decreased carbon dioxide retention.
• Prolonged vomiting can cause metabolic alkalosis.
• Emphysema leads to respiratory acidosis.
• Hyperventilation results in respiratory alkalosis.
• Increased angiotensin II results in elevated blood pressure, increased water and sodium retention.
• The renin-angiotensin-aldosterone system (RAAS) starts with renin secretion.
• Kidney medulla cells maintain normal volume by synthesizing organic solutes to match osmolarity.
• Proteins bind hydrogen ions at amino groups to buffer decreased pH in body fluids.
• Declining extracellular fluid pH leads to increased potassium reabsorption by kidneys.
• Pre-operative symptoms ("jitters") are due to sympathetic activation.
• Dehydration leads to increased ADH levels.

Electrolyte Imbalances and Other Considerations

• Decreased pH decreases urinary potassium excretion.
• Rapid organic acid increases lead to increased alveolar ventilation, and decreased blood pH.
• Severe hyperkalemia can cause skeletal muscle unresponsiveness and cardiac arrest.