Consequences of Fluid Loss from the GI Tract

• What are the main consequences of fluid loss from the gastrointestinal tract?

  • Hypovolaemia
  • Haemoconcentration
  • Ionic imbalance
• What is hypovolaemia and how can fluid loss from the GI tract cause it?

  • A decreased volume of circulating blood in the body.
  • Fluid loss from the GI tract (e.g., due to vomiting, diarrhoea, or bleeding) reduces extracellular fluid volume, leading to a drop in venous return, stroke volume, and cardiac output → triggering compensatory mechanisms to maintain perfusion.
• How does haemoconcentration result from GI fluid loss?

  Loss of plasma fluid (e.g. via diarrhoea or vomiting) leads to a relative increase in the concentration of blood cells and proteins, causing haemoconcentration.
• How does fluid loss from the GI tract cause ionic imbalance?

  Loss of electrolytes such as Na⁺, K⁺, and Cl⁻ through vomiting or diarrhoea disrupts normal ionic concentrations, impairing cellular and organ function.
• Which GI conditions commonly cause fluid loss leading to hypovolaemia?

  • Infectious diarrhoea (e.g. cholera, E. coli)
  • Inflammatory bowel disease (e.g. Crohn’s, ulcerative colitis)
  • Gastroenteritis
  • Vomiting due to gastritis or obstruction
• How does diarrhoea specifically contribute to fluid and electrolyte loss?

  Rapid expulsion of watery stool prevents reabsorption of water and electrolytes (Na⁺, K⁺, Cl⁻, HCO₃⁻), leading to dehydration and imbalance.
• What is the impact of vomiting on fluid and electrolyte balance?

  Vomiting causes loss of gastric fluids rich in H⁺, Cl⁻, and K⁺ → leading to metabolic alkalosis and hypokalaemia.
• How does cholera lead to hypovolaemia?

  Cholera toxin increases cAMP in intestinal epithelial cells → massive Cl⁻ and water secretion → profuse watery diarrhoea → severe fluid loss and hypovolaemia.
• Why does haemoconcentration occur during diarrhoeal diseases?

  Loss of isotonic fluid from plasma → decreased plasma volume → increased haematocrit and blood viscosity (i.e. haemoconcentration).
• What ionic imbalances are typical in prolonged diarrhoea?

  • Hyponatraemia (↓Na⁺)
  • Hypokalaemia (↓K⁺)
  • Metabolic acidosis (due to HCO₃⁻ loss)
• Which sensors detect hypovolaemia in the body?

  • High-pressure baroreceptors in the carotid sinus and aortic arch detect arterial pressure drops.
  • Low-pressure baroreceptors in the atria and pulmonary vessels detect decreases in blood volume.
  • Juxtaglomerular apparatus in the kidneys senses reduced renal perfusion.
• What immediate cardiovascular response occurs due to baroreceptor activation in hypovolaemia?

  Baroreceptor firing decreases → activates the sympathetic nervous system → causes:

  • ↑ Heart rate (tachycardia)
  • ↑ Cardiac contractility
  • Vasoconstriction (↑ total peripheral resistance)
  • Venoconstriction (↑ venous return)
• How does the renin-angiotensin-aldosterone system (RAAS) respond to hypovolaemia?

  ↓ Renal perfusion → juxtaglomerular cells release renin→ Converts angiotensinogen to angiotensin I→ ACE converts it to angiotensin II, which:

  • Causes vasoconstriction (↑ BP)
  • Stimulates aldosterone release from adrenal cortex → ↑ Na⁺ and water reabsorption in kidneys → ↑ blood volume
• What role does antidiuretic hormone (ADH) play in response to hypovolaemia?

  ↓ Blood volume & pressure → triggers hypothalamus → posterior pituitary releases ADH (vasopressin)→ Increases water reabsorption in the collecting ducts of the kidney→ Helps conserve fluid and restore plasma volume.
• What happens to urine output during hypovolaemia, and why?

  Urine output ↓ due to:

  • RAAS: Aldosterone promotes Na⁺ and water reabsorption
  • ADH: Increases water reabsorption→ Conserves fluid to restore blood volume and pressure.
• Why does hypovolaemia cause tachycardia?

  To compensate for ↓ stroke volume and maintain cardiac output (CO = HR × SV), the heart rate increases via sympathetic activation.
• How does vasoconstriction help in hypovolaemia?

  Vasoconstriction ↑ systemic vascular resistance → maintains mean arterial pressure despite low blood volume → preserves perfusion to vital organs (brain, heart).
• Which organs are prioritised for perfusion during hypovolaemia?

  • Brain
  • Heart→ Perfusion is maintained at the expense of skin, kidneys, and GI tract via sympathetic vasoconstriction.
• What are clinical signs of hypovolaemia?

  • Low blood pressure (hypotension)
  • Rapid heart rate (tachycardia)
  • Cool, pale skin (due to vasoconstriction)
  • Reduced urine output
  • Thirst
  • Dizziness or confusion (↓ cerebral perfusion)
• What triggers the release of antidiuretic hormone (ADH) in response to fluid loss from the GI tract?

  Fluid loss from the GI tract (e.g., through vomiting or diarrhea) leads to hypovolemia and increased plasma osmolality. These changes are detected by:

  • Osmoreceptors in the hypothalamus (sense ↑ osmolality)
  • Baroreceptors in the carotid sinus and aortic arch (sense ↓ blood volume/pressure)This stimulates the posterior pituitary to release ADH.
• What is the primary function of antidiuretic hormone (ADH) in response to fluid loss?

  ADH promotes water reabsorption in the distal convoluted tubule and collecting ducts of the nephron by increasing the insertion of aquaporin-2 channels into the apical membrane. This conserves water, reduces urine output, and helps restore plasma volume.
• How does ADH affect urine concentration following GI fluid loss?


  ADH increases water reabsorption, leading to:

  • Concentrated urine (↑ osmolality)
  • Decreased urine volume
  • This helps preserve body water and corrects dehydration resulting from GI fluid loss.
• What is the consequence of impaired ADH secretion during GI fluid loss?

  If ADH secretion is impaired (e.g., in diabetes insipidus), the kidneys cannot effectively reabsorb water, leading to:

  • Excessive water loss in urine
  • Worsening dehydration
  • Hypovolemia and hypotension
• Why is ADH crucial during prolonged GI fluid loss (e.g., diarrhoea)?

  Prolonged fluid loss leads to dehydration and low blood pressure. ADH plays a key role by:

  • Retaining water in the kidneys
  • Helping maintain blood volume and pressure
  • Preventing hypovolemic shock
• What cellular mechanism allows ADH to increase water reabsorption?

  ADH binds to V2 receptors on basolateral membranes of collecting duct cells → activates adenylate cyclase → increases cAMP → activates protein kinase A (PKA) → promotes aquaporin-2 channel insertion into the apical membrane → increased water permeability.
• What is dehydration and how does it relate to fluid loss from the GI tract?

  A state of negative fluid balance where fluid loss exceeds intake. In the GI tract, this commonly occurs due to vomiting or diarrhoea, leading to loss of water and electrolytes such as sodium, potassium, and bicarbonate.
• What are the main fluid and electrolyte losses associated with diarrhoea?

  Diarrhoea causes loss of large volumes of water, sodium, potassium, and bicarbonate. This can lead to dehydration, hyponatremia, hypokalaemia, and metabolic acidosis.
• How does vomiting lead to dehydration and electrolyte imbalance?

  Vomiting results in loss of gastric fluids rich in hydrogen and chloride ions, leading to dehydration, hypochloremia, and metabolic alkalosis. Repeated vomiting can also cause hypokalemia due to renal compensation.
• What cardiovascular changes occur during dehydration caused by GI fluid loss?

  Reduced blood volume (hypovolemia) leads to decreased blood pressure, tachycardia, and reduced tissue perfusion. Severe dehydration may result in hypovolemic shock.
• How does dehydration affect renal function?

  Dehydration decreases renal perfusion and glomerular filtration rate (GFR), leading to oliguria (low urine output) and potentially acute kidney injury if prolonged.
• What are neurological consequences of dehydration?

  Dehydration can cause confusion, dizziness, headaches, and in severe cases, seizures or coma due to electrolyte imbalances (e.g., hyponatremia).
• How does the body attempt to compensate for dehydration caused by GI fluid loss?

  Compensatory mechanisms include activation of the renin-angiotensin-aldosterone system (RAAS), increased antidiuretic hormone (ADH) secretion, and thirst stimulation to retain water and sodium.
• Why are infants and the elderly more vulnerable to dehydration from GI losses?

  Infants have higher fluid turnover and immature kidneys, while the elderly often have reduced thirst sensation and renal function, making them less able to compensate for fluid loss.