Module 2 Part I

What percentage of body weight is intracellular fluid (ICF) vs extracellular fluid (ECF)?

ICF = 40% of body weight, ECF = 20% of body weight.

What is the major intracellular cation and its concentration?

Potassium (K⁺), ~110 mmol/L.

What is the major extracellular cation and its concentration?

Sodium (Na⁺), ~140 mmol/L

Differentiate osmolarity from osmolality.

Osmolarity = solute particles per litre of water (Osm/L, volume-based); Osmolality = solute particles per kg of water (Osm/kg, mass-based).

What is the approximate formula for plasma osmolality?

2[Na⁺] + 2[K⁺] + [glucose] + [urea]

Where is ADH produced, and what stimulates its release?

Produced by the posterior pituitary; released in response to ↑ plasma osmolality or ↓ blood volume.

How does ADH act on the collecting duct to increase water reabsorption?

Binds V2 receptor → ↑ cAMP → activates PKA → insertion of AQP2 channels into apical membrane → ↑ water permeability.

What is daily sodium intake and main route of excretion?

Intake: 100–200 mmol/day; main excretion is renal.

What triggers renin release from the juxtaglomerular apparatus?

Low renal perfusion (e.g., hypovolemia, heart failure, shock).

Name the active hormone formed by ACE and its effects.

Angiotensin II; causes vasoconstriction and stimulates aldosterone release

What is the primary action of aldosterone in the kidney?

Increases sodium reabsorption and potassium excretion in the distal tubule.

Main clinical effect of hyponatraemia or hypernatraemia?

Neurological symptoms due to brain cell swelling (hyponatraemia) or shrinkage (hypernatraemia).

List two causes of hyponatremia.

SIADH, Addison’s disease, diuretics, vomiting, diarrhoea.

List two causes of hypernatremia.

Water loss (e.g., diabetes insipidus), excessive salt intake, mineralocorticoid excess (Conn’s syndrome).

What is normal extracellular potassium concentration?

~4 mmol/L.

How does acidosis affect potassium levels?

H⁺ enters cells in exchange for K⁺ → ↑ [K⁺] in ECF → hyperkalaemia.

List two causes of hypokalemia.

Diuretics, vomiting/diarrhea, aldosterone excess (Conn’s), Cushing’s syndrome.

List two causes of hyperkalemia.

Renal failure, Addison’s disease, acidosis, insulin deficiency, potassium-sparing diuretics.

Explain the role of ADH in water balance, including its regulation and mechanism of action on renal tubules.

• ADH is released from the posterior pituitary in response to ↑ osmolality or ↓ blood volume.

• Acts on V2 receptors in collecting duct cells → activates adenylyl cyclase → ↑ cAMP → activates PKA.

• Promotes synthesis and insertion of aquaporin-2 channels into the apical membrane, ↑ water reabsorption.

• Overall: lowers plasma osmolality and restores blood volume

Describe the Renin-Angiotensin-Aldosterone System (RAAS) and its role in sodium regulation.

• Trigger: low renal perfusion (hypovolemia, shock).

• Renin from JGA converts angiotensinogen → angiotensin I.

• ACE converts angiotensin I → angiotensin II.

• Angiotensin II causes vasoconstriction and stimulates aldosterone release from the adrenal cortex.

• Aldosterone acts in distal tubule to reabsorb sodium and excrete potassium, restoring ECF volume and blood pressure

Discuss the causes, symptoms, and pathophysiology of hyponatremia and hypernatremia.

• Hyponatraemia: Causes → water excess (SIADH, renal failure), sodium loss (Addison’s disease, vomiting, diarrhoea).

  • Symptoms: nausea, drowsiness (<130 mmol/L), confusion, seizures, coma (<110 mmol/L).

  • Pathophysiology: low Na⁺ → water moves into cells → cerebral oedema.

• Hypernatraemia: Causes → dehydration, excessive salt intake, mineralocorticoid excess.

  • Symptoms: weakness, lethargy (>150), seizures, and coma (>160).

  • Pathophysiology: high Na⁺ → water moves out of cells → neuronal dehydration

Explain potassium homeostasis, including normal distribution, regulation, and clinical disorders (hypokalaemia and hyperkalaemia).

• Distribution: ~98% intracellular (muscle, RBCs), ~2% extracellular (4 mmol/L).

• Regulation: intake, cellular shifts (insulin, acid-base balance, adrenaline), renal excretion.

• Hypokalaemia: Causes = GI loss, renal loss (diuretics, Cushing’s, Conn’s), redistribution (insulin, alkalemia).

• Hyperkalaemia: Causes = renal failure, Addison’s, acidosis, haemolysis, K⁺-sparing drugs.

• Clinical effects: arrhythmias, muscle weakness