sodium, water disorders

What is the major extracellular fluid (ECF) cation?

Sodium (Na+)

What does sodium regulate in the body?

ECF fluid, osmolality, and tonicity

How does sodium affect intravascular volume?

It determines intravascular volume based on Na+ concentrations.

Where does sodium absorption primarily occur?

In the gut, unregulated. (possibly through HT salt craving)

What regulates sodium reabsorption in the kidneys?

The renin-angiotensin-aldosterone system (RAAS)

What is the normal plasma sodium concentration range?

~140 mmol/L (135-145 mmol/L)

What is the sodium concentration in intracellular fluid (ICF)?

~10 mmol/L

What hormone regulates the overall mass of sodium?

Aldosterone

What hormone regulates sodium concentration?

Antidiuretic hormone (ADH)

Can low sodium concentration indicate low total sodium mass?

No, low sodium concentration does not mean low total sodium mass.

Example of sodium conc vs sodium mass

Chronic HF

In chronic heart failure, water retention lowers plasma osmolality despite an overall increase in total body sodium.

What percentage of Na+ filtered is reabsorbed in the kidneys?

99.5%

What percentage of Na+ is reabsorbed in the proximal convoluted tubule (PCT)?

70%-80%

What percentage of Na+ is reabsorbed in the loop of Henle (LoH)?

25%

What percentage of Na+ is reabsorbed in the distal convoluted tubule (DCT) and collecting duct (CD)?

8%

How do water and Cl- follow Na+ during reabsorption in the PCT?

They follow passively to maintain electrical neutrality and osmolality.

How is Cl- reabsorbed in the ascending loop of Henle?

Cl- is reabsorbed actively, and Na+ follows.

What hormone stimulates Na+ reabsorption in the DCT and CD?

Aldosterone (Ald)

What happens to K+ and H+ during Na+ reabsorption in the DCT/CD?

K+ is secreted and some H+ is secreted to maintain electrical neutrality.

What dictates Na+ reabsorption in the kidneys?

Pa detection at macula densa cells (JGA) stimulates renin release by granular cells.

What factors stimulate renin release?

Decreased renal arterial Pa, increased B-adrenergic activity, and increased prostaglandins.

What is the sequence of conversion from prorenin to Ang-II?

Prorenin → Renin → Ang-I → Ang-II, which can be converted into Ang-III by amino peptidase A.

What are the effects of Ang-II?

Stimulates aldosterone synthesis and secretion, causes vasoconstriction, promotes ADH release, releases adrenal catecholamines, and increases central sympathetic discharge.

What is the role of aldosterone in the body?

Aldosterone regulates sodium and potassium levels by promoting sodium reabsorption and potassium excretion in the kidneys.

How does aldosterone exert its effects at the cellular level?

Aldosterone binds to mineralocorticoid receptors in the cytosol, forming a complex that translocates to the nucleus to initiate transcriptional responses, increasing the expression of epithelial sodium channels (ENaC).

What is the consequence of increased expression of ENaC?

Increased expression of ENaC leads to enhanced sodium reabsorption from the renal tubules into the bloodstream, which is facilitated by the Na+/K+ ATPase pump.

What happens to potassium levels as a result of aldosterone action?

Aldosterone promotes potassium excretion into the urine, leading to decreased extracellular fluid potassium concentration (hypokalemia).

What feedback mechanisms are involved in regulating aldosterone secretion?

Negative feedback occurs through decreased extracellular volume (ECV), renal artery pressure, and sodium and water retention, which inhibit aldosterone secretion. Additionally, atrial natriuretic peptide (ANP) and dopamine also negatively inhibit aldosterone release.

What are the effects of excessive aldosterone secretion?

Excessive aldosterone secretion, known as primary hyperaldosteronism, can lead to hypokalemia and hypertension due to increased sodium retention.

What is the role of RAAS in blood volume control?

RAAS is part of the overall control of blood volume, with processes acting in synergy.

What mechanisms decrease blood volume?

Decreased blood volume occurs via mechanoreceptors in the left ventricle, carotid sinus, aortic arch, and renal afferent arterioles.

What are the consequences of decreased blood volume?

Consequences include increased sympathetic outflow from the CNS, increased RAAS, increased ADH, and increased thirst.

What effects do Angiotensin II, Aldosterone, and ADH have?

They produce vasoconstriction, venoconstriction, and renal retention of sodium and water.

What hormones are secreted alongside Aldosterone and cortisol?

Increased norepinephrine (NE) and epinephrine (E) secretion from the adrenal medulla is also observed.

HYPOVOLEMIA

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Hypovolemia DEF:

= usually deficiency of both Na+ and water

causes of hypovolemia can be divided into :

renal + non-renal causes

renal causes of hypovolemia

Tubulointerstitial injury (AKI - particularly problem) → if tubular cells are damage, cannot

reabsorb water / sodium (both are lost)

Side note: In chronic renal failure → hypervolaemia is more problem, kidneys cannot excrete H2O

■ Diuretics: thiazides (ENaC), loops (LoH) → strongest for Na+ loss & strongest for water (both lose

both)

■ Other drugs w/ low V as S/E: trimethoprim & pentamidine (through ENaC)

■ Mineralocorticoid deficiency (Addison's - hypoaldosteronism)

■ Mineralocorticoid resistance - rare

■ Medications antagonising MR (spironolactone, eplerenone → used in HTN & HF - cardiac

remodelling)

non-renal causes of hypovolemia

■ Haemorrhage

■ GI: diarrhoea ( → bicarbonate lost = acidosis), vomiting ( → chloride lost = alkalosis)

■ Skin: fever, exposure to heat

■ Resp mucosa via hyperventilation (NB in ICU - artificial ventilation)

■ Third spacing → aetiologies w/ ↑ vasc perm and hypoalbuminemia - loss of oncotic pressure

(albumin is main determinant of this in vasculature → in cirrhosis/liver pathology, loss of protein)

(sepsis, peritonitis, pancreatitis, burns)

side effects of hypovolemia

○ Orthostatic hypoT ⇒ ↓ >10-20 mmHg in BP on standing

○ Orthostatic tachycardia ⇒ ↑ >15-20 bpm upon standing

○ Dry mucous membrane ⇒ look under eyes, open mouth to look at whether tongue is dry (needs to glissen)

○ ↓ skin turgor

treatment of hypovolemia

○ Mild ⇒ oral hydration/replacement is sufficient

○ Severe ⇒ IV replacement

○ Isotonic saline (NaCl) vs dextrose (5%D/W = 5% dextrose in water) depending on whether pt is

hypo/normonatraemic or hypernatraemia