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MSC: Disease of major orgns > Sodium > Flashcards

Sodium Flashcards

1
Q

How does water move and its relation to sodium?

A
  • Water will move from an area of low osmolality to an area of high osmolality
  • As sodium moves, water will move
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2
Q

What is the location of the Kidneys?

A
  • Located between the 11th thoracic and 3rd lumbar vertebrae in the retroperitoneum on either side of vertebral column
  • The right kidney is lower than the left kidney
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3
Q

What are parts of the kidneys?

A
  • Renal Capsule
  • Renal Pelvis
  • Ureter
  • Renal Vein
  • Renal Artery
  • Renal Medulla
  • Renal Cortex
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4
Q

What is the gross anatomy of the kidneys?

A
  • Dimensions: 13 x 6 x 4 cm
  • Weight: ~150 g each
  • Cardiac output: Receives 20 – 25% of which 90% supplies the renal cortex
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5
Q

What are parts of the nephron?

A

Functional unit of kidney and contains approx 1 million

  • Renal Artery and Vein
  • Glomerular Capsule/Bowmans Capsule
  • Proximal Convoluted Tubule
  • Loop of Henle: Thin descending loop, Thin ascending loop, Thick Ascending loop
  • Distal Convoluted Tubule
  • Collecting Duct
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6
Q

How does sodium reabsorption take place?

A
  • <1% filtered Na+ is excreted in the urine
  • Therefore, >99% filtered Na+ must be reabsorbed via a process of tubular reabsorptiom which involves PROTEIN CARRIERS and ION-SPECIFIC CHANNELS
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7
Q

How does Sodium reabsorption take place in the Proximal Convuluted Tubule?

A

There is secondary active transport in PCT. Energy from basolateral through Na+-K+-ATPase. This creates favourable inward gradient for Na+

  • Na+-H+ ANTIPORTERS: Most Na+ reabsorbed in exchange for H+. It also allows reabsorption of HCO3-
  • Na+-SOLUTE CO-TRANSPORTERS: Allows simultaneous reabsorption of various organic & inorganic solutes
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8
Q

How does the Loop of Henle absorb Sodium?

A

​Basolateral membrane

  • Secondary active transport due to energy from basolateral Na+-K+-ATPase. This creates favourable inward gradient for Na+
  • Cl- leaves cell via channel which creates favourable inward gradient for Cl-.

Apical membrane

  • NKCC2 CO-TRANSPORTER: Na+ reabsorbed with K+ & 2x Cl-. Potassium is recycled back via ROMK1
  • Mg2+ & Ca2+ REABSORPTION: K+ movement drives reabsorption of Mg2+ & Ca2+
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9
Q

How does the Counter-Current System work?

A
  • Descending limb is permeable to H2O and some NaCl
  • The Ascending limb is impermeable to H2O and able to transport NaCl into the interstitium via NKCC2
  • This helps create a gradient within the medulla that gets more concentrated as the loop enlongates.
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10
Q

How does efficiency of the counter current system change?

A
  • Efficiency depedns on the length of the loop of Henle
  • JUXTAMEDULLARY NEPHRONS are more important for this process as they are longer
  • Cortical nephrons make little contribution due to them being shorter in length
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11
Q

How does the DCT reabsorb Sodium?

A

Basolateral

  • Secondary active transport through energy from basolateral Na+-K+-ATPase. This creates favourable inward gradient for Na+
  • Cl- leaves cell via channel which creates favourable inward gradient for Cl-

Apical

  • Na+ reabsorbed with Cl-
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12
Q

How does the Collecting Duct reabsorb Sodium?

A
  • In CD, luminal concentration of Na+ can be lower than intracellular Na+ so can’t set up concentration gradient!!

APICAL SODIUM CHANNEL

  • Na+ channel is electrogenic. Electronegativity allows Na+ entry into the cell. K+ is secreted simultaneously to balance charge
  • Intracellular electronegativity generated by Na+-K+-ATPase
  • Controlled by ALDOSTERONE
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13
Q

Which conditions are diuretic prescribed?

A
  • Hypertension
  • Heart failure
  • Liver cirrhosis
  • Nephrotic syndrome
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14
Q

What is the effect of Diuretics?

A
  • Cause NEGATIVE FLUID BALANCE
  • Decreases renal NaCl reabsorption and increases urinary losses of Na+ and therefore H2O
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15
Q

What are the main classes of Diuretics?

A
  • Loop Diuretics
  • Thiazide Diuretics
  • Potassium-sparing
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16
Q

What is the action of Loop Diuretics?

A

Promote excretion of 20-25% filtered Na+ at max dose

  • TARGET: Thick ascending limb of the Loop of Henle
  • INHIBIT: NKCC2
  • ACTION: Compete with Cl- for binding sites on NKCC2
17
Q

What is the action of Thiazide Diuretics?

A

Promote excretion of 3-5% filtered Na+ at max dose (Less potent than Loop Diuretics)

  • TARGET: Distal convoluted tubule
  • INHIBIT: NaCl cotransporter
  • ACTION: Compete with Cl- for binding sites on NaCl cotransporter
18
Q

What are Potassium Sparing Diuretics?

A

Promote excretion of 1-2% filtered Na+ at max dose. Avoid renal K+ wasting

  • TARGET: Principle cells of collecting duct
  • INHIBIT: ENaC
  • ACTION: Decrease the number of open Na+ channels inhibiting the channel directly (amiloride) or competitively inhibiting aldosterone binding to MR (spironolactone, eplenerone)
19
Q

What is the Renin-Angiotensin Alsoterone system?

A
  • Renin released which cleaves angiotensinogen to angiotensin 1
  • Angiotensin is converted to angiotensin 2 by the Angiotensin converting enzyme (ACE)
  • Angiotensin 2 leads to proudction of Aldosterone which leads to sodium and water rentention.
  • This leads to systemic volume expansion
20
Q

Where is Renin secreted from?

A
  • Synthesized and secreted by juxtaglomerular cells which are part of juxtaglomerular apparatus (JGA
  • They are specialised smooth muscle cells that are sensitive to arteriolar stretch ie. sense changes in ECF volume
  • Sodium is the main determinant of Renin Secretion
21
Q

Where is ACE mainly found and which proteins does it act on?

A

Dipeptidyl carboxypeptidase highly concentrated in the lungs. It acts to cleave dipeptides from a range of substrates:

  • Angiotensin I
  • Bradykinin
  • Substance P
  • Enkephalins
22
Q

Describe the Angiotensinogen metabolism

A

Angiotensinogen

  • 60 kDa, α2-globulin
  • Produced by the liver
  • Normally present in the plasma at a concentration of 1 mmol/L

Angiotensin 1

  • Formed from the cleavage of a decapeptide from angiotensinogen which is catalysed by RENIN
  • INACTIVE

Angiotensin 2

  • Formed from the cleavage of a dipeptide from angiotensin I
  • Catalysed by ACE
  • ACTIVE
23
Q

What are the main effects of Angiotensin 2?

A

SYSTEMIC VASOCONSTRICTION

  • Increases blood pressure

Na+ AND H2O RETENTION

24
Q

How does Angiotensin 2 increase Na+ and H2O retention?

A
  • Stimulates ALDOSTERONE release
  • Stimulates ADH release (­H2O retention)
  • Increases tubular reabsorption of Na+ & H2O
25
Q

What is Aldosterone?

A
  • Steroid hormone produced by the zona glomerulosa cells in the Adrenal Glands that acts as a mineralcorticoid
  • Aldosterone freely diffuses into CD cells and binds to mineralocorticoid receptor (MR)
26
Q

What is the effect of Aldosterone?

A
  • Increase in number of open Na+ channels so increased Na+ reabsorption & hence H2O reabsorption
  • Increased Na+ transport out of cell via Na+-K+-ATPase so Intracellular K+ increases
  • Increased K+ secretion as a result
27
Q

How can the RAAS mechanism be altered for therapy?

A

ACE Inhibitors (e.g. captopril, lisinopril, ramipril)

  • Produce vasodilation by inhibiting production angiotensin II
  • Block breakdown of bradykinin therefore increased levels contribute to vasodilator action of ACE-I

Angiotensin II receptor blockers (e.g. candesartan, losartan)

  • Receptor antagonists, dilate arteries and veins reducing arterial pressure and load on heart
  • Promote renal excretion Na and H2O

Aldosterone receptor blockers (e.g. spironolactone, eplerenone)

  • Antagonise actions of aldosterone in DCT resulting in excretion of Na and H2O
28
Q

What is structure of ADH?

A
  • Nonapeptide
  • MW = 1084 Da
  • Rapidly metabolized by Liver and Kidney
  • t1/2 = 15 – 20 mins
29
Q

What is the role of ADH?

A

Decrease the amount of urine produced by increased reabsoprtion of H2O

30
Q

How is ADH synthesised and secreted?

A

Synthesized by HYPOTHALAMUS

  • Supraoptic nuclei (SON)
  • Paraventricular nuclei (PVN)

Secreted by:

  • POSTERIOR pituitary
31
Q

What is action of ADH?

A
  • Binds to ADH receptor (V2) in the kidneys
  • This increases the aquaporin channels inserted into the apical membrane of the collecting duct
  • This increases the amount of water reabsorption
32
Q

Where are ADH receptors located?

A
  • V1(v1a): Located in smooth muscle of mesenteric artery. It causes vasoconstriction
  • V2: Located in Kidney. It leads to anti-diuresis
  • V3(v1b): Located in Pituitary Gland. It leads to release of ACTH
33
Q

What are ‘other’ causes of ADH secretion?

A
  • Nausea
  • Pain
  • Surgery
  • Pregnancy
  • Angiotensin II
  • Low Cortisol
34
Q

How is ADH secretion controlled?

A
  • Increased Extracellular fluid osmolality: increase in plasma osmolality stimulates ADH release & thirst
  • Decreased Extracellular fluid volume: decrease in plasma volume (without a change in osmolality) stimulates ADH release
  • Others
35
Q

How does increased ECF osmolality cause ADH release?

A
  • Increase ECF osmolality
  • ALL cells in the body become dehydrated and ALL cells in the body shrink including hypothalamic osmoreceptors
  • Loss of H2O from hypothalamic osmoreceptors leads to activation of “stretch-inactivated cation channels”
  • There is depolarization of the cell
  • This leads to stimulation of ADH secretion and synthesis
36
Q

How does decrease in ECF volume cause ADH release?

A
  • Detect decrease ECF volume
  • Massive increase in ADH secretion
  • Maximum urine concentration achieved

MSC: Disease of major orgns (23 decks)

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