Hormonal and Non-hormonal Control and Regulation of Solutes

Question 1

Atrial natriuretic peptide

Answer 1

Heart is an endocrine organ
Increases excretion of salt and water and adapts over time
Circulating ANP is a measure for severity of congestive heart failure because elevated levels indicate volume expansion (paradoxical diuresis

Question 2

Uradilatin

Answer 2

Peptide secreted by distal tubule and collecting duct when BP and ECFV increases
Only local effects
Inhibits NaCl and water reabsorption in medullary collecting duct

Question 3

Recycling of urea

Answer 3

1. Cortical and outer medullary collecting ducts, ADH increases water permeability, but it does not increase urea permeability
2. Urea concentration of tubular fluid increases
3. Inner medullary collecting ducts, ADH increases water permeability and increases transporter facilitated diffusion of urea, UT1
4. Creates a larger concentration gradient for urea and diffuses down gradient into interstitial fluid

Question 4

Diabetes insipidus

Answer 4

Hyperosmotic contraction
ADH insufficiency (decreased secretion, decreased renal response)
Inability to concentrate urine
Hypovolemia due to increased urine flow
Hypotension possible
Positive free water clearance (water deprivation has negative)

Question 5

Syndrome of Inappropriate ADH secretion

Answer 5

Hypoosmotic expansion
Excessive secretion
Hypovolemia due to decreased water excretion, hyponatremia, metabolic acidosis
Constitutive activation of V2 receptor in collecting duct similar but plasma ADH would be undetectable due to feedback suppression of secretion

Question 6

Excessive aldosterone

Answer 6

Hyperosmotic expansion
Increased reabsorption of salt and water produces hypervolemia, suppresses ADH, water excreted, hypernatremia (not seen with short term)
Increases secretion of H+ -> metabolic acidosis
Secondary HTN

Question 7

Deficient aldosterone secretion

Answer 7

Hypoosmotic contractionLoss of salt and water, hypovolemia
Decreases excretion of H+ -> metabolic acidosis -> opposed by proximal tubule
Increased reabsorption of salt and water in proximal tubule attempts to maintain volume -> increases bicarbonate reabsorption -> alkalosis -> increased secretion of K (possible hypokalemia)
Low blood volume stimulates ADH -> reabsorption of water without salt -> hyponatremia
ECFV decreases but ICFV increases
Spironolactone: aldosterone receptor blocker, will still have aldosterone

Question 8

Adding 2L isotonic saline

Answer 8

Isoosmotic expansion

Pee out water and salt

Question 9

Diarrhea

Answer 9

Isoosmotic contraction

Plasma Na concentration normal

Question 10

Osmotic diuresis

Answer 10

Increase in urine flow caused by presence of urine of substance not normally present or present in greater concentration
Usually causes a negative K balance
Glycosuria one of most common causes

Question 11

Control of K balance

Answer 11

Normally tight control
Hypokalemia is an independent risk factor for ventricular fibrillation and sudden cardiac death and severely exacerbates risk of events in pts with coexisting heart disease

Question 12

Flow effects on K excretion

Answer 12

Elevated tubular flow causes physiological regulation of plasma K
K excretion driven upward by increased urine flow, with no negative feedback
Increased tubular flow increases K secretion in distal tubule and CCD
Increased tubular flow increases K excretion

Question 13

Measuring K balance

Answer 13

Plasma K concentration not reliable because vast majority is intracellular
The key is [K+] of tubular cells, if it increases more K diffuses into tubular fluid

Question 14

Tubular Na and K excretion

Answer 14

Increased distal tubular Na load -> increase diffusion of Na into cells of distal tubule -> stimulates Na/K pump and increases intracellular K in tubular cells -> increases K secretion and excretion

Diuretics that inhibit Na reabsorption in Loop and early DT will increase K excretion

Question 15

Water diuresis and K excretion

Answer 15

Excess water decreases plasma Na and ADH
Results in water-induced diuresis
Increased tubular flow in MCD
Water induced diuresis and antidiuresis have little effect on K balance because their two effects cancel out.

Question 16

Volume expansion compensation

Answer 16

Decreased reabsorption of sodium chloride and bicarbonate in PT and decreases aldosterone causing metabolic acidosis (chronic leads to negative K balance)

Question 17

Volume contraction

Answer 17

Causes increased secretion of aldosterone which increases K secretion
Reabsorbed water at all costs to maintain CO
With increased PT water reabsorption, increased anion reabsorption (including bicarbonate), metabolic alkalosis
Increased aldosterone increases H+ and K secretion

Question 18

Increased extracellular K

Answer 18

Increases K excretion

Question 19

Aldosterone and K

Answer 19

Aldosterone promotes K excretion
1. Increase # of Na pumps
2. Increase # of Na channels
3. Increase serum glucocorticoid kinase increases Na channels and activates K channels
4. Stimulates channel activating protease which increases Na channels
5. Increases permeability of K
Net effect is K pumped into tubular cells and does not get reabsorbed

Question 20

Acid base status on K balance

Answer 20

Intracellular K and H interact and they can displace each other
Increased intracellular H drives K out of cell
Alkalosis shifts K from ECF into cell (which increases K excretion)
Acute metabolic acidosis causes decreased K excretion and hyperkalemia and decreases K permeability and metabolic energy for Na/K pump
Chronic causes increased K excretion but also hyperkalemia
Acute or chronic, plasma K often elevated until cellular depletion so severe it crashes

Question 21

Ca balance

Answer 21

Ca in plasma 45% bound to proteins, binding depends on pH (alkalosis increases affinity)
99% of FL reabsorbed, 80% in PT is paracellular, DT is transcellular by active transport
Ca-ATPase is primary active transporter and Na/Ca exchanger secondary active antiporter

Question 22

PTH

Answer 22

Secretion is inhibited by high levels of Ca and stimulated by low plasma levels
Required for life, increases plasma Ca through increased renal reabsorption, release from bone, and increased activation of Vitamin D to form calcitriol
Does not increase reabsorption of Ca in PT but promotes it in cortical TAL and DT

Question 23

Calcitonin

Answer 23

Increases deposition of Ca in bone

Question 24

Calcitriol

Answer 24

Promotes absorption of Ca and P in SI and assists PTH

Question 25

Linkage of Na and Ca

Answer 25

PT and cortical TAL reabsorption of Na and Ca are parallel
Loop diuretics: inhibit reabsorption of Ca because they inhibit reabsorption of Na, hypoclacemia
Thiazide: since reabsorption of Ca is transcellular in DT, it is not linked to Na and will increase Ca reabsorption, hypercalcemia

Question 26

Renal regulation of P

Answer 26

Usually reabsorbed at max rate
Diets high in P decrease max renal reabsorption rate
PT: 3Na/1P symportor (NPT2) and P/anion antiporter, almost entirely transcellular

Question 27

Interaction of P and Ca in renal failure

Answer 27

Chronic renal failure, the ability of kidneys to excrete P is often impaired
Lowers plasma free Ca and thus PTH increases, which mobilizes P from bone
Ca salts in heart, weak bones, , suppresses formation of calcitriol which exacerbates hypocalcemia (2nd hyperparathyroidism)