Hormonal and Non-hormonal Control and Regulation of Solutes Flashcards
Atrial natriuretic peptide
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
Uradilatin
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
Recycling of urea
- Cortical and outer medullary collecting ducts, ADH increases water permeability, but it does not increase urea permeability
- Urea concentration of tubular fluid increases
- Inner medullary collecting ducts, ADH increases water permeability and increases transporter facilitated diffusion of urea, UT1
- Creates a larger concentration gradient for urea and diffuses down gradient into interstitial fluid
Diabetes insipidus
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)
Syndrome of Inappropriate ADH secretion
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
Excessive aldosterone
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
Deficient aldosterone secretion
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
Adding 2L isotonic saline
Isoosmotic expansion
Pee out water and salt
Diarrhea
Isoosmotic contraction
Plasma Na concentration normal
Osmotic diuresis
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
Control of K balance
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
Flow effects on K excretion
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
Measuring K balance
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
Tubular Na and K excretion
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
Water diuresis and K excretion
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.
Volume expansion compensation
Decreased reabsorption of sodium chloride and bicarbonate in PT and decreases aldosterone causing metabolic acidosis (chronic leads to negative K balance)
Volume contraction
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
Increased extracellular K
Increases K excretion
Aldosterone and K
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
Acid base status on K balance
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
Ca balance
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
PTH
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
Calcitonin
Increases deposition of Ca in bone
Calcitriol
Promotes absorption of Ca and P in SI and assists PTH
