Session 4 Flashcards
How does solute move across the PCT cells and enter interstitium
Solvent follows solute, solute transported primarily water follows passively
Driver for movement of solute across PCT cells into interstitium
- Increased osmolarity of ICF as solute transported into PCT
- Water from nephron lumen moves down gradient into PCT until equilibrated
- Transient increase in ICF volume
- 3Na-2K-ATPase moves Na+ into interstitium and water follows
What solute enters the cell across the luminal (apical) membrane
Sodium
What is the Net effect on the osmolarity of the PCT epithelial cells to the movement of sodium
No change as increased osmolarity of PCT cells means water follows
Which ions move in 3Na-2K-ATPase
3 Na+ out
2 K+ in
Primary driving force in interstitium for movement of solute and solvent from interstitium into peritubular capillaries
Hydrostatic pressure increased
Primary driving force in peritubular capillaries for movement of solute and solvent from interstitium into peritubular capillaries
Higher oncotic pressure (lower hydrostatic), left oncotic proteins behind
What is the function of the tight junctions between tubule cells
Barrier to prevent diffusion of transporter, channel and pump proteins between apical and basolateral membrane. Maintain polarity
Percentage and location of sodium iron reabsorption along nephron
PCT 67%
LOH asc 25%
LOH desc 0%
DCT 5%
CD 3%
Percentage and location of sodium ions and water reabsorption along the nephron
PCT 65%
LOH asc 0%
LOH desc 10%
DCT 0%
CD 5%
What causes release of renin
Fall in plasma sodium leads to fall in ECF volume
Renin is released by
- increased sympathetic innervation (granular cells of JGA)
- Wall tension in afferent arterioles fall, granular cells detect this which stimulates renin release
- Decreased sodium to macula densa (if less NaCl reaches the macula densa, it i stimulated to secrete prostaglandins, acts on granular cells to simulate renin release)
Angiotensin II effects
Directly vasoconstricts efferent arterioles within the glomerulus
Stimulates zona glumerulosa of adrenal cortex to release aldosterone
What does aldosterone do
Directly increases Na+ reabsorption from DCT with ENAC channels
Releases ADH
Stimulate thirst
Prostaglandin synthesis
Decrease in effective circulating volume stimulates cortical prostaglandin synthesis
How does JGA respond if BP is high
ATP release
How does JGA respond if there is a drop in BP
Renin release, prostaglandin release
Prostaglandin synthesis occurs in
Cortex, medullary interstitial cells, collecting duct epithelial cells
Result in vasodilators and renin release
What is ANP (atrial natureric peptide)
Produced by cardiac atrial cells in response to an increase in ECF volume (high bp)
ANP acts to
-Inhibit Na+/K+/ATPase and close Na+ channels of CD and DCT, reducing Na+ reabsorption, water and Na+ excretion increased
- Vasodilate afferent arterioels increasing GFR
- Inhibit aldosterone secretion and ADH release
- Decrease renin release
What happens in high blood pressure to hydrostatic and oncotic pressure
NaCl intake increases so ECF increases
Hydrostatic pressure increases and oncotic pressure decreases, NaCl and water reabsorption by the PCT decreases
Effectors of change in renal sodium excretion when renal artery BP increases
Reduced Na-H antiporter and reduced Na-K-ATPase activity in PT
Reduction in sodium resorption in proximal tubule (Glomerular tubular balance)
Reduction in water Resorption in PT
Pressure natriuresis and diuresis
Summary of increased BP
Inhibits Na-K-ATPase and reduce ENAC expression
Decreased Na resorption DCT/CD
Increase in hydrostatic pressure of peritubular capillaries (pressure natriuresis and diuresis)
Summary of decreased BP
Prostaglandin release
RAAS activated (ANG II causes constriction of efferent arteriole and release of aldosterone)
Aldosterone increases expression of ENAC, stimulates ADH and thirst
Hypoperfusion due to congestive cardiac failure leads to
Na+ and water retention by the kidneys, leading to oedema, kidneys sense as hypovolemia, resulting in compensation by retaining NaCL and water to increase CFV
Stimulates low BP response
Increased pulmonary venous pressure results in
Transudation from the capillaries in the lungs and in pulmonary oedema
Management involves reducing the fluid load e.g. diuretics, ACE inhibitors, nitrates, vasodilators
First line diuretic
Furosemide
What is hypervolaemia
Fluid overload, XS of total body sodium and water, leads to expansion of ECF compartment
Hypervolaemia due to
Kidney retention of sodium and water
Reduced effective arterial volume e.g. CCF
XS sodium or fluid intake
Cirrhosis
Hyperaldosteronism
Hypovolemia can lead to
Shock
What is shock
A medical emergency in which the vital organs are not adequately perfused
Anaerobic metabolism and inefficient clearance of metabolites
Tiredness, dizziness, thirst
Vasodilation occurs in vital organs (heart lung brain) to maintain blood supply
Leads to acute tubular necrosis in kidney
A severe decrease in circulating volume stimulates sympathetic activity to maintain BP by
Tachycardia
Peripheral vasoconstriction
Increase in myocardial contractility
To counteract excessive vasoconstriction in Hypovolemic shock what happens in kidneys
Prostaglandins are secreted, maintains adequate blood flow through kidney and sufficient GFR
2 major consequences of loss of large amounts of fluid
Volume depletion (decreases tissue perfusion), electrolyte and acid-base disturbances
What is hypertensive renal disease
Renal autoregulation maintains Renal function despite variations in systolic BP
Arteriosclerosis of major renal arteries, hyalinization of small vessels with intimal thickening
Can lead to chronic renal damage (hypertensive nephrosclerosis) and a reduction in the size of the kidneys
Renal causes of secondary hypertension
Impaired Na+ and water excretion increasing blood volume
Stimulation of renin release
Renal artery stenosis, reduces perfusion of kidney, XS RAAS
Negative feedback loop for ADH
Increased ADH causes decreased renal water excretion
Decreased osmolarity inhibits ADH secretion
Negative feedback loops that begin with the anterior hypothalamus
Changes in BP have an effect on the
Response to changes in osmolarity
(Volume is more important)
Thirst is stimulated by
Increase in plasma osmolarity
Symptoms of diabetes insipidus
Polyuria, polydipsia, low urine osmolality (dilute)
Too little ADH in diabetes insipidus is
Inability to reabsorb water from the distal part of the nephron due to failure of secretion or action of ADH
What is hypernatremia
Less prevalent clinically
More than 140mmol/L
Causes of hypernatremia
Osmotic diuresis
Fluid loss without replacement
Diabetes insipidus
Incorrect intravenous fluid replacement
Primary aldosteronism
Features of hyponatremia
Low sodium very common in hospital patients
Serum conc of Na lower than
130/135mmol/L
Symptoms: neurological, agitation, nausea, focal neurology, coma
Causes of hyponatraemia
Diuretics
Water overload or retention
Increase in ADH secretion
Increased plasma osmolality
Increased plasma osmolality
Diuretics/renal failure
Peritonitis/Burns
D and V
Hyponatraemia is generally caused by
Water loss than sodium directly
Reference range of serum osmolality
275-295 mosm/kg
How do you calculate osmolarity
2 Na + glucose + urea (all in mmol/L)
What does hypovolemic hyponatremia tell us
Nonrenal loss e.g. GI, sweating, ascites, burns, cerebral salt-wasting syndrome
People with inappropriate ADH secretion are generally
Uvoelemic
Treatments for hyponatraemia
Fluid restriction
Pontine demyelination can occur with rapid correction
Infusion of hypertonic saline and furosemide
