W04: RENAL PHYSIOLOGY Flashcards
Define the functions of the kidney.
Filtration and excretion of substances from blood plasma / cardiac output
Describe the mechanisms of glomerular filtration, tubular reabsorbtion and secretion, and handling of solutes and water by the kidneys.
- GLOMERULAR FILTRATION governed by glomerular capillary pressure and autoregulation
- TUBULAR REABSORPTION facilitated by carrier mediated transport systems and utilisation of Tm
* Tm = capacity d/t saturation. Exceeded = substrate enters urine - ACTIVE SECRETION of protein-bound substances from the peritubular caps to the proximal tubule. Via Tm-limited carriers.
List the three basic renal processes.
- FILTRATION which forms @ glomerular capillaries to produce protein-free filtrate of plasma
- REABSORPTION regaining substances body needs while excreting substances body doesnt need or via active secretion
- TUBULAR SECRETION substances from PERITUBULAR CAP. TO TUBULE LUMEN providing 2º route into tubule
Explain why normally only filtration occurs at the glomerular capillaries.
Due to Pglom.cap.»_space; π
Pressure here is higher as the AFFERENT ARTEIROLE is short and wide = little resistance to flow = blood has high hydrostatic pressure
+ narrow efferent arterioles = HIGH POST CAPILLARY RESISTANCE exceeds oncotic. pressure (π)
*autoregulation effective over a range of 60-130mmHg
if P falls = dilatation and vice versa
*autoregulation is intrinsic and independent of hormones and nerves
Explain why normally only reabsorption occurs at the peritubular capillaries.
Within the efferent arteriole, resistance is offered along its entire length, there is a large P drop so that hydrostatic pressure is very low, ie PPC 15mmHg thus FACILITATING REABSORPTION INTO THE NEPHRON with ONCOTIC FORCES FAVOURED (π)
π is high d/t remaining proteins plus large volume lost as well
List some of the factors which can influence glomerular filtration.
Pgc dependent on arteriolar diameters (aff. and eff) subject to:
- SYMPATHETIC VC NERVES = constriction, greater sens of afferent
- CIRCULATING CATECHOLAMINES = afferent primarily constricted
- Angiotensin II = constriction of efferent at [low], both at [high]
Explain what is meant by the renal plasma threshold for glucose.
= 10mmoles/l (glucose)
Threshold is when SATURATION OCCURS, and where Tm occurs when looking at transport rate.
- governed by limited number of carriers
- Tm is set high to ensure optimum reabs. in non diabetic [glucose]
Explain the significance of the active reabsorption of Na+ ions at the proximal tubule.
Majority of reabs occurs in PROXIMAL TUBULE via ACTIVE TRANSPORT (not by Tm) thereby creating a ▲Na+ across tubule wall
passive from lumen driven by active transport:
tubule (high) | epithelial (low) | ISF (high)
proximal tubule membrane unique numerous microvilli allow the permeability of sodium ions.
*Cl- follow ▲elec. = H20 follows, out of the tubule
= thereby concentrating the substances left in the tubule
Describe the way in which K+ ions are handled by the kidney.
Thanks to the active transport of Na+ and the osmotic consequences, ⇧[K] (tub. lumen) facilitating passive solute diffusion.
Describe the essential features of the loops of Henle which enable them to act as countercurrent multipliers.
ASCNEDING LIMB actively co-transports Na+ and Cl- OUT OF TUBULE into ISF but is IMPERMEABLE TO H20 = diluting filtrate
meanwhile
DESCENDING LIMB is freely permeable to H20 but impermeable to NaCl = H20 moves out (remember LOOP) to equate osmolarity
H20 moves to interstitium and draws NaCl further in (ascending)
H20 is then reabs into the vasa recta
1) concentration increases down descending and bends
2) concentrated fluid delivered to ascending
3) concentration decreases upon ascent
200mOsm difference between ascending and interstitium
Explain the crucial importance of maintaining K+ homeostasis.
K+ is a MAJOR CATION = ECF[K+] = ~4mmols/l
⇧5.5mm = hyperkalaemia = ventricular fib.
⇩3.5mm = hypokalaemia = hyperpolarisation = cardiac arrythmias
After filtered, K+ reabs @ proximal tubule
+K+ secretion regulated by ALDOSTERONE
⇧K+ excretion induces negative feedback on aldosterone
Significance of Tm
Tm is used to regulate certain substances
when set low = achieve early saturation = excretion thus ensuring plasma regulation
Significance of proximal tubule and urea
only moderately permeable to urea therefore only around 50% reabs = remainder stay in the tubule
+tubule is impermeable to inulin and mannitol
Passive Na transport across the tubule
SGLT cotransporter (Tm) facilitates transport if [Na] high. and where [Glc] low.
GLUT protein and NaKATPase on basolateral membrane
Tubule relationship with drugs and pollutants
Naturally non-polar thus easily reabsorbed alongside osmotic forces
BUT
They become polar compounds and massively reducing permeability = excretion
Action of FRUSEMIDE on LoH
Inhibit the active transport of NaCl @ ascending LoH preventing horizontal osmol. gr.
= 300mOsm. everywhere ensuring isotonic concentrations of urine in Patients.
Significance of the countercurrent multiplier
Establishes horizontal gradient allowing concentration and eventual redilution of fluid
+~20% initial filtrate loss
+fluid entering distal tubule more dilute (from 300mOsm to 100mOsm)
= concentrating of medullary interstitium
= hypotonic fluid to distal convoluted tubule
Significance of the Vasa Recta
Peritubular capillaries of the juxtamedullary nephrons act as countercurrent exchangers.
Hairpin arrangement prevents carrying away NaCl and consequently abolishing the horizontal gr.
instead equilibrates solutes but doesn’t draw water
1) provide O2 for medulla
2) removes volume from interstitium
ADH & its Secretion
1º by plasma osmolarity = ⇧when osmotic pressure = ⇧ADH-secreting neurone discharge rate
therefore ⇧ADH release from posterior pit.
Osmoreceptors; neuronal discharge in the ant. hypo. and detect changes in cell stretch (d/t h20 loss/gain)
osmolarity changes induce vast increases/decreases in ADH = high gain system and very sensitive
2º ECF VOLUME affects ADH secretion
ADH Action @ Tubule
Binds to membrane receptor
actives cAMP
Cell inserts AQP2 water pores in apical membrane
Ensuring water absorbed by osmosis in the blood
= ⇧permeability(H2O) @collecting duct
ADH effect on urine
insertion of aquaporin in CD = permeable to water
ADH(+) = production of concentrated urine
ADH(++) = small volume of highly conc. urine via equilibration at each level
*observed in water deficit and retention
ADH(-) = impermeable to H2O thus LARGE VOL OF DILUTE URINE compensating for H2O excess.
d/t impermeability of H20 down the CD, remains hypotonic
Role of urea
with ADH(+), urea is concentrated along the CD and then moves out down the conc. gr towards the medullary tip and REABS.
amplified in ADH(++) and urea moves out from CD into interstitiium reinforcing interstitial gr. in thin LoH
= uraemia occurs (⇧urea => goes to vasa recta)
ECF volume effects on ADH + pressure receptors significance
⇧ECF vol = ⇩[ADH] and vice versa
- low pressure R located in atria and great veins = detect circulatory ‘fullness’
- high pressure R located in carotid and aortic arch baroreceptors
- haemorrhage
- volume expansion
Other stimuli affecting ADH
(+): pain, emotion, stress, exercise, nicotine, morphine
*
*truamatic sx inductes ADH secretion thus H2O intake to be monitored
(-) alcohol suppresses ADH
DIABETES INSIPIDUS
ADH deficiency d/t hypothalamic areas compromise = CENTRAL DIABETES INSIPIDUS
or CD insensitive to ADH = PERIPHERAL D. INSIPIDUS
*often 2º to hypercalcaemia or hypokalaemia so resolves when ions corrected
> ADH Tx
