Physiology Flashcards
A) Functions of kidney:
- Regulation of water & electrolytes balance
- Regulation of arterial blood pressure (short term: RAAS & long term: Na– H2O excretion)
- Regulation of acid base balance (elimination of acids + regulation of buffer stores)
- Excretion of waste (urea & creatinine) and foreign chemicals (drugs & food additives)
- Endocrine function (erythropoietin → RBCs, activation of vitamin D3, renin secretion)
- Paracrine function (PGs & BK → regulation of RBF)
- Gluconeogenesis
Mechanisms of RBF Autoregulation When BP ↑
Myogenic mechanism:
↑ BP –> stretch of vascular wall —> open stretch gated Ca++ channels —> Ca++influx —> contraction of smooth muscles of afferent arterioles
Tubuologlomerular feedback:
↑ BP —>↑ RBF & GFR —>↑reabsorption of Na & Cl —> ↑ delivery of solutes into macula densa —>macula secretes adenosine –> acts on receptors —> VC of afferent
Mechanism of RBF autoregulation for when BP↓
Myogenic:
↓ BP–> Relaxation of smooth muscles of afferent arterioles
Tubuloglomerular feedback:
↓ BP—> ↓ RBF & GFR—->
↓reabsorption of Na & Cl—-> ↓ delivery of solutes into macula densa —> macula densa: VD of afferent & VC of efferent
Functions of mesangial cells
- Support glomerular capillaries by mesangial matrix.
- Mesangial cells contract —> ↓ filtration surface area.
- Phagocytose immune complex & secretes cytokines.
- Removes debris and aggregated proteins from glomerular membrane.
- Have receptors for vasoactive substances.
Factors affecting GFR
Look at booklet
Give the Na reabsorption in the proximal tubule
65% of filtered Na is reabsorbed in PCT
First half of PCT: Co transport with AA, glucose, phosphate and sulfate, counter transport Na-H counter transporter
Late half of PCT: Na is reabsorbed with Cl passively
Give the Na reabsorption in the Loop of henle
Thin descending limb: Only water reabsorption, No na transporter
Thin ascending limb: No water reabsorption, Na is reabsorbed with Cl passively
Thick ascending limb: 25% of filtered Na is reabsorbed by Co transporter that carries Na, K and Cl. Most K refluxes back into lumen via K channels
Give the Na reabsorption in Distal tubule
Early distal tubule: Na is reabsorbed with Cl by NaCl cotransported
Late distal tubule & collecting duct: Less than 10% of filtered Na is reabsorbed prinicpal cells in exchange with K under aldosterone control.
passive diffusion of Na and K in into principal cells
Regulation of Na excretion
- GFR (glomerulo-tubular balance)
- ↑GFR —>↑ Na and water reabsorption.
- Mechanism: renal tubules reabsorb constant percentage of Na rather than constant amount.
- Importance:
o Prevent overloading of DCT when ↑GFR
o Prevent inappropriate loss of Na or water in - Rate of flow: slow rate —> ↑ Na reabsorption
- ABP.
- Pressure diuresis & natriuresis: ↑ GFR —> ↑ Na & water excretion.
- Mechanism: ↑ ABP —> ↓ Angiotensin II —> ↑ HP in peritubular capillary —-> ↑ HP in renal interstitial fluid —> enhance back leak of Na into tubular lumen –>↓ Na reabsorption & ↑ excretion.
Give the hormonal control for increase of Na reabsorption
Aldosterone: ↑ number of Na+ – K+ ATPase pump in basolateral border.
Glucocorticoids: weak mineralocorticoid activity
Angiotensin II: activate aldosterone secretion, Act directly on PCT stimulate Na —- K ATPase pump
Sex hormone: estrogen
Sympathetic stimulation
- VC of afferent. —> ↓ GFR
- Activate renin —> ↑ RAAS
- Increase Na reabsorption by PCT & thick ascending limb of loop of Henle.
Hormones that decrease Na reabsorption
ANP: increase NaCl excretion. Relaxation of mesangial cells, VD of afferent & VC of Efferent –> increase GFT —> increase Na filtration & reabsorption
PGE2: inhibit Na–K ATPase & Na channels
Endothelin: increase PGE2
Give an account on the obligatory water reabsorption
Proximal tubule: 65% of water is reabsorbed
in proximal tubule by osmosis. Movement of water is facilitated by insertion of aquaporin 1 channels
Loop of Henle:
in descending limb: highly permeable to water by osmosis due to gradual increase in medullary ISF
Early distal tubule & collecting duct: impermeable to water continued dilution of tubular fluid
Give an account on the facultative water reabsorption
In late distal tubule & cortical collecting duct:
↑ADH —-> ↑ number of aquaporin 2 channels —> 8% of filtered water is reabsorbed by osmosis into the interstitium of the cortex.
In medullary duct: 4.7% of filtered water is reabsorbed into medullary hypertonic interstitium —> concentrated urine
Give an account on the mechanism producing hyperosmotic renal medullary interstitium
Countercurrent multiplier system (function of juxtamedullary nephrons of loop of Henle)
Ascending limb:
Thick segment: active reabsorption of solute
Thin segment: passive reabsorption of NaCl
Descending limb: high permeable to water and less permeable to solutes. Water diffuses from descending limb to medullary interstitium by osmosis
Give an account on the mechanism producing hyperosmotic renal medullary interstitium
Countercurrent exchanger system of vasa recta
Descending limb of vasa recta:
Solutes diffuse from medullary ISF into blood along concentration gradient. Water diffuses from blood to ISF
Ascending limb of vasa recta: Solutes diffuse back into medullary ISF along concentration gradient. Water diffuse into vasa recta
Give an account on the mechanism producing hyperosmotic renal medullary interstitium
Contribution of urea
- Urea contributes about 40% of osmolarity of renal medullary ISF.
- At inner medullary CD–> urea moves into medullary ISF —> adding to hyperosmolarity (movement is facilitated by ADH)
- High protein diet –> concentrated urine & vice versa.]
Give an account of the disorders of urine concentration
Diabetes insipidus: polyuria & polydipsia. Polydipsia keeps the patients alive
Syndrome of inappropriate ADH secretion (SIADH)
Water retention –> ECF expansion.
Compare between water diuresis and osmotic diuresis in causes, mechanism, outcome, ADH
Water diuresis: ingestion of large amounts of water. Mechanism: ↑H2O –> ↓ plasma osmolarity –> ↓ ADH —> ↓ facultative reabsorption. Large amount of urine which is very diluted. ADH inhibited
Osmotic diuresis: Large amount of un-reabsorbed solute in tubular fluid.
Mechanism:
a) Un-reabsorbed solutes –> hold water inside tubules –> ↓ obligatory water reabsorption.
b) water retention —>↓ active reabsorption of Na —>↓
Na concentration —> Na retention + ↓ medullary
osmolarity.
Outcome: decrease H2O reabsorption and increase Na
ADH: normal or increased
Give an account on the K handling in renal tubules
K reabsorption: 65% in PCT. In thick ascending limn–> its 25%. In DT and CD it is dependent on K intake
K excretion: By principal cells depending on K intake and aldosterone level. In basolateral border K moves by Na/K ATPase. IN luminal border K moves via electrochemical gradient, K channels, and K–Cl co transporter
Give an account on the glucose reabsorption by renal tubules
All glucose is reabsorbed in early PCT
At luminal border: Glucose transported with NA with SGLT-2. Glucose is carried against concentration gradient
At basolateral border: Glucose is carried along concentration gradient by GLUT-2
Define tubular transport maximum
Tubular transport maximum: maximum amount of actively transported substances that can be reabsorbed per minute
Draw the curve and label each part. Define splay and cause of splay
Splay: is the region of reabsorption curve where reabsorption is reaching saturation but not fully saturated
Heterogeneity of the nephrons
Define Glycosuria and give its causes
Presence of glucose in urine in large amount
Caused by DM and congenital defect in glucose transport
Give the secretion of hydrogen & reabsorption of bicarbonate
Reabsorption of bicarbonate: HCO3- is reabsorbed mainly in PCT (85%), thick ascending loop of Henle (10%) & CD (4.8%). CO2 from blood combines with H2O which from a buffer system
Secretion of hydrogen: H is secreted in all parts of renal tubule except of loop on Henle. In PCT, thick parts of loop on Henle & early DCT–>2ry active transport Na —H counter transport.
