Renal Flashcards
1
Q
How does the kidney handle potassium? What other major ions are involved in potassium transport in the nephron? How do hydrogen ions influence potassium transport in the nephron?
A
- K is filtered, reabsorbed and secreted in the kidneys
- Freely filtered in the glomerulus (600meq/day)
- Reabsorbed in the PCT (65%), ascending LOH Na-K-2Cl co-transporters (25%) and CD
- Secreted at the DCT and CD with rate of secretion proportional to flow of tubular fluid and under influence of aldosterone
- High K, less reabsorbed and more secreted -> Net effect is increased excretion of K - Ions involved in K transport
- Na+ via the Na/K ATPase, Na-K-2Cl co-transporter
- H+ via the H-K ATPase - K transport is coupled to H
- High H+ concentration = Low K secretion due to H-K ATPase pump
2
Q
What factors influence K secretion?
A
- Rate of secretion of K proportional to rate of flow of tubular fluid through distal nephron
- Increase flow = increase K secreted - H+ ions affect K secretion as H and K is coupled through H-K ATPase
- In acidosis with high H+ concentration, less K+ secreted - Influence of aldosterone
- Aldosterone promotes Na reabsorption and K secretion - Na delivery to collecting ducts
- Increase Na = Increase K secretion - K reabsorption at proximal tubules
- Less K reabsorbed at PCT = more K secreted to be excreted
3
Q
Describe how ADH/Vasopressin acts on the kidney. What factors influence ADH secretion? What hormonal changes are evident after drinking a large amount of water?
A
- ADH is secreted by the posterior pituitary in response to increase osmolality and reduce hydrostatic pressure
- Acts on G-protein receptor in kidneys
- Activates adenyl cyclase to produce cAMP
- Acts on V2 receptors
- Triggers insertion of Aquaporins 2 into collecting ducts of kidney
- Increases water permeability and reabsorption
- Reduce osmolality and increase hydrostatic pressure
- Also acts on V1 receptors -> causes vasoconstriction - Factors influencing ADH secretion
- Increase ADH: High osmolality (osmoreceptors), low hydrostatic pressure (baroreceptors), Angiotensin II, N+V, pain, stress, exercise, drugs (carbamazepine)
- Reduce ADH: Low osmolality (osmoreceptors), high hydrostatic pressure (baroreceptors), ETOH - Drinking large amount of water reduces plasma osomolality (osmoreceptors) and increases hydrostatic pressure (baroreceptors)
- Changes evident after 15 mins of water ingestion
- Reduce ADH secretion -> diuretic effect -> excrete water -> reduce plasma osmolality
- Inhibits renin-angiotensin stimulation
4
Q
What is thirst and what causes it?
A
- Thirst is an appetite controlled by hypothalamus and triggered by
- Increased osmolality -> sensed by osmoreceptors -> triggers thirst -> increase H20 consumption -> reduce plasma osmolality
- Hypovolaemia/reduce hydrostatic pressure -> sensed by baroreceptors and renin-angiotensin system
- Psychogenic
- Dry mucus membranes
- Prandial -> Habit or learned response
5
Q
What is the definition of glomerular filtration rate? What is the normal GFR? List some factors that affect the GFR. What substances act on the mesangial cells to change GFR? What are mesangial cells?
A
- Glomeruli filtration rate is
- Amount of fluid filtered by kidney at the glomerulus PER UNIT TIME - Normal GFR = 125mls/min
- Factors affecting GFR follows Starling’s law
- Difference in hydrostatic pressure
- Difference in oncotic pressure
- Permeability and thickness of glomerulus capillaries
- Surface area mediated by mesangial cells
- Intrarenal interstitial pressure -> Altered in obstruction, ureteric edema
- Systemic BP
- Age - Substances acting on mesangial cells to
- Increase GFR: ANP, Dopamine, cAMP
- Reduce GFR: NA, vasopressin, Angiotensin II - Mesangial cells are
- Contractile cells that help to regulate GFR
- Located in glomerulus
6.
6
Q
Describe the neurological pathways involved in normal micturition. Describe the muscles involved in micturition. What prevents vesico-ureteric reflux?
A
- Neurological pathways in micturition
- Innervated by sacral spinal nerve roots (S2 - S4)
- Facilitated and inhibited by higher neural centres
- Can be voluntarily controlled until maximum volume reached
- First urge to void at 150mls, marked fullness at 400mls
- Volume distends stretch receptors in bladder
- Sends signal up spinal afferent fibres
- Signal travels down parasympathetic efferent fibres
- Triggers contraction of detrussor muscle
- Voluntary control of external urethral sphincter via pudendal nerves
- Voluntary control of perineal muscle which relaxes for micturition
- No sympathetic fibres input - Muscles involved in micturition
- Bladder has smooth muscles -> Detrussor muscles, circular, longitudinal muscles
- External ureteric sphincter -> Relaxes for micturition
- Perineal muscles -> Relaxes for micturition
- Abdominal muscles -> Contracts for micturition
- Bulbocavernous muscle -> Contracts in males for micturition - Vesico-ureteric reflux
- Prevented by oblique insertion of ureter into posterior bladder wall
7
Q
How does the countercurrant mechanism enable the kidney to concentrate urine? What is the role of urea in the countercurrant mechanism? How does urea reach the interstitium?
A
- Countercurrant mechanism is the increasing gradient of osmolality in the medullary pyramids
- Produced by counter-currant multipliers -> LOH -> Water diffuses out of descending LOH (Aquaporin) and NaCl diffuses out of ascending LOH (Na-K-Cl CT)
- Maintained by counter-currant exchanges -> Vasa recta -> Water diffuses into ascending vessel and NaCl diffuses into descending vessel
- Water bypasses the system
- NaCl is maintained in the medullary pyramids
- Urea also helps maintain the osmolality - Urea contributes to the osmolality gradient in medullary pyramids
- Urea moves out into the interstitium by
- Facilitated diffusion by urea transporters
