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Flashcards

Week 3

Dolu Falowo Foundations 3 English 28 cards

Cards in this deck (28)

  1. 1What is the key function of the thick ascending limb?To create a hyperosmolar interstitial space in the medulla to drive water loss from the descending limb and cortical collecting duct
  2. 2Describe the permeability of the descending limbPermeable to water which leaves filtrate due to osmotic force
  3. 3Describe the permeability of the thick ascending limb-Many tight junctions, no paracellular movement of water
    -Uses NKCC2 cotransporter to move Na+/K+/2Cl- out of the filtrate on the apical membrane. Electrically neutral channel
    -K+ leaks into the filtrate via leak channels. K+ recyling is needed to maintain cotransporter function as [Na+]>[k+]
  4. 4What is furosemide? Uses? Side effects?-Diuretic acting on ascending loop of Henle
    -Blocks NKCC2 cotransporter, allowing 20% of filter Na+ to be excreted
    -Leads to natriuresis and diuresis
    -Used: cardiac/renal failure
    -S/e: hypokalaemia leading to cardiac dysrhythmias (when used with digoxin), hypovolaemia, mild metabolic alkalosis, loss of Mg2+/Ca2+
  5. 5Describe the osmolality countercurrent system-In the loop of Henle, the descending and ascending limbs lie next to each other
    -Na+ and Cl- are pumped out of the thick ascending limb, increasing osmolality in the medulla
    -Water leaves the ascending limb due to the solute in the medulla
    -Osmolality increases down the descending limb and decreases up the thick ascending limb
  6. 6Describe Na+ absorption in the distal tubuleThere is a cotransporter for Na+/Cl- on the apical membrane to move Na+ out of the filtrate
  7. 7What is tiazides/thiazide-like drugs? Uses/side-effects?-Diuretics which act on the distal tubule
    -Blocks Na+/Cl- cotransporters
    -Uses: antihypertensive (decreases circulationg volume). Used with furosemide
    -S/e: increased uric acid, hyperglycaemia, hyponataemia
  8. 8Describe Na+, K+ and water transport in the collecting ducts-Na+ is reabsorbed via ENaCs
    -K+ is excreted via leak channels
    -Water leaves the filtrate via AQP2 (variable expression)
  9. 9What is spironolactone? Uses? S/e?-Diuretic acting on collecting ducts
    -Blocks effects of aldosterone (prevents Na+ reabsorption and K+ excretion)
    -Uses: heart failure
    -S/e: menstual disorders, testicular atrophy, hyperkalaemia
    Furosemide is normally combined with spironolactone to cancel out K+ effects
  10. 10What is eplerenone?More specific mineralocorticoid inhibitor with fewer s/es but more expensive
  11. 11Describe urea cycling-In the collecting duct, urea diffuses out via UT-A1 channels (increased by ADH)
    -Urea increases osmotic pressure in the medulla + aids water reabsorption from descending limb
    -Urea re-enters the descending limb via UT-A2 channels
  12. 12What is ADH?-Synthesised in the hypothalamus
    -Released from posterior pituitary from hypothalamic neurones
    -Acts in distal tubule/collecting duct to increase AQP2
  13. 13How does ADH regulate AQP2 levels?1) ADH binds to V2 receptors on the basolateral membrane (a GPCR)
    2) This initiates Gs, producing cAMP
    3) SHORT TERM: PKA is produced, leading to insertion of vesicles containing AQP2 onto the apical membrane
    4) LONG TERM: On the nucleus, there is positive transcription, leading to more AQP2 synthesis to be put into vesicles for future use
  14. 14Describe the effect of osmolality and flow rate in the nephron with no ADH-Dilute urine is produced so low osmolality in the distal tubule
    -The collecting ducts/distal tubule have a low permeability to water due to no AQP2
    -Urea remains high in urine
    -Flow is increased, as little water is absorbed
  15. 15Describe the effect of osmolality and flow rate in the nephron with max. ADH-Osmolality is increased in the distal tubule as AQP2 is inserted
    -Concentrated urine is produced
    -Increased urea reabsorption (increasing osmolality in the medulla)
    -Flow is reduced
  16. 16How does ADH affect urea transport?Urea transporter UT-A1 is regulated by ADH in the same way as AQP2
  17. 17How do cells in the medulla survive high osmolalities?They accumulate a range or organic osmolytes
  18. 18What is diabetes inspipdus? 2 types?Central: loss of ADH secretion
    Nephrogenic: loss of sensitivity to ADH (ie. problem with V2 receptors)
    -Polyuria (low osmolality), dehydration, hypovolaemia -> causes polydipsia
    -Can become hypernatraemic
  19. 19Describe central diabetes inspidusCauses: head injury, tumours, infection
    -Give desmopressin: ADH analogue (not ADH- short half life)
    -Thiazide diuretics: protects against hypernatraemia, encourages proximal tubule water reabsorption, increase in AQP
  20. 20Describe nephrogenic diabetes insipidus-Less common
    -Causes: toxicity (lithium), hypercalcaemia, mutations in V2/AQP2
    -Do NOT treat with desmopressin (insensitive to ADH anyway)
    -Treat: thiazaide diuretic, low salt diet
  21. 21Describe SIADH (syndromes in inappropriate ADH)-Excess ADH
    -Related to head injury
    -Produces concentrated urine
    -Hyponatraemic (body retains water)
    -Treatment: fluid restriction, urea- extra ends in urine drawing water with it. Acts as an osmotic diuretic)
  22. 22What is the vasa recta?-Efferent arterioles from the glomeruli that run into portal vessels. They plunge from the cortex deep into the medulla
    -Take water and solvents from the interstitial space after absorption by the tubules/vice versa
  23. 23What are the 2 mechanisms for autoregulation of renal blood flow?-Myogenic response
    -Tubuloglomerular reflex
    Does not need external control eg. hormones/impulses
  24. 24Describe the myogenic response-Above normal b.p. renal blood flow is constant
    -In hypotension, renal blood flow is not corrected leading to renal failure
    -An increase in perfusion pressure causes vasoconstriction, increasing resistance and reducing flow rate
    -Only a small change in afferent arterial diameter is needed to correct a change in pressure
    -Purpose is to correct glomerulus from hypertension
  25. 25Describe tubuloglomerular feedback1) High single nephron GFR
    2) High delivery of Na+ to distal tubule
    3) High activity of NKCC2
    4) Macula densa cells sense high Na+ and release ATP
    5) ATP is broken down into adenosine, causing vasoconstriction of afferent arterioles
    6) GFR falls
  26. 26Describe renal innervation-Dense plexus innervating renal vasculature
    -Efferent nerves: sympathetic, releasing noradrenaline to cause vasoconstriction (ie. in hypotension)
    -Afferent neurones: sensory nerves
  27. 27Equation for calculating GFR?GFR= (urine flow rate x conc of creatinine in urine) / conc. of creatinine in plasma
  28. 28Equation for calculating renal blood flow?RBF: (urine flow rate x conc of PAH in urine) / conc. of creatinine in PAH

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Renal tubular function 2 Urine concentration and dilution Renal blood supply
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Dolu Falowo
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