Fichas
Week 3
Fichas del conjunto (28)
- 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
- 2Describe the permeability of the descending limbPermeable to water which leaves filtrate due to osmotic force
- 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+] - 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+ - 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 - 6Describe Na+ absorption in the distal tubuleThere is a cotransporter for Na+/Cl- on the apical membrane to move Na+ out of the filtrate
- 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 - 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) - 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 - 10What is eplerenone?More specific mineralocorticoid inhibitor with fewer s/es but more expensive
- 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 - 12What is ADH?-Synthesised in the hypothalamus
-Released from posterior pituitary from hypothalamic neurones
-Acts in distal tubule/collecting duct to increase AQP2 - 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 - 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 - 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 - 16How does ADH affect urea transport?Urea transporter UT-A1 is regulated by ADH in the same way as AQP2
- 17How do cells in the medulla survive high osmolalities?They accumulate a range or organic osmolytes
- 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 - 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 - 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 - 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) - 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 - 23What are the 2 mechanisms for autoregulation of renal blood flow?-Myogenic response
-Tubuloglomerular reflex
Does not need external control eg. hormones/impulses - 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 - 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 - 26Describe renal innervation-Dense plexus innervating renal vasculature
-Efferent nerves: sympathetic, releasing noradrenaline to cause vasoconstriction (ie. in hypotension)
-Afferent neurones: sensory nerves - 27Equation for calculating GFR?GFR= (urine flow rate x conc of creatinine in urine) / conc. of creatinine in plasma
- 28Equation for calculating renal blood flow?RBF: (urine flow rate x conc of PAH in urine) / conc. of creatinine in PAH
Información
- Descripción
- Renal tubular function 2 Urine concentration and dilution Renal blood supply
- Creado por
- Dolu Falowo
- Visitas
- 2
- Valoración