lecture 4

Question 1

function of kidney

Answer 1

central regulator of homeostasis; we take in more than we need to replace that which we have ‘used up’ - kidney regulates

Question 2

purpose of filtration

Answer 2

no pumps for excess H2O or urea; production of urine through glomerular filtration but can’t afford to lose all of water and small molecules that pass through filter

Question 3

why control reabsorption and secretion

Answer 3

take in more salt and water than needed; reabsorb 99% ultrafiltrate; maintain solute balance, plasma concentration and pH

Question 4

define osmolarity

Answer 4

measure of osmotic pressure exerted by solution across perfect semi-permeable membrane; all concentrations of different solutes (mmol/l) added together - each ion counted separately

Question 5

what is osmolarity dependent on

Answer 5

number of particles in solution, not nature of particles

Question 6

normal plasma osmolarity vs urine osmolarity

Answer 6

285-295 mosmol/l for plasma (controlled), 50-1200 mosmol/l for urine (changes massively)

Question 7

effect on water movement if solute present at equal concentrations either side of semi-permeable membrane

Answer 7

no net effect

Question 8

transcellular vs paracellular

Answer 8

depends on how tight junctions are

Question 9

passive movement

Answer 9

protein independent transport (lipophilic) - linear, protein dependent transport (hydrophilic) - limited by number of protein channels available

Question 10

active movement

Answer 10

primary: dependent on amount of ATP; secondary: dependent on amount of primary ATP

Question 11

water transport

Answer 11

low to high osmolarity through aquaporins or tight junctions

Question 12

increase rate of passive uptake system

Answer 12

store channel proteins in vesicles and place in membrane

Question 13

protein reabsorption

Answer 13

endocytosis of protein and receptor; drop pH in endosome, protein dissociates from receptor which goes back to membrane

Question 14

transport maxima

Answer 14

doesn’t apply to individual cells (whole system); can vary dependent on circumstances - at high specific solute concentrations can’t absorb any more - maximum (Tm); Tm basal and stimulated (e.g. glucose - becomes present in urine; diabetes mellitus; also vitamins B and C)

Question 15

secretion opposite to reabsorption

Answer 15

H+, K+, choline, creatine, penicillin, other drugs secreted

Question 16

non-uniform reabsorption of Na+

Answer 16

most in proximal tubule, then loop of Henle (generate high concentrations of urine when conserving water), then distal convoluted tubule; variable amount in collecting duct (regulated most tightly by aldosterone and ADH)

Question 17

proximal convoluted tubule

Answer 17

dense brush border, mitochondria for Na+ reabsorption, large SA

Question 18

thin descending limb of loop of Henle

Answer 18

fewer mitochondria, loose tight junctions (reabsorb water)

Question 19

thick ascending limb of loop of Henle

Answer 19

lots of mitochondria for Na+ reabsorption

Question 20

distal convoluted tubule

Answer 20

less mitochondria than thick ascending limb of loop of Henle

Question 21

collecting duct

Answer 21

some mitochondria

Question 22

proximal convoluted tubule basolateral membrane

Answer 22

constant Na+ exchange out of cell for K+ to maintain resting potential - requires energy (primary)

Question 23

early proximal tubule

Answer 23

Na+ co-transported in apical membrane with glucose and amino acids (secondary), glucose and amino acids move out basolateral; Na+ entry down large electrochemical gradient can bring about uphill entry of glucose and amino acids and exit of H+

Question 24

early proximal tubule

Answer 24

Na+ in, H+ out - binds to HCO3- and water diffuses in by osmosis (regeneration of H+ in cell); carbonic anhydrase activity leads to Na+ reabsorption and increased urinary acidity

Question 25

passive reabsorption

Answer 25

urea, water

Question 26

active reapsorption

Answer 26

glucose, amino acids, Na+, K+, Ca2+, vit C, uric acid

Question 27

net secretion by proximal convoluted tubule

Answer 27

route of excretion for some substances, some drugs enter tubular gluid here and act further down nephron

Question 28

descending limb of loop of Henle

Answer 28

loose tight junctions so water reabsorbed, draws in Na+ and K+, squamous epithelium with few mitochondria

Question 29

ascending limb

Answer 29

cuboidal epithelium, few microvilli, many mitochondria; Cl- actively reabsorbed with Na+ passive reabsorption with it, HCO3- reabsorbed, impermeable to water as tight tight junctions; hypo-osmolar fluid leaves loop of Henle; loop diuretics block Na+/K+/Cl- cotransporter

Question 30

distal convoluted tubule

Answer 30

proximal: cuboidal epithelium, few microvilli; complex lateral membrane with interdigitations with Na+ pumps; if block lumen membrane Na+/Cl-, more Na+ in from blood so more Ca2+ out, so more Ca2+ absorbed from lumen - increase plasma Ca2+ (thiazides drug); numerous large mitochondria; Na+ and Cl- cotransporter linked to Ca2+ reabsorption; specialisation at macula densa in glomerulus (near distal convoluted tubule) detects changes in [Na+] of filtrate

Question 31

distal convoluted tubule: distal

Answer 31

sodium reabsorbed dependent on aldosterone

Question 32

collecting duct

Answer 32

sodium reabsorbed dependent on aldosterone, adjustment of Na+, K+, H+, NH4+; water reabsorbed under ADH control; impermeable to water without ADH; tight junctions so very little paracellular transport

Question 33

principal cell

Answer 33

important in Na+, K+ and water balance mediated by Na+/K+ pump

Question 34

intercalated cell

Answer 34

important in acid-base balance (mediate via H-ATP pump)

Question 35

single gene defects: renal tubular acidosis

Answer 35

hypercholermic metabolic acidosis, impaired growth, hypokalemia; not secreting H+; occurs distally or in early proximal; failure to reabsorb filtered HCO3- from urine; leading to urinary wastage of HCO3- and acidaemia (low blood pH)

Question 36

single gene defects: Bartter syndrome

Answer 36

mutation in ascending loop of Henle; excessive electrolyte secretion due to mutation in Na+/Cl-/K+ transporter in apical membrane, antenatal: premature birth, polyhyramnios; severe salt loss, moderate metabolic alkalosis; hypokalemia; hyponatraemia; renin and aldosterone hypersecretion

Question 37

single gene defects: Fanconi syndrome

Answer 37

increased excretion of uric acid, glucose, phosphate, bicarbonate; proximal tubules; increased excretion of low molecular wieght proteins
associated with renal tubular acidosis type 1 (Dent’s disease): CIC-5 mutation: drop pH in endosome as H+ out, Cl- in so increases electrochemical gradient so more H+ in separately - impaired in proximal tubule so receptor can’t dissociate as pH too low - lack of absorption as endosome required