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Physiology and Pharmacology > Gene Models and Nephron Function 1 - 3 > Flashcards

Gene Models and Nephron Function 1 - 3 Flashcards

1
Q

urine pathway

A

blood in through afferent arteriole
into glomerular capillaries
glomerular filtration - % of plasma moved from capillary into bowmanns capsule, whatever isnt leaves via efferent arteriole then into peritubular capillaries and into venous blood
ultrafiltrate moves through nephron and secretes urine

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2
Q

filtration

A 
glomerulus
125ml/min
filters plasma
180L/day
permits - H2O and small mol
restricts - blood cells and proteins
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3
Q

ultrafilrate consists of…

A

protein free plasma

1% filtered protein (albumin), reabsorbed by proximal tubule, doesnt appear in urine

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4
Q

tubular transport

A

apical = lumen of tubule
basolateral = peritubular capillary
transcellular reab - apical to baso, using specific transport proteins
transcellular secretion - baso to apical, lost in urine
paracellular secretion or reab - between cells, tight junctions, lets ion, solutes and water through

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5
Q

genes and transport

A

human genome = 33,000 genes
several hundred renal genes
knockout and transgenic mouse models
inherited renal disease symptoms

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6
Q

proximal tubule

A

protein free ultrafiltrate
bulk reab - 70% filtrate
contains lots of mitochondria - needs ATP to reabsorb

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7
Q

proximal tubule ion channels

basolateral membrane

A

Na/K ATPase - primary transport protein, hydrolyses ATP to move 3Na out and 2K in, also keeps intra cell [Na] low, so high extra cell and creates gradient
K channel - sets up driving force for Na uptake at apical mem, key for setting -ve mem pot

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8
Q

proximal tubule ion channels

apical membrane

A

SGLT1/2 - Na/glucose proteins, brings Na into cell, creates electrochemical driving force, uses Na to also bring in glucose which will leave at basolateral
NaPi2 - NA/phos transporter, uses Na to bring phos too, important role in ability to retain phosphate for bone formation etc

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9
Q

NaPi2 knockout

A

mouse cant make protein for transporter
lose ability to reab across apical mem
= less Pi reab
= more loss in urine
= issues in renal mineralisation
= cant maintain normal plasma phosphate level
= precipitates with calcium = kidney stones

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10
Q

proximal tubule

bicarbonate reabsorption

A

NHE3 - Na/H exchanger on apical mem, as Na enters, H leaves and binds with HCO3 to form H2CO3
carbonic anhydrase sits on apical membrane on extra cell surface causing H2CO3 to dissociate into CO2 and H2O
CO2 is freely permeable and diffuses down conc grad into cell
H2O moves in via aquaporins, down gradient
H2CO3 in cell dissociates, HCO3 and Na leave via Na/bicarb transporter on baso mem
critical in regulating plasma pH

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11
Q

renal NHE3 knockout

A

cant secrete H so cant reab HCO3
= acidosis
inhbiition of H secretion = inhibits Na and HCO3 transport = fall in fluid reab = drop in plasma HCO3 = pHfalls due to HCO3 compensation

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12
Q

trasnport maximum of glucose

A

substances reab via membrane carriers e.g. glucose and amino acids
inc plasma glucose = inc rate of filtration - glucose is freely filtered
up to renal threshold, everything filtered is reabsorbed = nothing in urine
then reaches transport maximum Tm (375mg/min) = all proteins are busy
after this you begin to see glucose in urine - important threshold for diabetes

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13
Q

secretion by proximal tubule - 2 systems

A

organic cations/anions
rapid removal
removal of plasma protein bound substances
foreign compounds e.g. penicillin - need much higher dose than you think

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14
Q

loop of henle

A 
concentrates urine
reabs Na, Cl, Mg, Ca and water
site of action for loop diruetics
thin descending limb - water out
thin ascending limb - Na and Cl out
thick ascending limb - Na and Cl out
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15
Q

thick ascending limb

A

Na/K ATPase and K channels - same as proximal tubule = setting -ve mem pot and low intracell Na sets driving force for Na influx at apical mem
Na, K and 2 x Cl co transport protein on baso mem uses electrical driving force for influx of Na to bring in 2 x Cl and K, Na leaves via ATPase, Cl accumulates in cell
allows Cl to move down gradient and leave cell, net reab Na/Cl creates driving force for transport of H2O in other segments - sets up osmotic gradient
protein classed as beta subunit (accessory) - regulates a transport protein, CLCK (in baso) only works when barttin is present
recycles K coming in, outer medullary potassium helps set -ve mem pot on apical mem and allows K to recycle - essential for normal function of thick ascending limb
if K levels in tubular fluid arent high enough, NKCC2 wont work
absorption of Na/Cl drives absorption of Ca/Mg - paracellular transport

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16
Q

Bartters syndrome

A

genetic inheritance, reccessive, loss of function mutations: NKCC2 mutation = no NaCl reab
salt wasting - losing too much Na/Cl in urine
polyuria = inc urine flow rate - H2O follows Nacl
dec in ECF vol = hypotension (low BP)
hypokalemia = low K in plasma
metabolic alkalosis = inc pH, too alkaline
hypercalciuria = too much Ca in urine
nephrocalcinosis = kidney stones
Cl cant leave through CLCK, if [cl] too high in cell, it stops NKCC2 from transporting: no NaCl reab
Barttin = CLCK cant work
ROMK = stops K recycling so tubular fluid K too low, cant support function of NKCC2

17
Q

ROMK knockout

A

fractional excretion (FE) = amount in urine/amount filtered
100% = all filtered - excreted
<100% = some reab
>100% = some secreted
compare wildtype to knockout, differences in FE = tubular defect

18
Q

loop diuretics

A

furosemide - inhibit NKCC2 so inhibit NaCl reab - lose in urine, so inhibits H20 reab
bumetanide - used for excess ECF vol = higher urine flow rate
treats high bp
side effects - Bartters like symptoms e.g. plasma K, pH, Ca
barters protection

19
Q

early distal tubule

A 
reab Na, Cl
reab Mg
sensitive to thiazide diuretics
NCC in apical mem - Na, Cl, co transport protein
Mg loss pathway unknown
20
Q

Gitelmans syndrome

A 
inherited, recessive
salt wasting and polyuria
hypotension
hypokalaemia 
metabolic alkalosis
hypocalciuria - very litte Ca in urine
mutation in NCC = loss of func, no Na Cl reab = salt wasting, hypotension
21
Q

mouse mutations and transport

A

xenopus oocyte studies
inject RNA of protein were interested in
oocyte processes it as normal
if a transport protein - it moves it to membrane = can do functional analysis
put radioactive Na outside oocyte, see how much ends up inside

22
Q

thiazide diuretics

A

early distal tubule
block NaCL co transport protein
treats inc bp
side effects = gitelmans like symptoms

23
Q

protection from hypertension

A

mutation in ROMK/NCC - gitelmans

mutation in NKCC2 - bartters

24
Q

late distal

A

links to connecting tubules (links late distal to cortical) ——> cortical collecting ducts

  • conc of urine
  • reab Na and H2O
  • secretion of K and H
25
Q

late distal and cortical collecting ducts cell types

A

2 mixed types
principle - Na/H2O reab, K and H2O secretion
intercalated - alpha IC and beta IC - dynamic, shifts depending on body needs, H secretion and reab, HCO3 reab and secretion

26
Q

principle cells

apical

A

ENaC - regulates Na absorption, epithelium channel
ROMK - K lost in urine - hypokalemia
aquaporin 2 - rate limiting step, water channel, H20 goes down osmotic gradient

27
Q

principle cells

baso membrane

A

Kir2.3 - driving force for Na influx with Na/K pump
AQP3/4 - constiutively active
inc Na in cell = inc H secreted = high pH

28
Q

dieseases with principle cells

A

diabetes insipidus - AQP2 issues, cant reab H2O = lost in urine
liddles syndrome - ENaC mutation = hypertension
pseudohypoaldosteronism - aldosterone = hormone

29
Q

amiloride

A

potassium sparing diuretic, agonist of ENaC - blocks net reab of Na = blocks reab H2O = loss of gradient so K doesnt leave cell into urine

  • inc urine production
  • treatment for hypertension
30
Q

alpha intercalated cells

A 
apical = proton pump, H secreted to urine
baso = AE1 - HCO3, Cl exchanger (anion exchanger 1)
31
Q

beta intercalated cells

A

flipped version on alpha
apical = AE1, anions secrete into tubular fluid and lost in urine
baso = proton pump for reab of H, Cl channel for net reab of Cl

32
Q

medullary collecting duct

A

low Na permability

high H2O and urea permeability in presence of vasopressin

33
Q

acute renal failure

A 
reversible 
fall in GFR over hrs/days
causes = pre renal, renal and post renal
impaired fliud and electrolyte homeostasis 
accumulation of nitrogenous waste
lasts 1 week
treatment = dialysis
34
Q

general symptoms of acute renal failure

A

hypervolaemia - low ECF vol, oliguria due to low GFR
hyperkalemia - lack of K secretion
cardiac excitability - sits closer to threshold of action potential
acidosis - H accumulation as not lost in urine, depression of CNS
high urea/creatinine - impaired mental function, nausea

35
Q

oliguria

A

fall in GFR

e.g. car accident - crushed muscles = intracell contents released = K higher in cell = released due to pressure change

36
Q

oliguria

pre renal

A

perfusion

poor renal perfusion due to hypotension

37
Q

oliguria

renal cause

A

rhabdomyolysis (release of myoglobin from damaged muscle) - toxic effect on tubules
high K - lack secretion and release from damaged cells - tachycardia
low HCO3 = acidosis

38
Q

treatment of oliguria

A

IV saline - dilutes K in plasma - treats hyperkalemia
HCO3 - bring level to normal
dialysis if oliguria persists

Physiology and Pharmacology (17 decks)

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