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104 theme 3 > formation of urine > Flashcards

formation of urine Flashcards

1
Q

the process of urine formation

A

glomerulus - filtration of blood
proximal tubule - reabsorption of filtrate, secretion into tubule
loop of henle - concentration of urine
distal tubule - modification of urine
collecting duct - final modification of urine

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2
Q

what is the glomerulus

A

afferent arteriole into network of glomerular capillaries to efferent arterioles (narrower to build pressure)
capsular space
distal tubule loops around to top from loop of henle

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3
Q

force for filtration in glomeruli

A

blood pressure

differing diameter of afferent and efferent arterioles

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4
Q

what is GFR

A

125 mL/min (180 L/day)
=rate at which glomerular filtrate is produced
can be measured clinically and used to indicate renal function

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5
Q

structure of glomeruli

A 
afferent arteriole 
bowman's capsule 
glomerular filtrate out via proximal tubule 
renal corpuscle 
efferent arteriole
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6
Q

what is glomerular filtration

A

first stage of urine formation
ultrafiltration - filtration on a molecular scale
small molecules filtered and large molecules and cells remain in blood

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7
Q

how does glomerular filtration work

A

depends on 2 factors BP and renal blood flow
filtrarte has to pass through
pores in glomerular capillary endothelium
the basement membrane of BC’s (inc contractile mesangial cells)
epithelial cells of BC (podocytes) via filtration slits into capsular space

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8
Q

forces involved in glomerular filtration

A

pressure out= Pgc and PIEbs
pressure in= PIEgc and Pbs
GC- glomerular capillary hydrostatic pressure
BS- bowman’s space oncotic pressure (almost 0)

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9
Q

how to work out filtration pressure

A

(Pgc)-(Pbs+PIEgc)
about 45, 25, 10 mmHg
about 10mmHg overall

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10
Q

how does net filtration pressure change

A

10mmHg to 0
as PIEgc (plasma protein pressure inc from an osmotic pressure of 25 to 35mmHg)
reduced by time blood leaves capillaries

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11
Q

does GFR change with BP

A

remains constant even when systemic BP changes

involves regulatory mechanism known as autoregulation of renal blood flow

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12
Q

what is autoregulation of blood flow

A

renal blood flow subject to autoregulation over a range of BPs (90-200mmHg)
persists in denervated and isolated perfused kidneys so not neuronal or hormonal but a local effect

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13
Q

what are the two hypothesises for autoregulation

A

myogenic - due to response of arterioles to stretch (Starling’s law) egg BP dec so arterioles constrict for constant renal blood flow and GFR
metabolic - renal metabolic modulate afferent and efferent arteriolar contraction and dilation
most likely in combo

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14
Q

how does GFR rely on diameters of afferent and efferent arterioles

A

GFR drop
dilate afferent and constrict efferent
and opposite if inc

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15
Q

what dilates and constricts the afferent arteriole

A

dilate - prostaglandins, ANP, dopamine, NO, kinine

constrict - NA, endothelin, adenosine, ADH

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16
Q

what dilates and constricts the efferent arteriole

A

dilate - adenosine via A2a and 2b Rs, NO)

constrict - Ang II

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17
Q

how can changes in GFR alter systemic blood pressure

A

drop in filtration pressure, causes drop in GFR
lower GFR means less Na+ enters PT
macula densa senses a change in tubular Na+ levels
stimulates juxtaglomerular cells to release renin into blood
ang II
vasoconstriction
inc BP to inc filtration pressure and GFR returns to normal

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18
Q

what is the RAAS

A 
homeostasis disturbed eg dec GFR 
renin release 
angiotensin activated 
elevation of BP and blood vol 
homeostasis restored, inc GFR 
homeostasis, normal GFR
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19
Q

what does the RAAS do

A 
inc sympathetic activity 
tubular Na+ reabsorption 
renal gland release aldosterone 
vasoconstriction
pituitary gland release ADH
also works in brain to inc thirst
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20
Q

what can happen to RAAS in hypertension

A

dysregulated and over activated

drugs

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21
Q

how does reabsorption in proximal tubule occur

A

60-70% filtered water, Na+, HCO3-, Cl-, K+ and urea are reabsorbed from PT
almost complete reabsorption of glucose, AAs, small amount of filtered proteins
driving force Na+/K+

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22
Q

how does Na+/K+ ATPase drive reabsorption

A

pumps Na+ out against gradient
req ATP
3Na+ out and 2K+ (which rapidly diffuses out)
water follows Na+, cotransport with glucose

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23
Q

what does the Na+/K+ ATPase do

A

keeps sodium low in PT cells (<30mM)

Cl- follows Na+ by facilitated diffusion, Phosphate and sulphate also co-transported with Na+

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24
Q

how is water reabsorbed from the PT

A

movement of solutes reduces osmolarity of tubular fluid and inc it in interstitial fluid
net flow from tubule lumen to lateral spaces trans (AQP channels in apical and basolateral surfaces) and para cellularly
not active, follows sodium

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25
Q

what are aquaporins

A

specific water channels located in cell membranes

4 major ones of 13 identified

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26
Q

what are aquaporin 1s

A

abundant distribution in PT

also other parts of tubule where water is reabsorbed (eg desc LOH)

27
Q

what are AQP2s

A

present in CD on apical surface

channel expression controlled by ADH

28
Q

what are AQP3s

A

present on basolateral surface of tubular cells involved in water reabsorption

29
Q

how is glucose reabsorbed from PT

A

high in filtrate
low glucose in cell
diffuse to low conc in peritubular capillary
via co transport with Na+

30
Q

what are the types of glucose transporters

A

S1 in PCT 90%
SGLT2 - low aff, high cap in and GLUT2 out
S3 in PST 10%
SGLT1 in - high aff, low cap and GLUT1 out
apical to basolateral

31
Q

what happens to glucose transporters if you’re diabetic

A

overloaded = urinary excretion of glucose as at max transport capacity of glucose (Tm - transport maxima)

32
Q

what are new drugs for controlling type 2 diabetes

A

SGLT2 inhibitors eg dapagliflozin

stop glucose transported, out in urine without entering blood too bring levels down to avoid complications

33
Q

downside of SGLT2 inhibitors

A

inc risk of UTIs

could be used in healthy to lose weight (hypoglycaemia)

34
Q

further reabsorption in PT

A

K+ 70%, passive via tight junctions (para)
urea 40-50% passive down conc gradient
AAs 7 independent transport processes dep on type of AA
proteins reabsorbed from PT via receptor-mediated endocytosis

35
Q

how are proteins absorbed in PT

A

small amounts pass into filtrate via G
reabsorbed via pinocytosis (vesicles transported into cells, degraded by lysosomes and AAs return to blood)
only limit transport capacity
proteinuria sign of G damage and impending renal failure

36
Q

how does secretion into PT occur

A

some subs can’t be filtered so specialised pumps in PT transport from plasma into nephron
two kinds of pumps (inc OAT, URAT)
for organic acids
and for organic bases

37
Q

how is PAH secreted into PT

A

para-amino hippurate sec from blood into pt with a-KG or other di/tri carboxylates and transported out in exchange for another anion present in pt lumen
not endogenous so can be used as tool to measure tubular secretion

38
Q

organic acids secreted into urine by pt

A 
camp 
bile salts
hippurates (not PAH, synthetic)
oxalate
prostaglandins
urate (uric acid)
39
Q

organic bases secreted into urine by pt

A 
creatinine
dopamine
adrenaline 
noradrenaline 
histamine 
choline 
thiamine, guanidine
40
Q

how much water, sodium, glucose and AAs are absorbed ed in PT

A 
65% Na and water 
glucose 100%
proteins and AAs 100%
organic anions and bases sec 
remaining fluid to loop of henle
41
Q

What does the LOH do

A

tubular fluid further modified to conc urine further whilst recovering fluids and solutes
2 stages
extraction of water in desc limb and extraction of Na and Cl in asc limb
more important in juxtamedullary

42
Q

what is the desc limb

A

thin
cells flat, no active transport of salts
freely permeable to water via AQP1
some passive movement via tight junctions

43
Q

what is the asc limb

A

think
tubular wall impermeable to water
specialised Na/K/2Cl co transporters to reabsorb (+ve charge repels Ca2+, Mg2+)

44
Q

how does filtrate move through the LOH

A 
fluid entering from PT is isotonic 
water reabsorbed 
by tip row filtrate is hypertonic 
solutes then pumped out. 
by end (entering distal tubule) its hypotonic
300-1200-150 mOsm
45
Q

what is countercurrent multiplication

A

how fluid goes iso, hyper to hypotonic
creates a large osmotic gradient in medulla
facilitated by Na/K/Cl transport
permits passive reabsorption of water on other side of tube

46
Q

how does the urea play a part in countercurrent multiplication

A

active transport of NaCl contributes, remainder is urea
freely filtered at G, some reabs in PT but LOH and DT impermeable
can diffuse out of CD into medulla down conc gradient to add to osmolarity of medullary interstitium

47
Q

how much of each molecule is reabsorbed in the LOH

A 
Water 15%
Na and K 20-30%
Cl 50%
some urea sec (varies, CD)
remaining fluid enters DT
48
Q

what does the DT do

A

further adjustment of urine
active absorption and secretion of solutes
Na and Cl actively reabsorbed from tubular fluid
exchanged for K or H, sec into fluid

49
Q

how does the DT adjust urine

A

Na and Cl exchanged for K throughout
Na exchanged for K in late DT and early CD
involves specialised principal cells, sensitive to aldosterone

50
Q

what do principle cells do

A

late DT and early CD
K+ secretion (swap for Na+)
aldosterone sensitive
exchange part of RAAS

51
Q

what does aldosterone do

A

RAAS inc sec by adrenal glands
interact with R-aldo
inc Na channels, K channels and Na/K pump
inc Na+ reabsorption, inc H2O reabsorption ad inc BP

52
Q

what are intercalated cells

A

Na exchange for H in entire DT and early CD
a or b types
acid base regulation

53
Q

what do a intercalated cells do

A

secrete acid (H+)
via H/Na or H/K exchange
involving ATPase or H+ATPase
reabsorbs HCO3-

54
Q

what do B intercalated cells do

A

secrete bicarb via pendrin

reabsorb H+/acid

55
Q

what is the collecting ducts

A

impermeable to water and solutes

altered by ADH

56
Q

What is ADH

A

most important hormone that regulates water balance
nonapetide
aka vasopressin
released from posterior pituitary gland after hypothalamic inputs
plasma half life 10-15min
ADH acts on V2Rs on basal membrane of principle cells in DT/CD leading to activation of AQP2 via camp (water only)

57
Q

how does ADH modify urine volume

A

maximal ADH
CD permeable with max AQP2 insertion, <66% water in CD, delivery of fluid low so conc urine
opposite if well hydrated
300ml to 30L/day

58
Q

what results from a lack of ADH

A

Diabetes insipidus - treated via synthetic ADH
two forms
nephrogenic
neurogenic

59
Q

what is nephrogenic diabetes insipidus

A

due to inability of kidney to respond normally to ADH

treated via chlortalidone (diuretic) and indomethacin (ant-inf)

60
Q

what is neurogenic diabetes insipidus

A 
due to lack of ADH production by brain 
treated via
desmopressin (ADH analogue)
Vasopressin 
Carbamezapine (anti-convulsive)
61
Q

what are the other types of diabetes insipidus and the opposite syndrome

A

dipsogenic
gestational
other extreme syndrome of inappropriate ADH (SIADH) - XS ADH due to head injury, unwanted drug effect - hyponatraemia and fluid overload
treated via V2 blockers (ADH inhibitors)

62
Q

other substances that affect ADH

A

synthesised in hypothalamus and stored in pituitary
agents inc ADH are nicotine, ether, morphine, barbiturates
inhibit
alcohol

63
Q

what happens to all the water and solutes reabsorbed from the tubule

A

taken back into peritubular vessels and vasa recta surrounding tubule

104 theme 3 (15 decks)

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