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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
what are aquaporins
specific water channels located in cell membranes | 4 major ones of 13 identified
26
what are aquaporin 1s
abundant distribution in PT | also other parts of tubule where water is reabsorbed (eg desc LOH)
27
what are AQP2s
present in CD on apical surface | channel expression controlled by ADH
28
what are AQP3s
present on basolateral surface of tubular cells involved in water reabsorption
29
how is glucose reabsorbed from PT
high in filtrate low glucose in cell diffuse to low conc in peritubular capillary via co transport with Na+
30
what are the types of glucose transporters
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
what happens to glucose transporters if you're diabetic
overloaded = urinary excretion of glucose as at max transport capacity of glucose (Tm - transport maxima)
32
what are new drugs for controlling type 2 diabetes
SGLT2 inhibitors eg dapagliflozin | stop glucose transported, out in urine without entering blood too bring levels down to avoid complications
33
downside of SGLT2 inhibitors
inc risk of UTIs | could be used in healthy to lose weight (hypoglycaemia)
34
further reabsorption in PT
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
how are proteins absorbed in PT
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
how does secretion into PT occur
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
how is PAH secreted into PT
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
organic acids secreted into urine by pt
``` camp bile salts hippurates (not PAH, synthetic) oxalate prostaglandins urate (uric acid) ```
39
organic bases secreted into urine by pt
``` creatinine dopamine adrenaline noradrenaline histamine choline thiamine, guanidine ```
40
how much water, sodium, glucose and AAs are absorbed ed in PT
``` 65% Na and water glucose 100% proteins and AAs 100% organic anions and bases sec remaining fluid to loop of henle ```
41
What does the LOH do
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
what is the desc limb
thin cells flat, no active transport of salts freely permeable to water via AQP1 some passive movement via tight junctions
43
what is the asc limb
think tubular wall impermeable to water specialised Na/K/2Cl co transporters to reabsorb (+ve charge repels Ca2+, Mg2+)
44
how does filtrate move through the LOH
``` 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
what is countercurrent multiplication
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
how does the urea play a part in countercurrent multiplication
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
how much of each molecule is reabsorbed in the LOH
``` Water 15% Na and K 20-30% Cl 50% some urea sec (varies, CD) remaining fluid enters DT ```
48
what does the DT do
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
how does the DT adjust urine
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
what do principle cells do
late DT and early CD K+ secretion (swap for Na+) aldosterone sensitive exchange part of RAAS
51
what does aldosterone do
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
what are intercalated cells
Na exchange for H in entire DT and early CD a or b types acid base regulation
53
what do a intercalated cells do
secrete acid (H+) via H/Na or H/K exchange involving ATPase or H+ATPase reabsorbs HCO3-
54
what do B intercalated cells do
secrete bicarb via pendrin | reabsorb H+/acid
55
what is the collecting ducts
impermeable to water and solutes | altered by ADH
56
What is ADH
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
how does ADH modify urine volume
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
what results from a lack of ADH
Diabetes insipidus - treated via synthetic ADH two forms nephrogenic neurogenic
59
what is nephrogenic diabetes insipidus
due to inability of kidney to respond normally to ADH | treated via chlortalidone (diuretic) and indomethacin (ant-inf)
60
what is neurogenic diabetes insipidus
``` due to lack of ADH production by brain treated via desmopressin (ADH analogue) Vasopressin Carbamezapine (anti-convulsive) ```
61
what are the other types of diabetes insipidus and the opposite syndrome
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
other substances that affect ADH
synthesised in hypothalamus and stored in pituitary agents inc ADH are nicotine, ether, morphine, barbiturates inhibit alcohol
63
what happens to all the water and solutes reabsorbed from the tubule
taken back into peritubular vessels and vasa recta surrounding tubule

104 theme 3 (15 decks)

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