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sem 2 renal > renal blood flow and glomerular filtration > Flashcards

renal blood flow and glomerular filtration Flashcards

1
Q

what is the functional unit of kidney?

A

nephron

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2
Q

avg length of a nephron

A

4cm

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3
Q

what are the 2 elements of a nephron?

A

glomerulus and tubule

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4
Q

how many nephrons per kidney?

A

1 million

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5
Q

can the kidney regenerate new nephrons?

A

no

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6
Q

how do the tubules along the nephron connect with the blood supply?

A

peritubular capillaries

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7
Q

what are the diff types of capillaries a nephron has?

A

peritubular and glomerular

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8
Q

glomerular capillaries come into close contact with what?

A

the nephron in the Bowman’s capsule

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9
Q

name the 2 stages of urine formation

A
  1. glomeruli produce the liquid

2. tubules modifies its volume & composition

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10
Q

where does the majority of fluid that is forced out into the Bowman’s capsule go?

A

majority of fluid is reabsorbed when it comes into contact with peritubular capillaries again.

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11
Q

what is the consequence if you don’t reabsorb fluid?

A

you may become volume depleted

- hypovolaemia

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12
Q

as the blood flows into the nephron, where does it go?

A

it flows in via the afferent arteriole, down into the glomerular capillaries which are situated in the bowman’s capsule and then flowing out again through the efferent arteriole

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13
Q

why do we have such a huge filtration rate?

A

you need a big filtration rate in order to flush out the waste products (which then go into our urine) to keep levels in the blood low

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14
Q

how is glomerular fluid formed?

A

passive ultrafiltration of plasma across the glomerular membrane

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15
Q

what is the glomerular filtration rate (GFR) set by?

A

(i) autoregulation:

(ii) renal sympathetic vasomotor nerve activity

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16
Q

what does the glomerulus consist of?

A

a clump of capillaries & Bowman’s capsule

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17
Q

small solutes (NaCl, glucose, urea) - concentration in glomerular fluid

A

the concentration in glomerular fluid = the concentration in plasma

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18
Q

plasma proteins - concentration in glomerular fluid

A

almost zero

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19
Q

Proteinuria

A

protein in the urine

-sign of renal/urinary tract disease

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20
Q

the glomerular membrane sieves out solutes from plasma based on what?

A

their molecular size

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21
Q

what drives glomerular fluid formation?

A

an imbalance of Starling’s forces

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22
Q

what 2 pressures act in the opposite direction to the high capillary pressure?

A
  • colloid osmotic pressure exerted by proteins in the blood
  • pressure in the Bowman’s space

but net filtration force pushes fluid out

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23
Q

what happens to blood pressure and plasma concentration as the blood flows through the capillary from the afferent end to the efferent end?

A
  • there is a slight drop in pressure

- plasma gets more concentrated due to fluid loss

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24
Q

what happens to the plasma COP (colloid osmotic pressure) as the blood flows from the afferent to efferent end?

A

COP rises because fluid is lost from capillaries, hence the protein is getting more concentrated thereby exerting a greater force driving fluid back from the tubule into the peritubular capillary

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25
Q

podocytes and pedicels

A

invaginated epithelial layer of the bowman’s capsule which coats the outer surface of the capillaries
-pedicels are the foot processes of the epithelial cell

26
Q

what are the gaps in between the foot processes/pedicels?

A

filtration slits

27
Q

what can travel through the fenestrations

A

Anything that’s dissolved in water can easily travel through fenestra and basal lamina (a matrix of various proteins) as long as there is a suitable channel through these proteins

28
Q

how are the filtration slits subdivided?

A

subdivided into much smaller slits (4nm wide) created by a cytoskeletal arrangement of proteins nephrin and podocin

29
Q

why can’t albumin pass through the filtration slits?

A

it would but the slits are further sub divided into a ladder of much smaller slits, and albumin gets trapped here

30
Q

how far can ferritin travel?

A

travel freely through the fenestra, but pile up at the basal lamina and they don’t enter through the filtration slips because of their size

31
Q

how far does myeloperoxidase (albumin-size protein) travel?

A

held up at the filtration slits, none penetrates into the urinary space

32
Q

describe the structure of the glomerular membrane

slide 15 and 20 diagrams

A

3 sieves in series of increasing fineness

  1. fenestrated capillaries
  2. basement membrane
  3. filtration slits of podocytes
33
Q

why does proteinuria occur?

A

if the BM or the filtration slits are damaged

34
Q

nephrotic syndrome

A

albumin getting through the layers into the bowmans capsule

35
Q

how can GFR be controlled?

A

intrinsic or extrinsic control

36
Q

explain what is meant by intrinsic control

A
  • GFR is held constant (120ml/min)
  • Important for capacity of tubules to reabsorb filtrate not be overwhelmed by excessive GFR
  • the mechanism holding GFR constant is an internal one called ‘autoregulation’
37
Q

are changes in urine production usually due to changes in GFR?

A

no, usually due to changes in tubular reabsorption

38
Q

explain “auto regulation” further

A

GFR & renal blood flow are held constant over a range of arterial pressure

This is important because blood pressure drives GFR, and blood pressure changes throughout the day, meaning the GFR would change and fluid would be forced out, causing dehydration

So, the whole system is regulated to make sure the GFR remains constant throughout your normal day-to-day fluctuations in blood pressure

39
Q

if there was no auto regulation what would happen?

A

a relatively small increase in bp (from 100-125mmHg) would cause a similar 25% increase in GFR

and, if tubular reabsorption remained constant then urine flow would increase by 30-fold, depleting blood volume very quickly

this is why when things happen to alter your blood pressure (persistent hypotension) this will start being deterimental

40
Q

what are the 2 mechanisms responsible for keeping GFR and renal plasma flow constant?

A

Bayliss myogenic response
-direct vasoconstriction of afferent arteriole with increase in perfusion pressure

Tubuloglomerular feedback (TGF)
-flow-dependent signal detected in macula densa that alters tone of afferent arteriole
41
Q

which mechanisms responds to slower BP fluctuations, over intervals of 20 seconds or great?

A

tubuloglomerular feedback

42
Q

Bayliss myogenic response

A

increase in perfusion pressure leads to an immediate increase in vessel radius (few seconds only), so blood flow goes up briefly

Bayliss observed that this resulting stretch of smooth muscle in the afferent arteriole quickly results in contraction and a reduction in diameter & increase in resistance - readjustment to an intermediate value within about 30s

43
Q

explain the relevance of the bayliss myogenic response on kidney function

A

if we increase the pressure in the artery the afferent arteriole constricts and becomes very narrow, reducing the flow going into the glomerular capillaries and maintaining that pressure. If the pressure is maintained, the GFR will not change

44
Q

what detect the stretch in the afferent arteriole?

A

myogenic stretch receptors in the wall of the afferent arteriole

45
Q

when does auto regulation fail, and what happens as a result?

A

when you go below a certain pressure, e.g. in hypotension, shock and haemorrhage

results in olguria, which is failed urine output.

46
Q

Myogenic

A

contraction that originatesfrom the cell itself and not from an external source

47
Q

How does contraction of afferent arteriole regulate glomerular capillary pressure ?

A

the afferent arteriole drops pressure by constricting and therefore increasing the resistance, reducing the flow into the capillaries and maintaining the pressure in the capillaries so GFR doesn’t change

48
Q

afferent arterioles are resistance vessels - what does this mean?

A

they alter resistance to maintain GFR in the capillaries

49
Q

what comes back into contact with the afferent and efferent arterioles?

A

the distal convoluted tubule

50
Q

what are juxtaglomerular cells?

A

modified smooth muscle cells in walls of afferent arteriole proximal to glomerulus – store inactive pro-renin

the areas is known as the macula dense

51
Q

Tubulo-glomerular feedback (TGF)

A
  • GFR increases
  • flow through tubule increases, and flow past macula dense increases
  • increase in [NaCl] and osmolarity in DCT, which is sensed by the macula densa
  • paracrine/vasoactive agents diffuse from the macula dense to the afferent arteriole
  • afferent arteriole constricts, increasing resistance
  • hydrostatic pressure in the glomerulus decreases
  • GFR decreases (restored)
  • superimposed on this is the RAAS system
52
Q

what can renal sympathetic nerves do?

A

reduce GFR by resetting autoregulation to a lower level (from 120 to 100)

53
Q

in which 3 situations does resetting of autoregulation to a lower level via renal sympathetic nerves occur? why does this occur?

A
  1. standing upright (orthostasis)
  2. heavy exercise
  3. haemorrhage
  • the role is to conserve body fluid volume during physical stress
  • conserve blood loss and cardiac output (haemorrhage)
54
Q

what can these sympathetic actions by aided by? (during shock)

A

circulating vasoconstrictor hormones such as adrenaline, angiotensin and vasopressin

55
Q

Two major clinical disorders of the GFR

A
  1. Glomeruli too leaky to plasma protein: nephrotic syndrome (eg. Filtration slit disordered by nephrin deficiency)
  • Proteinuria (because the glomerular basement membranes become damaged and more leaky. basement membranes becomes thicker, maybe due to deposition of immunoglobulins)
  • Hypoproteinaemia
  • Oedema
  1. GFR too low (more common)
    chronic glomerulonephritis (infection) nonfunctioning glomeruli
    When GFR < 30 ml/min, this is chronic renal failure.
56
Q

why does nephrotic syndrome cause oedema?

A

loss of proteins from the plasma means oncotic pressure isn’t as high anymore, so fluid isn’t absorbed at the venous end of the capillaries

57
Q

what usually happens to fluid at the venous end?

A

usually fluid is reabsorbed at the venous end because the oncotic pressure at this point is higher than the capillary pressure

58
Q

what happens to any fluid left that isn’t reabsorbed at the venous end?

A

any fluid left enters the lymphatic system as tissue fluid

59
Q

chronic glomerulonephritis appearance

A

fibrosed glomeruli, virtually no blood flow or red blood cells, so no glomerular filtrate produced

60
Q

treatment for patient with chronic glomerulonephritis

A
  • dietary restriction, renal dialysis

- or a renal transplant if match available

sem 2 renal (10 decks)

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