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GU 1 > 4/5 - Nephron Function > Flashcards

4/5 - Nephron Function Flashcards

1
Q

Starling forces?

A

Govern the movement of water and solutes between the plasma and ISF. Hydrostatic pressure forces water and solutes out of the blood while plasma proteins are not filtered and exert oncotic pressure inwards. In normal capillaries there is a small outwards fluid shift that is controlled by the lymphatics.

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2
Q

The glomerulus?

A
  • very leaky capillary tuft due to fenestrated epithelium

- located between 2 arterioles

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3
Q

How much of the plasma volume in the glomerular capillaries is filtereD?

A

20%

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4
Q

What is the normal GFR for both kidneys?

A

125ml/min

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5
Q

How is GFR primarily regulated?

A

Changes in glomerular hydrostatic pressure and so BF to the glomerular capillaries. For the kidneys to tightly regulate ECF osmolality and pH GFR needs to be constant.

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6
Q

How does renal autoregulation work?

A
  • changes in systemic BP should change GFR but usually doesn’t
  • works to maintain constant pressure and BF in the glomerulus and so constant GFR over a range of systemic BPs (MAP of 80-160)
  • renal autoregulation involves fb mechanisms that cause dilation/constriction of the afferent arteriole or constriction of the efferent arteriole
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7
Q

LOH?

A

Important in production of dilute or conc urine

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8
Q

How can the medulla be divided?

A

Outer medulla and inner medullary. Boundary is where the short loop nephrons (superficial ones) end

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9
Q

Thiazide diuretics?

A

Block the NaCl cotransporters in the early distal convoluted tubule

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10
Q

Furosemide diuretics?

A

Block the NKCC2 channels in the Thick Ascending Limb. Promotes urine output and salt excretion

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11
Q

2 primary cell types in the late distal convoluted tubule, connecting tubule and collecting duct

A

Principal cells and intercalated cells

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12
Q

Principal cells?

A

Reabsorb na and secrete k

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13
Q

Potential side effect of thiazide diuretics?

A

Block the na/cl cotransporter is early distal conv tubule. Means more na arrives at the ENac channel in the late distal tubule causing more K+ to be secreted by the ROMK channel causing hypokalaemia which can cause ventricular arrhythmias

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14
Q

What is the target of K+ sparing diuretics

A

ENaC i.e. amiloride. Others work by the inhibition of aldosterone

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15
Q

What does aldosterone do

A

Steroid hormone released by the adrenal cortex. Binds receptor and enters nucleus of principal cells to increase activity of existing ENaC channels in late distal conv tubule and increases transcription of ENaC and Na/K ATPases so increases Na abs and K+ secretion

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16
Q

How does spirolactone work

A

Inhibits aldosterone so is a weak K+ sparing diuretic

17
Q

Intercalated cells?

A

Important for acid base balance and K+ absorption. Usually secrete H+ via H atpase and H/K ATPase. Some of the H+ is used to reabsorb the little HCO that wasnt reabsorbed in the prox tubule but some is also freely secreted into the urine and so is a way to rid the body of acid.
Means pH is dropped as H+ is being secreted like in proximal tubule BUT some is being secreted WITHOUT HCO3- reabsorption

18
Q

How is new HCO3- generated in the intercalated cells?

A

Some CO2 and H20 is generated by metabolism

19
Q

Diffusion trapping

A

pH can only drop to 4.5 which is not sufficient to secrete all dietary H+ - therefore NH4+ is formed and trapped in the lumen and is another way to void acid. (ammonia forms ammonium ion)

20
Q

What happens to the water in the late distal conv tubule, connecting tubule and CORTICAL collecting duct?

A

Depends on the level of ADH (anti-diuretic hormone). Causes aquaporin water channels to be inserted in the apical membrane causing water to be absorbed (conc urine - 300mOsm). Made by the hypothal and released by the posterior pituitary in response to changes in osmol and BP. The channel insertion/response is rapid.

21
Q

What happens with water in the outer medulla collecting ducts?

A

Same thing - h20 extraction by osmosis using ADH regulated channels and the outer medulla salt gradient

22
Q

If you drink lots of water what happens to adh?

A

Reduced and so more is excreted whereelse if you infuse the same amount of normal saline osmol hasn’t changed so the level of ADH doesn’t change and there won’t be much of a change of urine output

23
Q

How is the conc gradient in the inner medulla established?

A
  • gradient is made up of both NaCl and UREA
  • when adh is high water is reabsorbed and as a result of this the conc of urea becomes very high in the cortical collecting duct
  • adh increases both urea and h20 permeability of the inner medulla collecting ducts
  • urea is then deposited in the interstitium and the water causes the conc of NaCl to drop
  • NaCl then moves out of the tip and ascending limb into the interstium by osmosis
24
Q

What are the 2 theories for the conc gradients in the 2 different parts of the medulla?

A
  1. Short loop countercurrent

2. Long loop passive hypothesis

25
Q

What can the osmol of the interstium reach?

A

2300 mOsmol

26
Q

How does the vasa recta influence the medullary conc gradient?

A

The counter current exchange by the vasa recta helps to preserve the osmotic gradient and carries water away that has been extracted

27
Q

What happens when adh is low?

A
  • water is not reabsorbed in the distal nephron and cortical collecting duct so the conc of urea does not increase
  • the inner medulla is permeable to urea even when adh is low
  • if the conc of urea in the interstitium is greater than that in the collecting duct then the urea will diffuse out of the intersitum into the collecting duct and be excreted (wash out)
  • this means that as long as ADH is low then urea levels in the medulla will be low
  • when adh increases then urea is deposited in the medulla again
28
Q

Compare the inner medulla to the outer medulla

A

Outer:
- the nacl gradient is formed by the countercurrent multiplication mechanism
Inner:
- nacl and urea gradient are formed by a passive mechanism that is dependent on high adh levels

29
Q

Summary of the proximal convoluted tubule

A
  • reabsorbs 2/3 of water, inorganic ions, 90% of hco3- and 100% glucose and AAs
  • na coupled transport dominates
  • filtrate is isosmotic to plasma (300) as water follows the Na
  • the pH only slightly drops as most of the H+ is used to reabsorb HCO3-
  • some new HCO3- is made by glutamine metabolism
30
Q

LOH summary

A
  • the thick ascending limb PUMPS out NaCl but is impermeable to water
  • countercurrent mechanism is established by short loops in the outer medulla (300-600 mOsm grad)
  • in the long loops when adh is high NaCl moves from the tip and acending thin limb into the inner medulla by osmosis, urea is deposited in the inner medulla by the collecting duct
  • the inner medulla conc gradient is established (600-1200 mOsm) and draws water in from the descending thin limb and collecting duct to concentrate the urine (taken away by vasa recta)
31
Q

Distal tubule summary

A
  • the early distal tubule is impermeable to water and more nacl is absorbed (blocked by thiazide diuretics like Furosemide)
  • urea becomes concentrated
32
Q

Late distal tubule, connecting tubule and collecting duct summary

A

What happens here depends on ADH

  • no adh and is imperm to water, nacl continues to be reabsorbed by ENaC which is the target of K sparing diuretics and the urine stays dilute
  • in the presence of adh water is reabs and urine becomes conc. the intercalated cells secrete H+ where some is used to reabs hco3- while some is freely excreted
33
Q

Medullary collecting duct summary

A
  • similar to cortical collecting ducts except in the presence of adh the tubule becoems more permeable to urea and it is deposited in the interstitum and NaCl moves via osmosis out of the thin descending limb to the interstitum
  • additional H+ is excreted via diffusion trapping

GU 1 (19 decks)

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