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Urinary > Ion transport and handling > Flashcards

Ion transport and handling Flashcards

1
Q

Describe bicarbonate reuptake in the PCT

A
  • NHE draws Na+ in and H+ out
  • H+ and HCO3- make H20 and CO2 (w/ help from carbonic anhydrase)
  • Which are reabsorbed
  • Carbonic anhydrase then converts H20 and CO2 back into HCO3- and H+
  • H+ extruded again via NHE and anion exchanger draws the HCO3- back into the blood
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2
Q

Name a diuretic which inhibits NHE action

A

Amiloride

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3
Q

Describe how chloride is reabsorbed in the EARLY PCT

A

K- Cl cotransporter on basal side removes Cl-
Anion exchanger on apical side removes formate (HCOO-) and moves Cl- in.
Formate in loop of its own- removing H+ in cell so AE extrudes it then picking one up in the lumen so it can diffuse back in.

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4
Q

How is chloride reabsorbed in the late PCT?

A
  • Most of HCO3- has been reabsorbed
  • so Cl- is the major anion
  • so more and more will be reabsorbed paracellularly
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5
Q

How is phosphate reabsorbed in the PCT?

A

co transported with Na+ on apical side

faciliated diffusion removes it on the basal side

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6
Q

How is glucose reabsorbed in the nephron

A

in PCT, SGLT2 cotransports glucose in with sodium

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7
Q

How are amino acids reabsorbed in the nephrons?

A

cotransport w/ sodium at the PCT

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8
Q

How is albumin reabsorbed in the PCT?

A

Receptor mediated endocytosis
Lyosome degrades albumin to aminoacids which diffuse in to capillaries by facilitated diffusion
In glomerular damage, albumin filtered greatly increases, this system cannot uptake all the extra albumin, which si why you start getting it lost in blood

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9
Q

Above what conc of plasma glucose do you start to excrete it in urine?

A

7 mmol/L

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10
Q

How is vitamin B12 reabsorbed in the PCT?

A

B12 binds to transcobalmin. This complex is recognised by megalin receptor which causes receptor mediated endocytosis. o

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11
Q

How is calcium and magnesium reabsorbed in the nephrons?

A

When Ca2+ is high it can be reabsorbed by paracellular diffusion alone.
When its not TRPV6 will reabsorb it down a conc gradient . Vitmain D (activated by PTH) binds to vit D receptor, which activated transcellular transport of Ca2+ to the basal membrane

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12
Q

How are non endogenous organic acids secreted into the nephron?

A

Na+ and a- ketogluterate move into the cell by cotransport.
An antiporter removes the a- ketogluterate and moves the organic acid in to the cell from the blood.
An acid- base antiporter on the apical side removes the organic acid and swaps it for a base (HCO3-, Cl-, OH- ect).

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13
Q

Give examples of non endogenous organic acids which are secreted in the PCT?

A

Penicillins, PAH, histamine, choline, EDTA, thiazide diuretics ect

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14
Q

Describe the mechanism by which Na+ is reuptaken in the ascending limb of the loop of henle

A

NKCC2 cotransporter moves Na, K and 2x Cl- in all together

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15
Q

Name a drug which acts at the ascending limb by inhibiting NKCC2

A

loop diuretics- furosemide

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16
Q

Describe how sodium and chloride are reabsorbed in the DCT

A

KCICT (K+/Cl- cotransporter) and CIC-kb (Cl- remover) on the basal membrane remove Cl- from the cell.
Na+ and Cl- can therefor diffuse in together by the NCCT (Na/ Cl cotransporter).
ENaC also present allowing Na reabsorbtion

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17
Q

Which drugs act the DCT by inhibiting ENaC and NCCT?

A

NCCT inhibited by thiazides such as cholothiazide

ENaC inhibited by amiloride

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18
Q

Describe how Na+ is reabsorbed in the collecting ducts

A
  • ENaC present

- ROMK secretes K+ into lumen when Na+ moved in, to equal out intracellular charges

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19
Q

Why are PO4 and NH3 needed to buffer H+ in urine?

A

lots of H+ can be excreted without decreasing urine pH to a level that would damage the urethra

20
Q

Describe the two ways more H+ is excreted when blood pH is low

A
  • More creation of HCO3- in PCT= more NH4+ producion= more NH3 entering lumen, so more H+ can be buffered in filtrate (so more H+ lost)
  • More creation of HCO3- from CO2 and H2O in a- intercalated cells of the collecting ducts= more H+ produced= increased activity of H/ATPase, HPO4-2 buffers the H+ here
21
Q

How does furosemide (loop diuretic) decrease serum H+?

A

Inhibits NKCC, so causes hypokalaemia, hypokalaemia leads to increased H+ absorbtion into cells as k+ leaves the cells.
Also Cl- depletion causes increased H+ entry into cells.

22
Q

What controls the short term regulation of K+?

A

movement of K+ into and out of cells and (mainly) skeletal muscle

23
Q

Na/K/ATPase is responsible for putting K+ into cells, what will increase its activity? (3/4)

A
  • Insulin (meal= increased K+ but also increased insulin so K+ kept normal)
  • Catecholamines
  • High K+ in ECF
  • Aldosterone also has a minor affect on is
24
Q

Why can chronic disease lead to hyperkalaemia?

A

it decreases Na/K/ATPase actvitity

25
Q

What increased K+ expulsion from cells?

A

Acidosis
Exercise
High cell osmolarity/ low serum
cell damage

26
Q

What decreases K+ release from cells?

A

alkalosis

27
Q

What effect does K+ release from cells have during exersize?

A

Causes vasodilation–> good

But when levels increase v high, causes reduced excitability and contractability of cells, leading to fatigue

28
Q

What is the kidneys response to high serum K+?

A
  • Hyperkalaemia causes aldosterone release from zonagraulosa of adrenal glands
  • Aldosterone increases Na/K/ATPase, ENaC and K+ membrane permeability to increase K+ secretion at the collecting ducts
  • This system is effective until kidney function is very very bad- GFR can go as low as 15ml/min and you can still secrete excess K+
29
Q

What is the kidneys response to low serum K+?

A

Less aldosterone release, meaning less K+ secretion, however were unable to reabsorb all of it so you always need it from your diet

30
Q

Why does aldosterone released due to hypovolaemia not also cause hypokalaemia?

A

Becuase when aldosterone is released due to hypovolaemia, angiotensin is also present. Angiotensin inhibits ROMK, so negates aldosterones affect to make the collecting duct more permeable to K+, it also increases NCCT in the early DCT so there is less distal delivery of Na+, so less ENaC activity, so less K+ secretion. (aldosterone paradox)

31
Q

What causes hypokalaemia?

A
  • low dietary intake
  • increased entry into cells (metabolic alkalosis)
  • increased GI loss (vomiting and diarrhoea)
  • loop and thiazide diuretics
  • tubular acidosis (rare)
  • Mg2+ deficiency
32
Q

What effect does hypokalaemia have on membrane excitability

A

increases excitability because bigger K+ gradient

33
Q

What effect does hyperkalaemia have on membrane excitability?

A

decreases excitability because membrane potential decreases, so more Na+ channels will be inactivating, making propagation of action potentials

34
Q

What are the signs and symptoms of hypokalaemia?

A

weakness
polyuria
constipation
arrhythmias- U wave and eventually V fib

35
Q

How is hypokalaemia treated?

A

oral K+
Slow IV K+
Treating cause- eg giving Mg2+ if deficiency in this has caused the hypokalaemia

36
Q

How does Ca2+ travel in the plasma?

A

bound to albumin

37
Q

How does the body respond to low Ca2+?

A

PTH release increases which:

  • increases calcitriol release which causes increase Ca2+ absorption in the GI and increases bone resorption
  • stimulates osteoclasts (bone resorption)
  • Increases reabsorbtion in the DCT
  • Decreases PO4-2 reabsorbtion in the PCT
  • Calcitriol also helps facilitate the effects on the kidneys
38
Q

What causes hypocalcaemia?

A
  • Vit D deficiency
  • lack of PTH
  • loop diuretics, drugs cont. phosphate, gentamicin (decreases Mg2+)
  • reduced intake and malabsorbtion
  • pancreatitis
  • high phosphate or magnesium
  • ECF expansion
  • alkalosis (causes more binding with proteins- less free ionised ca2+)
39
Q

What are the signs and symptoms of hypocalcaemia?

A

Fatigue, muscle weakness, parasthesia, reduced CO, irritability, memory loss, confusion, hallucination and paranoia

40
Q

How is hypocalcaemia treated?

A

treat the cause
treat other ions
give vit D
Calcium supplementation

41
Q

Where is Mg2+ reabsorbed in the nephrons?

A

15% in the PCT and 60% in the TAL

42
Q

Describe how the kidney handles Mg2+ concentration changes

A

If Mg2+ increases, more will be filtered, the Tm will be exceeded and Mg2+ should return to normal.
If Mg2+ decreases, the TAL can detect that and increase transcellular transport slightly, but this has little effect, as a result hypomagnesia is hard for the kidneys to recover from

43
Q

What % of Mg2+ is normally absorbed in the gut and how much can this can increase by under conditions of hypomagnesia?

A

Normally 30-50%, but can increase uptake by upto 80% when needed.

44
Q

What can cause hypomagnesia?

A

malnutrition, malabsorbtion, diarrhoea, loop and thiazide diuretics, metabolic acidosis, alcoholism and many other things

45
Q

What are the signs and symptoms of hypomagnesia?

A

fatigue, muscle spasms, anxiety or depression, headache

If it gets worse (<0.4mmol/L)- cardiac dysrhythmias, hyperreflexia, tetany, seizures, hypokalaemia and hypocalcaemia

46
Q

How is hypomagnesia treated?

A

Treat cause

Give oral Mg salts or IV magnesium sulphate

Urinary (9 decks)

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