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REN > Potassium, calcium, sulphate and endocrine > Flashcards

Potassium, calcium, sulphate and endocrine Flashcards

1
Q

Where is the K reservoir?

A

Intracellular - 140mM

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2
Q

When is cellular equilibrium reached for K?

A

When [K]inside / [K]outside is constant

Usually 140/4

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3
Q

What ensures a resting membrane potential across the cell?

A

Na/K ATPase. Move 2K in to ensure that K concentration is conserved

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4
Q

Where does K distribute if administered IV?

A

Adds to ECS, some moves into ICS to establish the equilibrium bu this takes time to occur so ACUTE levels will remain in ECS.

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5
Q

What is the problem with a K build up in ECS?

A

If potassium builds up or there is a release from the intracellular reservoir without compensation it can be fatal. Causes arrhythmias.

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6
Q

What may cause a release of intracellular K?

A

Muscle damage, crush injury or burn injury

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7
Q

What are the causes of HYPERkalaemia?

A

Endstage renal failure, crush injuries, blood transfusion (RBC leak in storgae), cytotoxic drugs, insulin deficiency, overuse of K sparing diuretics.

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8
Q

What results from hyperkalaemia?

A

Cardiac arrhythmias

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9
Q

How is hyperkalaemia treated?

A

Treat the cause and restrict K in diet
Give insulin and glucose as this stimulates the uptake of K into cells by increasing the rate of Na/K ATPase due to insulin allowing glucose uptake for energy.

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10
Q

What causes HYPOkalaemia?

A

Diarrhoea, furosemide, insulin overdose (too much K sequestered into cells)

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11
Q

What results from hypokalaemia?

A

Cardiac arrhythmias

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12
Q

How is hypokalaemia treated?

A

Treat the cause and give K.
IV for acute or oral for chronic
Can target RAAS

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13
Q

What controls K movement in PT?

A

Reabsorbed passively across basolateral and moves paracellularly with water.
Main site for reabsorption

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14
Q

What controls K movement in Thick Ascending limb?

A

Reabsorption through NKCC2 but most cycles back into the filtrate to prevent a net movement

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15
Q

What controls K movement in DT to MCD?

A

SECRETION of K through apical channel ROMK. Under the control of ALDOSTERONE and is Ca activated.

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16
Q

What effect do diuretics have on K?

A

Diuretics will increase K secretion by increasing distal Na delivery and water into the filtrate, causing a fall in K concentration of the interstitium

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17
Q

How does aldosterone affect K?

A

Regulates K concentration.

High K = aldosterone release for ROMK secretions, Na conservation and water retention

18
Q

How is RAAS inhibited to prevent hypokalaemia?

A

ACEi
Sartans
ARBs
Stop aldosterone production in response to K

19
Q

How much calcium is filtered in the glomerulus

A

20% of plasma free Ca (10% of total Ca)

20
Q

How does calcium move in the renal system?

A

Reabsorbed in PT transcellularly through apical channels and active transport across the basal, in proportion to water.
Reabsorbed in TAL due to the +ve potential in the lumen created by NKCC and K recycling into filtrate, so Ca moves paracellularly following the electrical gradient. TAL is main area for reabsorption.

21
Q

What allows Ca movement through apical channels in PT?

A

Ca concentration in cells is low so a small permeability allows movement

22
Q

How does sulphate move in the renal system?

A

An anion of the filtrate that is reabsorbed in the PT using the Na gradient.
NaS1 cotransporter on the apical membrane, followed by anion exchange on the basal. Tm limited.

23
Q

What does the absence of NaS1 lead to?

A

Hyposulfatemia and hypersulfaturia

24
Q

What are the 3 endocrine functions of the kidney?

A

EPO
RAAS
Vit D

25
Q

Why is EPO equired?

A

For RBC production and increased haematocrit.

26
Q

Where is EPO synthesised and what stimulates it?

A

In mesangial cells of the renal cortex upon stimulation by hypoxia.
Low iron increases production as it is a cofactor of HIFalpha dioxygenases

27
Q

What mediates EPO release?

A

Mediated by the release of PG HIF-2.

Mediated during shock or hypovolaemia with a low BP by beta-adrenoreceptor and ATII

28
Q

How is the response mediated by HIF-2 different to the response mediated by ATII?

A

During shock the aim is to increase volume to raise BP but it is slow and is not effective for acute shock.

29
Q

What is the purpose of administering an anti-apoptotic agent?

A

To ensure that all EPO progenitor cells survive to increase production.

30
Q

What is the mechanism of action of EPO?

A

EPO binds to receptors in the BM to increase the production of proerythroblasts. The EPO receptor activates JAK2 TK to activate the intracellular pathways Ras/MAP and STAT TF.

31
Q

What does low EPO receptor expression lead to?

A

Higher EPO concentration as EPO binding is irreversible as the receptors are internalised and removed from circulation. Therefore more EPO is needed to increase the chance of binding to the remaining receptors

32
Q

What may renal failure present with due to its endocrine functions?

A

ANAEMIA (normochromic normocytic)

Low 1,25 vitD (loss of conversion and diet restrictions)

33
Q

Why doesn’t polycystic KD present with anaemia?

A

If enough parenchyma remains, EPO production is not lost as there is sufficient mesangial cells to continue producing.

34
Q

What is used to treat RF anaemia?

A

EPO analogues. They are modified to extend the half life via glycosylation

35
Q

Why is EPO abused in sport? What is the risk?

A

Used to increase endurance but carries an increases risk of thrombosis and reduced flow due to the increased haematocrit and viscosity.

36
Q

What is the role of the kidney in Vit D production?

A

Vit D from sun or diet is converted to 25 vitD in the liver and then to its active 1,25 vitD in the kidney.

37
Q

What controls Vit D activation in the kidney?

A

PTH stimulates

Calcitonin inhibits

38
Q

What is the effect of active vitD on the body?

A

Increases Ca and phosphate absorption in the small intestine and reduces excretion.

39
Q

Why can 25 vitD supplements be given to a pt with RF?

A

There are extrarenal areas in the body that have vitD hydroxylation functions

40
Q

What role does the renal system play in RAAS?

A

RENIN is secreted into the circulation from JG cells, upon a fall in BP. Acts at a distance to increase BP by vasoconstriction, increasing cortisol and aldosterone for Na and water retention.

REN (14 decks)

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