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Renal Final > 5. Regulation of K, Ca, PO4, and Mg > Flashcards

5. Regulation of K, Ca, PO4, and Mg Flashcards

1
Q

What are the symptoms of hypokalemia?

A

A SIC WALT
Alkalosis, shallow respirations, irritability confusion/drowsiness, Weakness, arrhythmias (tachycardia or brady), lethargy, thready pulse
decrease in intestinal motility, nausea, vomit

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2
Q

What is addison’s disease?

A

hypoaldosteronism resulting in hyperkalemia
Hypoaldosteronism increases water and salt excretion and reduces potassium excretion
Destruction of adrenals: aldosterone isnt secreted

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3
Q

What is the normal range of plasma K?

A

2% in ECF

3.5-5.0 mEq/l

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4
Q

What is the acute effect of low EC K concentration on resting membrane potential of excitable tissues?

A

It lowers the resting membrane potential and makes it harder to excite the tissue

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5
Q

What are some factors that cause K to move from ICF to ECF?

A

Hyperosmolarity, Cell lysis, Heavy exercise, acidemia, hypokalemia, alpha-adrenergic agnoists

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6
Q

What factors affect the movement of K from the ECF to the ICF?

A

Hyperkalemia, alkalemia, beta-adrenergic agonists, insulin

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7
Q

If K moves from the ECF to the ICF, something has to be changed to maintain electroneutrality. What is exchanged and what can result if there is a high amount of exchange?

A

H+ ion is exchanged and can cause acidosis in the ECF

Patients with hyperkalemia are at risk of acidosis.

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8
Q

Why are diabetics at risk for hyperkalemia?

A

Because insulin moves K into the cells. Without insulin, the K stays in the ECF and causes hyperkalemia

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9
Q

Patients that have alkalosis are prone to what levels of K in the ECF? why?

A

Hypokalemia. The reduced extracellular H concentration favors movement out of the cell and to maintain electroneutrality, K and Na enter the cell

Vice versa can happen. Too much acid will result in hyperkalemia

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10
Q

K is handled differently in different segments of the nephron. Where is most of the K reabsorbed? How much is reabsorbed? What is the method of reabsorption?

A

In the proximal tubule
67% reabsorbed
Paracellular- solvent drag and diffusion (+lumen)

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11
Q

Where is 20% of K reabsorbed in the nephron?

A

Thick ascending limb of henle by the Na,K,2Cl cotransport

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12
Q

Where is physiological control of K exerted in the nephron?

A

collecting duct by principal cells that either reabsorb or secrete K depending on body’s K balance.

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13
Q

What are the FIVE factors which affect K secretion in collecting duct?

A

ECF K concentration
Na reabsorption: negative luminal voltage attracts K
Luminal fluid flow rate: dilution of secreted K results in conc. gradient
Extracellular pH: K/H exchange
Aldosterone: Collecting duct, maintain electroneutrality

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14
Q

Most classes of diuretics increase Na and volume delivery to late distal tubule and CD, which ________ K secretion

A

increases

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15
Q

Less Na delivery to late distal tubule and CD causes ______ K secretion

A

less, and may cause hyperkalemia

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16
Q

If there is an increase in extracellular H what cation exchanges happen in the collecting duct principal cells? What results?

A

H/K exchange on interstitial side of cell. It will cause H/K exchange which lowers intracellular K concentration and thus decreases K secretion and increases plasma K

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17
Q

What is the major regulator of plasma K?

A

aldosterone,
It goes into the nucleus to increase the amount of K channels and Ka/K ATPase
aldosterone does not monitor Na concentration

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18
Q

The presence of high aldosterone causes a negative feedback to what system?

A

RAAS, so in a patient with high aldosterone there can be low plasma renin

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19
Q

A person with hyperaldosteronism, what would you expect the Na concentration to be? why?

A

Normal because along with Na reabsorption, water is reabsorbed, maintaining concentration

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20
Q

In a patient with hypoaldosterionism, what would you expect the level of plasma Na to be?

A

Low because, Na will decrease because we are no longer holding onto it and losing it at a higher rate

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21
Q

What is Conn’s disease?

A

hyperaldosteronism resulting in hypokalemia
Aldossterone secreting tumor in adrenal cortex
K secretion by CD is inappropriately stimulated

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22
Q

What do osmotic diuretics do?

A

e.g. mannitol: inhibit reabsorption of water and secondarily, Na in the proximal tubule and thin descending limb of henle. Generate osmotic pressure gradient

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23
Q

What do carbonic anhydrase inhibitors do?

A

Acetazolamide: inhibit NaHCO3 reabsorption in the proximal tubule
reduce Na reabsorption by their effect on carbonic anhydrase and 1/3 of proximal tubule Na reabsorption occurs in exchange for H (Na/H antiporter)
Long term creates metabolic acidosis
*only used for altitude sickness

24
Q

What are some examples of Loop diuretics?

A

Furosemide (lasix), bumetanide (bumex) and ethacrynic acid

25
Q

What is the function of loop diuretics?

A

inhibit Na/K/2Cl cotransporter by competing for Cl. Increases total RBF and dissipates high solute concentration of medullary interstitium
Lessens water reabsorption in descending limb of henle and medullary collecting duct

26
Q

What diuretics act on the distal convoluted tubule?

A

Thiazide

e.g. hydrochlorothiazide

27
Q

What are the actions of thiazide?

A

in the DCT..
inhibit Na/Cl cotransport
Increase Na and Cl excretion as well as K
Results in decreased Ca excretion

28
Q

What diuretics act on the collecting duct?

A

Potassium-sparing diuretics

Amiloride, triamtrene (block Na channels) and spironolactone (aldosterone antagonist)

29
Q

What are the actions of potassium-sparing diuretics?

A

in the collecting duct..
inhibit Na reabsorption, K secretion
Aldosterone antagonist
Often used in combination with other diuretic classes that increase K excretion but the diuretics themselves do not mess with K

30
Q

The use of diuretics is used for therapy of what condition?

A

hypertension

31
Q

What type of diuretic is used in patients with SIADH?

A

aquaretics (eg. demeclocycline)
water diuresis by blocking action of ADH on late distal tubule and collecting duct. Need to help kidneys excrete solute free water

32
Q

Ca can dampen action potentials by blocking what?

A

Na channels

33
Q

Low EC Ca can produce hypocalcemic ________

A

Tetany

34
Q

What is an enzyme cofactor, component of bone, part of cellular signaling and is involved in blood clotting?

A

EC Ca

35
Q

What is the normal total plasma Ca concentration range?

A

4.5-5 mEq/l

36
Q

How much Ca is protein bound?

A

45%

37
Q

What is the concentration of free plasma?

A

1.2-1.5 mM

only free Ca is biologically active

38
Q

Why does the increase of hydrogen ions in the plasma cause an increase in plasma free Ca?

A

Because H competes with Ca for bidning sites on plasma proteins. So if there is more H, the ions displaces Ca from the proteins therefore increasing the plasma free [Ca].

39
Q

Acidemia -> ? plasma free [Ca]

A

increase

40
Q

alkalemia -> ? plasma free [Ca]

A

decrease and can mimic hypokalemia

41
Q

What are the organs that help determine EC [Ca]?

A

Parathyroid, GI, Kidney, bone

42
Q

Describe how extracellular Ca is increased due to hypocalcemia?

A

Parathyroid senses low EC [Ca] and releases PTH. PTH in the blood creates a higher concentration of H which causes an increase in free plasma [Ca].
PTH also works on the kidneys by inducing the production of vitamin D (Calcitriol) which promotes resorption of Ca in the GI tract. PTH and Calcitriol also stimulates bone resorption. Kidneys also reabsorb more

43
Q

Where is most of the Ca reabsorbed in the nephron?

A

PT ~70%

44
Q

How much Ca is reabsorbed in the TAL? where is Ca reabsorption fine tuned?

A

~20%

fine tuned in the DT

45
Q

How is Ca reabsorbed in the proximal tubule?

A

Paracellularly and also transcellular route (intracellular Ca is very low which creates a concentration gradient. once in the cell it is transported out via Na/Ca exchange and Ca ATPase)

46
Q

How is Ca reabsorbed in the thick ascending limb of henle?

A

Paracellular. Despite the tight junctions becoming ‘tighter’, the + 6mV tubular potential drives the cations including Ca through the tight junction into the blood

K leak causes tubular urine to be positive

47
Q

How is Ca reabsorbed in the DCT?

A

via epithelial Ca channels

48
Q

How do thiazides lead to hypercalcemia?

A

It inhibits the Na/Cl symporter in early DCT on tubular lumen side. This lowers the Na intracellular concentration. In turn, this enhances the activity of Na/Ca exchanger on the basolateral surface. Creates a driving force for Ca reabsorption through epithelial Ca channels

49
Q

What is calbindin and what is its purpose in the distal tubular cell?

A

Calbindin is a vitamin D-dependent Ca binding protein.
It causes a greater reabsorption of Ca and helps bring calcium to the peritubular capillary side through Ca-ATPase and Ca/Na exchanger on basolateral side (mechanism unclear)

50
Q

Renal failure leading to the inability to make vitamin D can lead to what long term effect?

A

2ndary Hyperthyroidism

and bone becomes diseased and fibrotic

51
Q

PTH inhibits phosphate _________

A

Reabsorption

52
Q

How is phosphate reabsorbed in the proximal tubule?

A

On tubular side: 2Na/Pi

Blood: Pi/Anion

53
Q

What does PTH do to PO4 reabsorption

A

Increases the amount excreted. Decreases the amount reabsorbed and lowers the Tm

54
Q

What are the three forms of Mg in the plasma ?

A

60% free Mg
20% complexed with inorganic, small organic anions
20% bound to plasma proteins

55
Q

How much Mg is filtered into nephrons each day?

A

2 g Mg

56
Q

Where is the bulk of the filtered Mg reabsorbed? How much of the total amount of Mg filtered is excreted normally?

A

Thick ascending limb of henle by paracellular movement due to positive charge in lumen
and 10% is excreted

57
Q

What is the effect of loop diuretics on renal Mg handling?

A

Decreases the positive flow in lumen and decreases the Mg flow through paracellular junction. Thus increases the amount excreted.

Renal Final (8 decks)

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