Lec 47 K Balance Flashcards

1
Q

How does reabsorption proximally affect distal reabsorption?

A
  • if Na reabsorbed a lot in proximal it will affect how much K is absorbed in distal because less Na available
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2
Q

What percent of filtered K is net reabsorbed? Why is this important?

A

80-95%

there is such a huge range suggests need for K homeostatis

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3
Q

What factors balance to determine serum electrolyte conc?

A
  • intake
  • output
  • movement between plasma and intracellular space
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4
Q

Where is majority of K stored in body?

A

90% of K stored in cells

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5
Q

What two things favor renal secretion?

A
  • aldosterone

- elevated plasm K

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6
Q

What is immediate compensation for high plasma K?

A
  • increased activity of NA-K ATPase
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7
Q

How does insulin play a role in K storage?

A

insulin increases Na-K ATPase action

makes sense since most K comes from food

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8
Q

What are the 2 things that trigger aldosterone release from adrenal?

A
  1. angiotensin II triggers release

2. high K triggers release

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9
Q

Over what time frame is most K excreted

A

by 6-8 hrs after ingesting

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10
Q

What happens to K in PT?

A

67% of K reabsorbed in PT passively with Na and H2O

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11
Q

What happens to K in loop of henle?

A

20% reabsorbed via Na/K/2Cl cotransporter in LOH [thick ascending limb]

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12
Q

What happens to K in distal convoluted tubule and collecting duct?

A

Aldosterone and high serum K lead to secretion via principal cells

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13
Q

What would happen to your serum K level if you lost early reabsorption?

A

you would be hypokalemic since this is where most of reabsorption occurs

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14
Q

In thick ascending limb what happens to K conc?

A

K conc decreases below that of blood because you are reabsorbing water and not reabsorbing K

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15
Q

Why is low K conc in thick ascending limb important for principal cell function?

A
  • it means when you get to collecting duct there is a driving force for K to leave principal cells via K channel to enter lumen and be excreted
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16
Q

What determines amount of K secreted?

A
  • concentration

- electrochemical gradients

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17
Q

What 4 ways does aldosterone increase principal cell K secretion?

A
  1. increases number of Na-K ATPase on basolateral side
    - - increases Na out to interstitium
    - - increases K into cell
  2. increases potential of lumen
  3. increases activity of apical K channel = increase K secreted
  4. increases activity of apical Na channel = increase Na reabsorbed into cell
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18
Q

How does volume expansion alter K secretion?

A
  • if eat a ton of salt and water you have to pee like crazy
  • normally there is higher conc of K directly next to cell in lumen
  • if increase volume get increased luminal flow
  • decreases build up of K near cell so have even bigger K gradient = bigger driving force for K to enter lumen
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19
Q

What are the mech of hyperkalemia?

A
  1. high intake [uncommon]
  2. less going into cell
  3. too much going into cell
  4. less ouptut
20
Q

What could cause too much K to leave intracellular space and thus leave you hyperkalemic?

A

in cancer undergo chemo causes cells to explode and get lots of K from thos cells into blood stream

21
Q

What could cause decreased K output leading to hyperkalemia?

A
  • kidney disease
  • other physio problem takes presedence [ex. if hypotensive and high levels of aldosterone/angiotensin, you will aborb all Na proximally so don’t have Na distally to exchange with K to secrete K
  • problem with regulatory hormones
22
Q

How could being hypotensive lead to hyperkalemia?

A

will have high levels of aldosterone/angiotensin and you will absorb all Na proximally so don’t have Na distally to exchange with K to secrete K

23
Q

What are the mech of hypokalemia?

A
  1. low intake [very rare]
  2. more K going into cells than leaving
  3. too much outflow
24
Q

What are ways you could have more K going into cells than leaving?

A
  • drugs –> like insulin cause K to go into cells

- alkalemia

25
What are ways you could have too much K outflow
- GI excretion | - renal excretion
26
What do thiazide diuretics do?
- block NaCl transporter in distal tubule | - thus get more Na, more water, higher flow in collecting duct
27
What is normal Na range?
135-145 mEq/L
28
What is normal K range?
3.5-4.5 mEq/L
29
What is normal HCO3 range?
22-26 mEq/L
30
What does hyperaldosteronism do to K, BP, HCO3?
directly - increases Na reabsorption in principal cell --> HTN - increases K secretion in principal cell --> hypokalemia indirectly via aldo - increases H secretion and HCO3 reabsorption in alpha intercalated --> metabolic alkalosis
31
How does aldo cause hypertension?
- direct effect on principal cell, increases Na retention by increasing # open apical Na channel, increasing activity Na-K ATPase - increased Na reabsorption causes increase intravascular volume
32
How does aldo cause hypokalemia?
- direct effect on principal cell - increases # open Na channels apical which makes negative lumen potential - increases activity Na-K ATPase which increases cellular K - increases # luminal channels so K moves down concentration and electrochem gradient
33
What transporter throughout body turns on when hypokalemic?
- H/K exchanger [1 K out, 1 H into cell] | - will cause pH rise [less serum H]
34
What is affect of alpha intercalated cell on H and K?
- K reabsorption - H secretion - via H-K exchanger
35
What are potential treatment mech for hyperaldosteronism?
- block Na channel in principal cell --> gets ride of electrochemical gradient that helps drive K channel secretion - aldosterone antagonists
36
Is thiazide diuretic a good treatment for pt with hyperaldosteronism? why?
NO! - will cause higher distal flow which will maintain low lumen K - will have more Na in lumen to be reabsorbed so bigger electrochemical gradient and more Na coming into cell bigger electrochemical gradient and low lumenal K will drive more K secretion via K channel
37
What are 3 main effects of hyperaldosteronism?
- HTN [via increased Na reabsorption in principal] - hypokalemia [via principal cell] - increased serum HCO3 [via a intercalated secreting H and H/K exchanger throughout body]
38
What is effective blood volume?
the volume thats actually perfusing baroreceptors and glomerular arterioles
39
What percentage of extracellular fluid is effective blood volume?
20-25% of extracellular fluid
40
What regulates EBV
- pressure change sensed by baroreceptors | - compensation --> change TPR, change CO, change Na/water excretion
41
What is short term control vs mid term vs long term control of EBV/BP?
short term -> neural/ANS mid term --> TPR/CO long term --> renal
42
What is relationship EBV to ECV [extracellular volume]?
- blood vol and extracellular fluid usually go together but can be independent in pathological conditions
43
what happens to person in water -- EBV, ECV, ANP, aldo, Na?
- vertical immersion puts hydrostatic P on legs and redistributes blood volume centrally - sensed by baroreceptors that think you have high blood volume - so EBV increased but ECV the same - body attempts to normalize via hormones, ANP rises, aldo drops - urinary Na excretion increased to restore EBV to "normal"
44
What happens to EBV and ECF in cirrhosis?
in cirrhosis have low albumin - decreased plasma oncotic pressure - will get more filtration --> edema - expanded ECF, low EBV
45
What happens to EBV and ECF in CHF?
- low CO decreases MAP and high venous P increases capillary hydrostatic pressure - get more filtration --> edema - expanded ECF, low EBV
46
What are the main mediators of volume regulation
- sympathetics - RAA - ANP - ADH