Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology Part 2 > Lec 47 K Balance > Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What factors balance to determine serum electrolyte conc?

A
  • intake
  • output
  • movement between plasma and intracellular space
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where is majority of K stored in body?

A

90% of K stored in cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What two things favor renal secretion?

A
  • aldosterone

- elevated plasm K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is immediate compensation for high plasma K?

A
  • increased activity of NA-K ATPase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A
  1. angiotensin II triggers release

2. high K triggers release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Over what time frame is most K excreted

A

by 6-8 hrs after ingesting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What happens to K in PT?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What happens to K in loop of henle?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What determines amount of K secreted?

A
  • concentration

- electrochemical gradients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

What are ways you could have too much K outflow

A
  • GI excretion

- renal excretion

26
Q

What do thiazide diuretics do?

A
  • block NaCl transporter in distal tubule

- thus get more Na, more water, higher flow in collecting duct

27
Q

What is normal Na range?

A

135-145 mEq/L

28
Q

What is normal K range?

A

3.5-4.5 mEq/L

29
Q

What is normal HCO3 range?

A

22-26 mEq/L

30
Q

What does hyperaldosteronism do to K, BP, HCO3?

A

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
Q

How does aldo cause hypertension?

A
  • 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
Q

How does aldo cause hypokalemia?

A
  • 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
Q

What transporter throughout body turns on when hypokalemic?

A
  • H/K exchanger [1 K out, 1 H into cell]

- will cause pH rise [less serum H]

34
Q

What is affect of alpha intercalated cell on H and K?

A
  • K reabsorption
  • H secretion
  • via H-K exchanger
35
Q

What are potential treatment mech for hyperaldosteronism?

A
  • block Na channel in principal cell –> gets ride of electrochemical gradient that helps drive K channel secretion
  • aldosterone antagonists
36
Q

Is thiazide diuretic a good treatment for pt with hyperaldosteronism? why?

A

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
Q

What are 3 main effects of hyperaldosteronism?

A
  • 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
Q

What is effective blood volume?

A

the volume thats actually perfusing baroreceptors and glomerular arterioles

39
Q

What percentage of extracellular fluid is effective blood volume?

A

20-25% of extracellular fluid

40
Q

What regulates EBV

A
  • pressure change sensed by baroreceptors

- compensation –> change TPR, change CO, change Na/water excretion

41
Q

What is short term control vs mid term vs long term control of EBV/BP?

A

short term -> neural/ANS
mid term –> TPR/CO
long term –> renal

42
Q

What is relationship EBV to ECV [extracellular volume]?

A
  • blood vol and extracellular fluid usually go together but can be independent in pathological conditions
43
Q

what happens to person in water – EBV, ECV, ANP, aldo, Na?

A
  • 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
Q

What happens to EBV and ECF in cirrhosis?

A

in cirrhosis have low albumin

  • decreased plasma oncotic pressure
  • will get more filtration –> edema
  • expanded ECF, low EBV
45
Q

What happens to EBV and ECF in CHF?

A
  • low CO decreases MAP and high venous P increases capillary hydrostatic pressure
  • get more filtration –> edema
  • expanded ECF, low EBV
46
Q

What are the main mediators of volume regulation

A
  • sympathetics
  • RAA
  • ANP
  • ADH

Physiology Part 2 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions