Lec 47 K Balance Flashcards
How does reabsorption proximally affect distal reabsorption?
- if Na reabsorbed a lot in proximal it will affect how much K is absorbed in distal because less Na available
What percent of filtered K is net reabsorbed? Why is this important?
80-95%
there is such a huge range suggests need for K homeostatis
What factors balance to determine serum electrolyte conc?
- intake
- output
- movement between plasma and intracellular space
Where is majority of K stored in body?
90% of K stored in cells
What two things favor renal secretion?
- aldosterone
- elevated plasm K
What is immediate compensation for high plasma K?
- increased activity of NA-K ATPase
How does insulin play a role in K storage?
insulin increases Na-K ATPase action
makes sense since most K comes from food
What are the 2 things that trigger aldosterone release from adrenal?
- angiotensin II triggers release
2. high K triggers release
Over what time frame is most K excreted
by 6-8 hrs after ingesting
What happens to K in PT?
67% of K reabsorbed in PT passively with Na and H2O
What happens to K in loop of henle?
20% reabsorbed via Na/K/2Cl cotransporter in LOH [thick ascending limb]
What happens to K in distal convoluted tubule and collecting duct?
Aldosterone and high serum K lead to secretion via principal cells
What would happen to your serum K level if you lost early reabsorption?
you would be hypokalemic since this is where most of reabsorption occurs
In thick ascending limb what happens to K conc?
K conc decreases below that of blood because you are reabsorbing water and not reabsorbing K
Why is low K conc in thick ascending limb important for principal cell function?
- 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
What determines amount of K secreted?
- concentration
- electrochemical gradients
What 4 ways does aldosterone increase principal cell K secretion?
- increases number of Na-K ATPase on basolateral side
- - increases Na out to interstitium
- - increases K into cell - increases potential of lumen
- increases activity of apical K channel = increase K secreted
- increases activity of apical Na channel = increase Na reabsorbed into cell
How does volume expansion alter K secretion?
- 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
What are the mech of hyperkalemia?
- high intake [uncommon]
- less going into cell
- too much going into cell
- less ouptut
What could cause too much K to leave intracellular space and thus leave you hyperkalemic?
in cancer undergo chemo causes cells to explode and get lots of K from thos cells into blood stream
What could cause decreased K output leading to hyperkalemia?
- 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
How could being hypotensive lead to hyperkalemia?
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
What are the mech of hypokalemia?
- low intake [very rare]
- more K going into cells than leaving
- too much outflow
What are ways you could have more K going into cells than leaving?
- drugs –> like insulin cause K to go into cells
- alkalemia
What are ways you could have too much K outflow
- GI excretion
- renal excretion
What do thiazide diuretics do?
- block NaCl transporter in distal tubule
- thus get more Na, more water, higher flow in collecting duct
What is normal Na range?
135-145 mEq/L
What is normal K range?
3.5-4.5 mEq/L
What is normal HCO3 range?
22-26 mEq/L
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
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
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
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]
What is affect of alpha intercalated cell on H and K?
- K reabsorption
- H secretion
- via H-K exchanger
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
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
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]
What is effective blood volume?
the volume thats actually perfusing baroreceptors and glomerular arterioles
What percentage of extracellular fluid is effective blood volume?
20-25% of extracellular fluid
What regulates EBV
- pressure change sensed by baroreceptors
- compensation –> change TPR, change CO, change Na/water excretion
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
What is relationship EBV to ECV [extracellular volume]?
- blood vol and extracellular fluid usually go together but can be independent in pathological conditions
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”
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
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
What are the main mediators of volume regulation
- sympathetics
- RAA
- ANP
- ADH
