Exam3Lec4Sodium/Potassium/ElectrolytesBalance

Question 1

A decr in GFR leads to a ____ in Na+ excretion

Answer 1

decrease

Question 2

What can change with decreased blood pressure?

Answer 2

Filtration presure

Question 3

What is the equation for GFR?

Answer 3

GFR = Kf [PGC - PBC) - piGC ]

Question 4

What two hormones incr Na+ reabsoprtion?

Answer 4

Aldosterone and
Angiotensin II

Question 5

What type of hormone is Aldosterone and Angiotensin II?

Answer 5

Aldosterone: steroid hormone
Angiotensin 2: peptide hormone

Question 6

Does atrial natriuretic peptide (ANP) and BNP favor sodium reabsorption?

Answer 6

NO, its favors sodium excretion

Question 7

Which organ secretes aldosterrone and what is the fxn of aldosterone>

Answer 7

Adrenal gland secretes aldosterone and the fxn of aldosterone is to incr sodium reabsoprtion in the kidney

Question 8

Aldosterone incr Na+ Reabsorption in what segments of the nephron?

Answer 8

Late Distal Tubule and Collecting Duct

Question 9

Explain how aldosterone incr Na+ reabsorption

Answer 9

1. In the presence of Aldosterone, it stimulates the activation of the Na+ channel (ENaC) on the lumen side.
2. Once Na+ enters cytosol through the channel, aldosterone also incr activation of the sodium potassium pump to incr Na+ into the intertisum.

note that Na+ enters cytsol through a sodium channel that IS NOT voltage gates, just diffuses through the endothelial sodium channed (ENaC)

Question 10

How is angiotensin 2 formed?

Answer 10

1. Liver synthesizes Angiotensinogen and is excreted into the bs
2. Angiotensinogen is then turned into Angiotensin 1 by the renin enzyme.
3. Angiotensin 1 is then turned into Angiotensin 2 by ACE enzyme.

renin chops off the last 4 aa from Angiotensinogen to become angiotensin 1
ace removes 2 more aa from angiotensin 1 to beceom angiotensin 2

Question 11

What are 4 mechanisms of which angiotensin 2 can incr Na+ reabsorption

Answer 11

• incr Aldosterone
• decr Kf (surface area)
• incr Proximal Reabsorption directly
• incr Filtration Fraction (FF)

Question 12

Angiotensin II is a very powerful ____ hormone

Answer 12

vasoconstricting

Question 13

How does Angiotensin II incr filtration fraction (FF)?

Answer 13

Angiotensin II constricts both afferent and efferent arterioles but has more effect on efferent arteiole

You incr vasoresistance through vasoconstrition lowering plasma flow

Question 14

Because angiotensin II can increase Filtration what occurs to the GFR and RPF?

Answer 14

GFR remains unchanges and RPF decr

You incr vasoresistance through vasoconstrition lowering plasma flow
GFR remained unchanged b/c both aff and eff are constricted

Question 15

As a result of angiotensin 2 incr Na+ reabsoption, does the protein osmotic pressure incr or decr in peritubular capillaries and why?

Answer 15

It’s increased bc there is more plasma flow in GFR is filtered into proximal tubule. Lots of proteins are left behind inside the glomerular capillary so the protein osmotic pressure incr,

Question 16

What leads to the release of ANP (atrial natriuretic peptide) ?

Answer 16

Volume expansion of the heart leading to atrial stretch leads to the atrial cell releasing ANP

Question 17

What are the two main effects of ANP?

Answer 17

1. Vasodilation leading to lowering of blood pressure
2. Incr Na+ and H2O excretion

does both simultaneously
action s mediated by cGMP

Question 18

Similar Structures of the Natriuretic Peptides Family

Where is ANP found?

Answer 18

Atria and other tissues

has 1 disulfide bond

Question 19

Similar Structures of the Natriuretic Peptides Family

What is BNP? Where is it found?

Answer 19

BNP is an isoform of ANP. It is found in the brain, atria, and ventricles.

Question 20

Why is BNP important clinically?

Answer 20

It is an important indicator to assess the health of the heart. If someone has heart failure, they can look at BNP lvls

Question 21

Similar Structures of the Natriuretic Peptides Family

What is CNP? Where is it found?

Answer 21

CNP is an isoform of ANP. It is found in the CNS and vasculature

Question 22

Atrial Natriuretic Peptide (Factor)
ANP (ANF) ____ Na+ Reabsorption

Answer 22

Decreases

oppostire

Question 23

How does ANP/ANF/BNP decr Na+ reabsoprtion?

Answer 23

ANP/ANF/BNP incr cGMP activity and this inhibits Na+ reabsorption through inhibiting the sodium channel so Na+ comes in less,

Question 24

Actions of Atrial Natriuretic Peptide is mediated by?

Answer 24

cGMP

Question 25

Explain the action of Actions of Atrial Natriuretic Peptide when the blood volume incr

Answer 25

Question 26

A decr in protein osmotic pressure leads to what?

Answer 26

Increases Na+ Excretion (glomerulus) remember: GFR = Kf [PGC - PBC) - **piGC** ] ## Footnote Decreased Protein Osmotic Pressure Increases Na+ Excretion (glomerulus)

Question 27

How does a decreased Protein Osmotic Pressure increase Na+ excretion in the Proximal Tubule?

Answer 27

It lowers osmotic pressure in the PT capillary so less Na+ is reabsorbed back into the capillary and you see an incr is Na+ excretion/

Question 28

How does sympathetic innervation (epi and norepi) effect absorption?

Answer 28

It increases Na+ reabsoprtion

Question 29

Sympathetic incr increases Na+ reabsorption through which structures?

Answer 29

1. Arterioles 2. JG cells 3. Kf (surface area) 4. Tubule

Question 30

How does sympathetics (norepi or epi) incr Na+ reabsorption through the tubules?

Answer 30

it increases the active Na/K APTase by activating PP1 and thus increase Na reabsorption. ## Footnote Angiotensin 2 has a similar effect but different receptor.

Question 31

Increased blood flow to cortex results in?

Answer 31

Increased Na+ excretion

Question 32

Is the juxtamedullary nephron salt sparing or salt wasting?

Answer 32

Salt sparing ## Footnote because it has a longer loop of henle and they are more efficent in Na+ reabsoption

Question 33

Is the cortical nephron salt sparing or salt wasting?

Answer 33

Salt wasting ## Footnote b/c they don't reabsorb as much, bc shorter tubule less, sa for reabs

Question 34

What is pressure natriuersis/diuressis and what is it caused by?

Answer 34

Pressure natriuresis/diuresis is an increase of Na+ /water excretion Caused by an increase in arterial pressure in the absence of a change in renal blood flow and glomerular filtration rate.

Question 35

During pressure natriuresis/diuresis , In the range of autoreg, there is a wide range of change (incr) in arterial pressue, no change in RBF or GFR, and there is NO autoregulation of urine outflow leading to a large incr of urine outlflow. Why does this possibly occur?

Answer 35

possibly Because there is inhibition of Na+ and H2O reab in the proximal tubule ## Footnote hypothesis is thar an incr bp inhibiits antiporter (Na+/H+) decr Na+ reab

Question 36

What is this curve?

Answer 36

Renal functional curve ## Footnote if you have some Na or H20 retention, this can make your BP incr pass the equilibrium point then you kidney reaction incr alot, so you see incr excretion of H2O and salt (outake>intake) to lower back to equilibrium

Question 37

What does this graph represent?

Answer 37

Renal functional curve of someone with hypertension. The curve shifted to the right, so their equiibrium point incr. ## Footnote Pts with HTN have to operate in high BP in order to achieve that equilibrium

Question 38

What is Liddle syndrome?

Answer 38

an autosomal dominant disorder characterized by early, and frequently severe, **hypertension** associated with low plasma renin activity, metabolic alkalosis due to hypokalemia, and hypoaldosteronism.

Question 39

What causes liddle syndrome?

Answer 39

This syndrome is caused by disregulation of an epithelial sodium channel (ENaC) due to a genetic mutation. It does not breakdown/degrade fast enough so you have accumulation of sodum reabsoption. The increased sodium reabsorption leads to hypertension

Question 40

Review: ADH ____ tubular permeability to water

Answer 40

Incr ## Footnote remember: by phosph AQP2 it makes the whole tubule water perm. In the absence of ADH the channels are recycled and the apical membrane is again impermeable to water. It does this regulation at the corticla and medullar collecting duct

Question 41

Primary control of H2O excretion by ____.

Answer 41

ADH

Question 42

Primary control of H2O excretion is by ADH, what is the exception?

Answer 42

osmotic diuresis

Question 43

For osmotic diuresis, the reabsorption of water is dependent on what? Increased solute excretion nearly always results in what?

Answer 43

* The reabsorption of water is dependent on the **reabsorption of solutes**. * Increased solute excretion nearly always results in **increased urine flow** ## Footnote EX: (diabetes): so much glucose is being processed through tubule and it cannot reabsorb all of it so by the time it leaves the proximal tubule, glucose is left behind and receptors are sat, and its excreted in urine. B/c glucose has high osm , when you excrete glucose you take H20 with it.

Question 44

For osmotic diuresis, is the reabsorption of solutes dependent on the reabsorption of water?

Answer 44

NO ## Footnote The reabsorption of water is dependent on the reabsorption of solutes.

Question 45

What stimulates and inhibits ADH secretion/release?

Answer 45

1. Stimulated by: ATII 2. Inhibited by: ANP ## Footnote Secretion of ADH is stimulated by physiological factors, other hormones and drugs

Question 46

You have a patient with hypertension who you have been treating with a loop diuretic for 1 month. His initial plasma [K+] was 4.5 mEq/L and has decreased to 3.0 mEq/L. How much potassium has the patient lost ?

Answer 46

Potassium Intake = 100 mmoles/day PotassiumExcretion = 100 mmoles/day 90% urine 10% feces lost 21 mmol ## Footnote things to note: intake=output. Pt lost plasma K+ so ECF was lost, ICF unchanged.

Question 47

# Regulation of Potassium Excretion 100% of the filtered K+ is reabsorbed by the time it reaches what segment of the nephron?

Answer 47

the beginning of the distal tubule ## Footnote late distal and collecting duct is primarily K+ secretion

Question 48

What is the effect of aldosterone intake on potassium excretion?

Answer 48

Increase aldosterone intake daily, you excrete more K+. ## Footnote Those who start with a high plasma K+ concentration will always have high postassium excretion independent on K+ concentration. why? Aldosterone **increases** K+ Secretion & **K+** Stimulates K+ Secretion **directly**

Question 49

Aldosterone ____ K+ secretion and ____ stimulates K+ secretion ____

Answer 49

Aldosterone **increases** K+ Secretion & **K+** Stimulates K+ Secretion **directly** ## Footnote this is occuring at the distal tubule and cortical collecting duct more K+ in plasma drives K+ pump. K+ pump is more active. incr in K+ secretion

Question 50

What aldosterone stimulate simultaneously?

Answer 50

It simultaneously stimulates Na+ reabsoption and K+ secretion. ## Footnote presecne of aldosterone stimulaates Na+ channel and you have a lot more Na+ comein is, this stimulates the Na+K+ pump and more Na+ is reabsorbed.

Question 51

You have a patient with hypertension who you have been treating with a loop diuretic for 1 month. His initial plasma [K+] was 4.5 mEq/L and has decreased to 3.0 mEq/L. Why would a diuretic cause hypokalemia ?

Answer 51

1. Drugs like furosemie (loop diuretic) i can inhibit the reabsorption of Na+K+and 2Cl- by inhibiting the cotransporters located in the thick ascending limb. K+ would be excreted b/c its not getting reabsorbed 2. Aldosterone can incr Na+ reabsorption and incr K+ secretion 3. Drugs like thiazied can specifically inhibit NaCL cotransporters in the distal convulated tubule. So you see more sodium traveling through the tubule, and once it reaches the distal tubule and cortical collecting duct, Na+ stimulates aldosterone regulation mentioned in number 2. So you see that K+ is stimulated for secretion ## Footnote 1. see an incr of Na+and K+ INSIDE tubule

Question 52

What controls phosphate excretion and Ca2+ absorption?

Answer 52

PTH ## Footnote kidney failure: lots of phosphate buidlup b/c can't get rid of them

Question 53

Mg2+ is absorbed where? Mg2+ excretion of affected by what?

Answer 53

Mg2+ is absorbed in the **TAL** and excretion affected by **diuretics**.

Question 54

Parathyroid Hormone (PTH) ____ reabsorption of phosphate in the ____

Answer 54

Parathyroid Hormone (PTH) **decreases** reabsorption of phosphate in the **proximal tubule** ## Footnote it inhibits the Na+/HPO4-/SO4- co transporter on the lumen side. This INCR excretion when incr Ca2+ is released d/t bone breakdown, concentration HPO4 also incr so needs to be excreted

Question 55

Parathyroid hormone (PTH) ____ calcium reabsorption in the ____

Answer 55

Parathyroid hormone (PTH) **increases** calcium reabsorption in the **DT and CD** ## Footnote incr probabiity of "trippy channel"

Question 56

Besides PTH, what else can incr calcium reabsoprtion in DT?

Answer 56

Vitamin D

Question 57

Active form of Vitamin D is made where?

Answer 57

in the kidneys

Question 58

How is Mg2+ is reabsorbed in the TAL and how is its excretion affected by diuretics?

Answer 58

* Normally: the lumen is neutral bc of Na+ and K+ and 2Cl- being transposrted into the cell (+2-2=0). The Ca2+ and Mg+ which travels paracellualary is not being reabsorbed bc there is no charge from the lumen (no electrical gradient) to drive the paracellular pathway * With dieuretics: The loop dieuretic it incr reabsoprtion of Ca2+ and Mg+ because it inhibits the Na+K+2Cl- contransoprter. There is now a lot of Na+ and K+ sitting in the lumen in addition to the Ca2+ and Mg2+, so there is too many cations (too much positve charge) * Ca2+ and Mg+ now is reabsorbed through paracelleur pathway because there is now an electral gradient.