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Physiology: Exam 3 > Lecture 4: Sodium/Potassium/Electrolytes Balance > Flashcards

Lecture 4: Sodium/Potassium/Electrolytes Balance Flashcards

1
Q

How does changes in GFR affect Sodium (Na+) excretion?

GFR- Glomerular filtration rate

A
  • Decrease in GFR decreases Na+ excretion (increases Na+ reabsorption)

B/c filter less=excrete less

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2
Q

How does changes in blood pressure affect the GFR?

A
  • Decreasing blood pressure causes a decrease in PGC (which is the force driving filtration)
  • ↓BP=↓PGC=↓GFR

GFR=[(PGC-PBC)-πGC]

PGC=Hydrostaic glomerular capillary

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3
Q

True or False. Changes in blood pressure can decrease GFR which then decreases Na+ excretion.

A

TRUE

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4
Q

What is Aldosterone?

A

A steroid hormone excreted from the adrenal gland when Angiotensin II acts on it

Review Slide 6

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5
Q

What is the affect of increased Aldosterone on Na+ reabsorption?

A

Increased Aldosterone increases Na+ reabsorption

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6
Q

Where and how does Aldosterone increase Na+ reabsorption?

HIGH yield

A
  • At the late Distal Tubule and Collecting Duct there are eNaC channels (on lumen side) which are normally closed
  • Aldosterone opens these channels to allow more Na+ into the cell to be absorbed by the capillaries and increase activity of the already present Na+ pump

Review Slide 7

eNaC=epithelial sodium channels

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7
Q

List the 3 ways Aldosterone increases Na+ reabsorption in the late distal tubule and collecting duct

HIGH yield

A
  1. Aldosterone ↑ activity of eNaC channels by causing them to open (on lumen side)
  2. Aldosterone increases the # of Na+ channels present (on lumen side)
  3. Aldosterone ↑ activity of Na+/K+ pump (on the capilly side)
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8
Q

What is Angiotensin II?

A

Vasoconstricting peptide endocrine hormone

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9
Q

How is Angiotensin II produced?

A
  • Angiotensinogen is released from the liver into the vascular tissue
  • Renin is released from the kidney into the vascular tissue
  • Angiotensinogen w/ Renin is converted into Angiotensin I
  • Angiotensin I w/ ACE is then converted into Angiotensin II

Review Slide 9

ACE=Angiotensin Converting Enzyme

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10
Q

What affect does Angiotensin II have on Na+ reabsorption?

A

Angiotensin II increases Na+ reabsorption

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11
Q

List the ways that Angiotensin II increases Na+ reabsorption (4)

A
  1. ↑ Aldosterone
  2. ↓ Kf (surface area)
  3. ↑ Proximal Reabsorption (Na+/K+ exchanger activity)
  4. ↑ Filtration Fraction (FF)
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12
Q

How does Angiotensin II decrease Kf (surface area)?

Kf=filtration coefficient

A
  • Angiotensin II is a vasoconstrictior hormone that decrease surface area by acting on mesangial cell (in the glomerulus)
  • Less surface area decreases GFR, which decreases filtering of Na+
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13
Q

How does Angiotensin II increases Proximal Reabsorption?

A

Increases the Na+/K+ exchanger activity in the proximal tubule to increase Na+ reabsorption

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14
Q

How does Angiotensin II increase FF?

A
  • FF= GFR/RPF
  • Angiotensin II constricts both afferent and efferent arterioles (more effect on the efferent arteriole)
  • This constriction decreases RPF but GFR remains generallly unchaged d/t the stronger affect on the effferent arteriole
  • The ratio of an unchanged GFR and decreased RPF equals increased FF (inverse relationship)

Review Slide 10 of L4 & Slide 28 of L2

FF= Filtration Fraction
GFR= Glomerular Filtration Rate
RPF=Renal Plasma Flow

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15
Q

Why is there an increase in protein osmotic pressure in the Pertibular capillaries?

A

Because of a high FF all the plasma have been filtered out which decreases plasma: protein ratio which increases the oncotic pressure to drive Na+ reabsorption

Review Slide 10

NOTE: efferent arteiole becomes the pertibular capillaries

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16
Q

What is ANP?

A

Atrial natriuretic peptide

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17
Q

What triggers the release of ANP?

A
  • Volume expansion of the heart, specifically the atria will cause atrial streching which indicates high blood pressure
  • Indication of high BP causes the atria to release ANP

Review Slide 12

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18
Q

What are the effects of ANP of the body? (2)

A
  • Vasodilation: ↓ Blood Pressure
  • Increases Na+ and H2O secretion: ↓ BP
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19
Q

List the different types of natriuretic peptides and their location in the body

A
  • ANP: Atria, other tissues
  • BNP (an isoform of ANP): Brain, atria, ventricles
  • CNP (an isoform of ANP): CNS, vasculature
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20
Q

Why is BNP important clinically?

A
  • Important indicator to assess the health of the heart
  • Good index of CHF b/c there will be high levels of it in the blood plasma
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21
Q

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

A

Decreases

Opposite effect of Aldosterone

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22
Q

How does ANP or BNP decrease Na+ reabsorption?

A

In the Collecting Duct, ANP/BNP increases cGMP activity and this inhibits the Na+ channel so less Na+ comes in the cell→↓ Na+ reabsorption (↑Na+ Excretion)

NOTE: NOT the voltage-gated Na+ channels

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23
Q

Actions of Atrial Natriuretic Peptide are mediated by?

A

cGMP

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24
Q

Explain the actions of ANP on factors listed below when there is an expansion of blood volume

  • Atrial Stretch
  • ANP
  • GFR
  • Na+ excertion
  • Aldosterone
  • Blood Pressure
A
  • ↑ Atrial Stretch
  • ↑ ANP
  • ↑ GFR
  • ↑ Na+ excertion
  • ↓ Aldosterone
  • ↓ Blood Pressure

Review Slide 15

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25
Q

A decrease in protein osmotic pressure leads to what?

A
  • Increases Na+ Excretion
    (glomerulus)
  • Remember: GFR = Kf [PGC - PBC) - πGC]
  • ↓ πGC→more leaky capillaries allowing more filtrate out
  • ↓ πGC=↑GFR=↑ Na+ excretion

Review Slide 17

26
Q

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

A

It lowers osmotic pressure in the PT capillary so less Na+ is reabsorbed back into the capillary which causes an increase in Na+ excretion

Review Slide 18

Less Na+ reabsprtion b/c ↓π wants to get rid of H2O and Na+

27
Q

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

A

It increases Na+ reabsoprtion

28
Q

Sympathetic innervation increases Na+ reabsorption through which structures?

A
  1. Arterioles
  2. JG cells
  3. Kf (surface area)
  4. Tubule
29
Q

How does sympathetics (norepi or epi) increase Na+ reabsorption through the tubule?

A

it increases the active Na/K APTase by activating PP1 and thus increase Na reabsorption.

Angiotensin 2 has a similar effect but different receptor

30
Q

Increased blood flow to cortex results in?

A

Increased Na+ excretion

31
Q

Is the juxtamedullary nephron salt-sparing or salt-wasting? and explain why?

A
  • Salt-sparing
  • B/c it of a longer loop of Henle w/ increased SA which is more efficient in Na+ reabsorption
32
Q

Is the cortical nephron salt-sparing or salt-wasting? and explain why?

A
  • Salt-wasting
  • B/c of shorter tubule w/ decreased SA less efficient for Na+ reabsorption
33
Q

What is pressure natriuresis/diuresis and what is it caused by?

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

Review Slide 23

34
Q

Explain how inhibition of Na+ and H2O in the proximal tubule causes pressure natriuresis/diuresis

A

In the range of autoregulation

  • there is a wide range of change (increase) in arterial pressure
  • no change in RBF or GFR
  • NO autoregulation of urine outflow leading to a large increase in urine outflow

Review Slide 23

35
Q

What is the curve?and what is it showing

A
  • Normal Renal Function Curve
  • if you have some Na+ or H2O retention this can make your BP increase pass the equilibrium point
  • Then your kidney reacts, so you see increase excretion of H2O and salt (outake>intake) to lower back to equilibrium
36
Q

What does this graph?

A
  • Renal functional curve of someone with hypertension. The curve shifted to the right, so their equiibrium point increases
  • Pts with HTN have to operate in high BP in order to achieve that equilibrium
37
Q

What is Liddle syndrome?

A

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

Review Slide 28

38
Q

What causes Liddle syndrome?

A
  • 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 reabsorption.
  • The increased sodium reabsorption leads to hypertension

Review Slide 28

39
Q

Review: ADH ____ tubular permeability to water

A

Increases

Review Slide 32

40
Q

Primary control of H2O excretion is by ____.

A

ADH

41
Q

What is the exception for the control of H2O excretion?

A

Osmotic diuersis

42
Q

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

Increased solute excretion nearly always results in what?

A
  • The reabsorption of water is dependent on the reabsorption of solutes (not of water)
  • Increased solute excretion nearly always results in increased urine flow
42
Q

Give an example of osmotic diuresis, and explain what occurs

A

Diabetes: so much glucose is being processed through the tubule and it cannot reabsorb all of it so by the time it leaves the proximal tubule, glucose is left behind (b/c receptors are saturated) and its excreted in urine.
B/c glucose has high osm, when you increase glucose you take H2O with it.

43
Q

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

A

NO

The reabsorption of water is dependent on the reabsorption of solutes.

44
Q

What stimulates and inhibits ADH secretion/release?

A
  1. Stimulated by: ATII
  2. Inhibited by: ANP

Review Slide 35

Secretion of ADH is stimulated by physiological factors, other hormones and drugs

45
Q

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 ?

A
  • Potassium Intake = 100 mmoles/day
  • Potassium Excretion = 100 mmoles/day (90% urine 10% feces)
  • Lost 21 mmol

Remember: intake=output; Pt lost plasma K+ so ECF lost, ICF unchanged

46
Q

100% of the filtered K+ is reabsorbed by what segment of the nephron?

A

the beginning of the distal tubule

47
Q

Where is the location of primary K+ secretion?

A

Late distal and collecting duct

48
Q

What is the effect of aldosterone intake on potassium excretion?

A
  • Increase aldosterone intake daily, you excrete more K+
  • Those who start with a high plasma K+ concentration will always have high postassium excretion independent on K+ concentration.
  • B/c Aldosterone increases K+ Secretion & K+ Stimulates K+ Secretion directly
49
Q

Alodsterone ____ K+ secretion and ____ stimulates K+ secretion ____

A

Increases, directly

50
Q

Where is the effects of aldosterone occuring?

A

The distal tubule and cortical collecting duct (more K+ in plasma drives K+ pump. K+ pump is more active→increase in K+ secretion)

Review Slide 41

51
Q

What does aldosterone stimulate simultaneously? and explain how?

A
  • It simultaneously stimulates Na+ reabsorption and K+ secretion
  • Presence of aldosterone stimulates the Na+ channel and you have a lot more Na+ come in, this stimulates the Na+/K+ pump and more Na+ is reabsorbed.

Review Slide 41

52
Q

Why would a diuretic (ex. furosemide) cause a hypokalemia?

Hypokalemia= too little K+

A
  1. Drugs like Furosemide (loop diuretic) can inhibit the reabsorption of Na+/K+/2Cl- by inhibiting the cotransporters located in the thick ascending limb.
  2. Also w/ ↑ Na+/K+ excretion, too much Na+ will be absorbed and cause more K+ excreted @ the collecting duct
  3. Drugs like Thiazide. 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 (↑ Na+ reabsorption & ↑K+ secretion)

Review Slide 43

At DCT, ↑[Na+] excretion leads to the same effect in CT

53
Q

What can be used to prevent hypokalemia?

A

Drugs like Spironolactone to inhibit aldosterone at collecting duct

54
Q

What controls phosphate (HPO4-) excretion and Ca2+ absorption?

A

Parathyroid hormone (PTH)

NOTE: kidney failure-lots of phosphate buidlup b/c can’t get rid of them

55
Q

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

A

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

TAL=Thick Ascending Limb

56
Q

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

A

Parathyroid Hormone (PTH) decreases reabsorption of phosphate in the proximal tubule

it inhibits the Na+/HPO4-/SO4- co transporter on the lumen side. This increases excretion

57
Q

Parathyroid hormone (PTH) ____ calcium reabsorption in the ____

A

Parathyroid hormone (PTH) increases calcium reabsorption in the DT and CD

increases probabiity of “trippy channel”

58
Q

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

A

Vitamin D

59
Q

Active form of Vitamin D is made where?

A

in the kidneys

60
Q

How is Mg2+ and Ca2+ reabsorbed in the TAL and how is its excretion affected by diuretics

TAL=Thick Ascending Limb

A

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 increases 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, 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.

Review Slide 49

Physiology: Exam 3 (10 decks)

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