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ATSU - DeBoer > Physiology 2: Renal Handling of Electrolytes > Flashcards

Physiology 2: Renal Handling of Electrolytes Flashcards

Covers pages 38-53 in the Renal Handout.

1
Q

Explain the load-dependent phenomenon known as glomerulotubular balance.

A

Despite fluctuations in GFR, a fairly constant fraction (~65%) of the filtered Na and Water is reabsorbed in the proximal tubule.

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2
Q

When might someone have an increased filtered load and increased excreted load of Na?

A

Hypervolemic state; secondary to higher GFR.

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3
Q

When might someone has a decreased filtered load and decreased excreted load of Na?

A

Hypovolemic state; decreased GFR.

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4
Q

What 2 things can stimulate the Na+-H+ exchanger?

A

Stimulation by Angiotensin II as well as Sympathetics.

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5
Q

Explain Cl-driven Na_ reabsorbtion

A

Since other anions are preferentially used in the proximal proximal tubual this creates an increased and favorable gradient in the distal proximal tubual for Cl to be the major Anion and help drive Na+ absorption. Also helps maintain electronutrality.

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6
Q

Characteristics of THIN DESCENDING limb of loop of Henle, what is it permeable to and impermeable to? Result?

A
  • Tubular fluid entering the loop is isotonic.
  • It is permeable to water
  • It is IMPERMEABLE to solutes.

Therefore, water leaves and the tubular fluid OSMOLALITY INCREASES distally.

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7
Q

Characteristics of THIN ASCENDING limb of loop of Henle, what is it permeable to and impermeable to? Result?

A
  • IMPERMEABLE to water
  • permeable to solutes
  • Passive diffusion of
  • -NaCl “out”
  • -Urea “in”

Results in progressively more dilute tubular fluid (decreasing osmolality).

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8
Q

Characteristics of THICK ASCENDING limb of loop of Henle, what is it permeable to and impermeable to? Result?
What can stimulate or inhibit absorption here?

A

-Impermeable to water

  • *Na-K-2Cl pump
  • K is recycled
  • -net Na-2Cl reabsorption

Lumen “+” potential promotes reabsorption of Na+, Ca++, and Mg++ via the paracellular route.

Stimulated by ALDO and ADH
Inhibited by loop diuretics (lasix)

Na-H exchanger

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9
Q

Characteristics of DISTAL TUBULE, what is it permeable to and impermeable to? Result?

A
  • Na-CL co-transporter
  • NaK-ATPase

Impermeable to water - fluid becomes even more dilute

Blocked by thiazide diuretics (HCTZ)

Important in Ca++ reabsorption.

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10
Q

What types of diuretics (loop or distal tubule) are more efficacious and why?

A

Loop diuretics since there is more Na+ in the loop than in the distal tubule.

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11
Q

Characteristics of Collecting Ducts, what is it permeable to and impermeable to? Result?

A

Na and K channels present (passive movement)

NaK-ATPase

Rapid Na entry that produces a “-“ lumen potential that:

  • promotes K+ secretion
  • promotes Cl- reabsorption (paracellular pathway)

Stimulated by Aldosterone
Blocked by “K-sparring diuretics”

ADH sensitive region
-increases permeability to water

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12
Q

If you are reabsorbing Na+ what ion are you likely secreting?

A

K - potassium.

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13
Q

Aldosterone Effects in Principal Cells in Collecting Ducts:

A

Aldosterone:

  • increased Na+ reabsorption
  • increases K+ secretion
  • increases Cl- reabsorption
  • increases H+ secretion
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14
Q

Characteristics of Medullary Collecting Ducts, what is it permeable to and impermeable to? Result?

A

Functions parallel to the Cortical Collecting Ducts.

ALDO sensitive:

  • NA/Cl reabsorption
  • K/H secretion

ADH sensitive

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15
Q

Hypervolemia; definition, effects on secretion and other systems/factors

A

Increased ECBV
(-) RAAS
(+) ANP, BNP, Urodilatin

Na and water excretion increases but no change in osmolality.

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16
Q

Hypovolemia; definition, effects on secretion and other systems/factors

A

Decrease ECBV
(+) RAAS
(+) sympathetic

Na and water excretion decreases but no change in osmolality.

17
Q

Hypernatremia; definition, effects on secretion and other systems/factors

A

Increased plasma [Na]
(+) ADH release

excretion of free water decreases and plasma osmolality decreases

18
Q

Hyponatremia; definition, effects on secretion and other systems/factors

A

Decreased plasma [Na]
(-) ADH release

excretion of free water increases and plasma osmolality increases

19
Q

Primary stimuli for aldosterone release (4), and what can suppress it:

A
    1. Angiotensin II - increases in hypovolemic states and results in release of renin
    1. Hyperkalemia - K+ has a direct effect on zone glomerulosa cells of the adrenal to increase aldosterone release
      1. Hyponatremia - weak stimulus
      2. ACTH (Adrenocorticotrophic hormone) - weak stimulus

ANP and Dopamine can suppress Aldosterone secretion.

20
Q

Mechanisms of aldosterone action on the COLLECTING TUBULES (4): Net effect on Na, other effects on K+ and H+

A
  1. Increases NaK-ATPase activity
  2. Increases synthesis and insertion of Na+ channels
  3. Increases the provision of energy for active transport
  4. **The net effect is an increase in Na+ REABSORPTION

Increases K+ SECRETION from principal cells
Increases H+ SECRETION from intercalated cells

21
Q

Effects of increased Na+ intake:

A

Increases urine Na+
Decreases plasma renin
Decreases aldosterone
Increases ECBV

22
Q

Effects of decreased Na+ intake:

A

Decrease urine Na+
Increase plasma renin
Increase aldosterone
Decreases ECBV

23
Q

GFR effects on Na+ excretion:

A

Increased GFR = increased Na excretion

Decreased GFR = decreased Na excretion

24
Q

What is ANP, where does it come from and what is it a result of?
What are it’s effects?

A

ANP = Atrial natriuretic peptide

Released from myocytes in right atrium as a result of expansion of the vascular volume (low pressure centers).

Causes afferent arteriolar vasodilation (increased GFR but decreased FF)
Decreases peritubular capillary reabsorption
Inhibits Na+ reabsorption in collecting ducts

Inhibit ADH release, results in increased water secretion.

25
Q

What is BNP, where does it come from and what is it a result of?
What are it’s effects?

A

BNP = B-Type natriuretic peptide

Released from myocytes in right ventricle as a result of expansion of the vascular volume.

Causes afferent arteriolar vasodilation (increased GFR but decreased FF)
Decreases peritubular capillary reabsorption
Inhibits Na+ reabsorption in collecting ducts

Inhibit ADH release, results in increased water secretion.

26
Q

What is Urodilatin, where does it come from and what is it a result of?
What are it’s effects?

A

Hormone, secreted by distal tubule and collecting tubule of nephron.

Inhibits Na_ and water reabsorption in the collecting tubules/ducts.
Results in natriuresis and diuresis.

Activity is correlated with hypervolemia.

27
Q

What are the affects of Endogenous digitalis-like hormone? When is it secreted?

A

Levels increased as a response to volume expansion.

Reduces NaK-ATPase activity, thus decreases Na+, solute, and water reabsorption.

28
Q

Function of Norepinephrine and Angiotensin II in kidney:

A

Exert direct effects on proximal ruble that increase Na+ and water reabsorption.

Angiotensin II also stimulates that Na+/H+ exchanger via increased NaK-ATPase activity.

29
Q

Understand renin-angiontensin system in Na+ volume regulation; what causes release?

A

Precieved hypovolemia by juxtoglumulerular cells and this causes release of Renin.

Stimulation of B1 adrenergic receptors also causes renin release.

Renin catalyzes the conversion of angiotensinogen to angiotensin 1.

30
Q

Angiotensin II functions (10):

A
  1. Stimulates aldosterone secretion to increase Na+ and water reabsorption
  2. Causes systemic vasoCONSTRICTION to increase BP
  3. Stimulates thirst to increase water intake
  4. Stimulates ADH release to increase distal nephron H20 absorb.
  5. Causes greater vasoconstriction of efferent arterioles (compared to afferent)
    - -decrease RBF, helps maintain GFR, increases FF
  6. enhances norepinephrine biosynthesis
  7. Vasoconstriction in outer cortical afferent arterioles, shunts blood to JM nephrons w/ greater reabsorbtive capacity.
  8. Stimulates prostaglandin production to prevent over-vasoconstriction.
  9. Stimulates Na reabsorption
  10. Inhibits renin secretion (negative feedback)
31
Q

Things that increase Na excretion:

A 
Osmotic diuresis
Impairment anions in the filtrate (diffusion trapped)
Aldosterone deficit
--hypovolemia
--hyperkalemia
--metabolic acidosis
32
Q

Things the decrease Na excretion

A

Aldosterone excess

  • -hypervolemia
  • -hypokalemia
  • -metabolic alkalosis

Aldosterone escape?

33
Q

Low oncotic pressure causes and the net effect of it.

A

Cirrhosis - decrease in production of plasma proteins
Nephrotic syndrome: loss of protein in urine

-leads to decreased oncotic pressure and edema formation, eventually looks like a hypovolemia

ATSU - DeBoer (43 decks)

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