Brainscape's Knowledge GenomeTM

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


See full index

Renal Exam 2 > Regulation of Solutes/Ions > Flashcards

Regulation of Solutes/Ions Flashcards

1
Q

Renal Control of Potassium

-Results?

A

Changes in cardiac function, ECG changes

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

Effects on K concentration on ECGs

A

Slide 10

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

Factors affecting movement on K+ between intracellular and extracellular pools
-ICF (cells)–> ECF (movement out of cells)

A
  • Hypokalemia
  • Acidemia
  • Ischemia (cell damage)
  • alpha-adrenergic agonists
  • Heavy exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Factors affecting movement on K+ between intracellular and extracellular pools
-ECF–> ICF (cells) (movement into cells)

A

Hyperkalemia
Alkalemia
Beta-adrenergic agonists
Insulin

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

Factors affecting movement on K+ between intracellular and extracellular pools
-ECF–> ICF (cells) (movement into cells)-Hyperkalemia is seen in patients with what common disease?

A

Diabetes

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

When a patient is alkalotic, what is happening to:

  • H?
  • Na, K?
A

-H+ is being pumped out of the cells (to compensate for the decreased H+ in the ECF)
-Na and K are being pumped into the cells
(opposite for acidotic)–>hypokalemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Renal tubular handling of K

-Where is it reabsorbed?

A

-Mostly in the PT but also in the thick ascending limb via the Na, K, 2Cl cotransporter)

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

Renal tubular handling of K

-Where is physiological control exerted?

A
  • In the CD

- Principal cells either reabsorb or secrete K depending on body’s K balance

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

Five factors which affect K secretion in CD?

A
  • Extracellular K concentration
  • Na reabsorption
  • Luminal fluid flow rate (Na and water delivery)
  • Extracellular pH
  • Aldosterone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Five factors which affect K secretion in CD

-Na reabsorption?

A

Negative luminal voltage ‘attracts’ K

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

Five factors which affect K secretion in CD?

-Luminal fluid flow rate?

A

Dilution of secreted K resulting in conc gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Five factors which affect K secretion in CD?

-Extracellular pH?

A

K and H exchange across cell membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Five factors which affect K secretion in CD?

-Aldosterone?

A

Stimulates K secretion in CD to maintain electroneutrality when Na is reabsorbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

General rule of thumb

-Out of Na, H, and K-When one of these three is being absorbed?

A

The other 2 are going out of the cell to balance it out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What happens to urinary K excretion as plasma K concentration increases?

A

Urinary K excretion increases

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

Tubular flow rate affects K secretion in the distal nephron (graph)
-Patients on loop diuretics sometimes need to be supplemented with?

A

Potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Situations that alter K handling

-MOA of most diuretics?

A

Most classes of diuretics increase Na and volume delivery to late DT and CD which increases K secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Situations that alter K handling

-Low sodium diet?

A

Less Na delivery to late DT, CD–> less K excretion–>may cause hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Clinical application-How might hyperkalemia be treated?

A
  • By increasing downstream delivery of Na to the DT/CD

- Results in increased Na reabsorption and K secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Amount of potassium secreted in an acidotic patient versus an alkalotic patient?

A

An acidotic patient would secrete less potassium than normal (opposite for alkalotic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Effect of aldosterone on K?

A

Aldosterone stimulates K secretion in DT and CD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Effect of increased plasma K concentration on aldosterone?

A

Increased plasma concentration stimulates aldosterone secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

2 main presenting symptoms of hyperaldosteronism (Conn’s syndrome)?

A

Hypokalemia and metabolic alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What would be the plasma Na of a patient with hyperaldosteronism?

A

It would be normal or on the high end of normal (not extremely high) because water is being absorbed along with the sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Disorders of aldosterone secretion

  • Primary hyperaldosteronism (Conn’s syndrome)
    • Due to?
    • What happens to K secretion?
    • Consequence?
A
  • Aldosterone secreting tumor in adrenal cortex

- Inappropriately stimulated K secretion–>hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Disorders of aldosterone secretion

  • Hypoaldosteronism (Addison’s disease)?
    • Caused by?
    • What happens to K secretion?
    • Consequence?
A
  • Destruction of adrenals (no aldosterone secreted)

- Decreased K secretion in CD–>hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Disorders of aldosterone secretion

  • Hypoaldosteronism (Addison’s disease)
    • What would the sodium level be?
A

Low sodium level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Practice on slide 28

A

!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Diuretics

-What are they?

A

Drugs that increase urine excretion by inhibiting tubular solute and water reabsorption (increasing excretion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Diuretics

-Purpose?

A

To help eliminate excess volume to treat volume overload disorders (e.g. edema, CHF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Different classes of diuretics

  • Osmotic diuretics
    • MOA?
    • Example?
A
  • Inhibit reabsorption of water and, secondarily, Na

- Example-mannitol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Different classes of diuretics

  • Carbonic anhydrase inhibitors
    • MOA?
    • Example?
A
  • Inhibit NAHCO3 reabsorption

- Example-Acetazolamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Where do osmotic diuretics and carbonic anhydrase inhibitors act in the nephron?

A

Proximal tubule

34
Q

Loop diuretics

-Where in the nephron do they act?

A

Loop diuretics act at the loop of Henle

35
Q

Loop diuretics

-MOA?

A
  • Inhibit Na, K, 2Cl cotransporter by competing for Cl
  • Increases total RBF and dissipates high solute concentration of medullary interstitium
  • Lessens water reabsorption in descending limb and medullary CD
36
Q

Loop diuretics

-Caveat?

A

Powerful: require careful medical supervision

37
Q

Loop diuretics

-Examples?

A

Furosemide (lasix), bumetanide (bumex), ethacrynic acid

38
Q

Thiazide diuretics

-Where do they act in the nephron?

A

DCT

39
Q

Thiazide diuretics

-MOA?

A
  • Inhibit Na, Cl cotransport
  • Increase Na, Cl, and K excretion
  • Results in decreased Ca excretion
40
Q

Thiazide diuretics

-Example?

A

Hydrochlorothizazide

41
Q

“Potassium-sparing” diuretics

-Where do they act in the nephron?

A

Collecting duct

42
Q

“Potassium-sparing” diuretics

- MOA?
- Often used in combination with?
A
  • Inhibit Na reabsorption and K secretion

- Often used in combination with other diuretic classes that increase K excretion

43
Q

“Potassium-sparing” diuretics

-Examples?

A

-Amiloride, triamterene, spironolactone

44
Q

“Potassium-sparing” diuretics

-Triamtrene-MOA?

A

Blocks Na channels

45
Q

“Potassium-sparing” diuretics

-Spironolactone-MOA?

A

Aldosterone antagonist

46
Q

Summary of diuretics

A

Slide 34

47
Q

Renal control of Calcium

-Importance of EC Ca?

A
  • Affects activity of excitable tissues: nerve, muscle, myocardium
  • Enzyme cofactor, component of bone, cell signaling, blood clotting
48
Q

Ca can damage action potentials by?

A

-Ca can dampen action potentials by blocking Na channels

49
Q

Renal Control of Potassium

-What are the effects of extracellular K concentration?

A

Extracellular K concentration affects membrane potential and excitability of muscle and nerve tissue

50
Q

Low EC Ca can induce?

A

Hypocalcemic tetany

51
Q

Ca is required for?

A

Neuromuscular transmission

52
Q

Active vs inactive Ca?

A
  • 45% of plasma Ca is protein-bound-inactive

- ONLY free Ca is biologically active

53
Q

What is the Ca concentration in Bowman’s capsule? Why?

A

Only half of Ca in blood can be filtered because half of Ca is protein bound and proteins cannot be filtered through the glomerulus

54
Q

Effect of plasma pH on free Ca?

A

H compete with Ca for binding sites on plasma proteins

55
Q

Acidemia-increased H–>?

A

Increased free Ca in plasma (opposite for alkalemia)

56
Q

Patient with acidosis is at risk for?

A

Hypercalcemia (alkalotic patient is at risk for hypocalcemia)

57
Q

How does EC Ca affect the myocardium?

A

Affects contractile strength

58
Q

Hypocalcemia-What does PTH do when released:

-3 MOA?

A
  • Causes the kidneys to activate vitamin D (calcitriol)
  • Causes GI tract to reabsorb more Ca from diet
  • Causes resorption of bone by osteoclastic activity
59
Q

Where is the majority of Ca reabsorbed?

A

PCT

60
Q

Mechanism of PT Ca reabsorption

-2 routes?

A
  • Paracellular-between the cells

- Transcellular-intracellular calcium is very low compared to tubular fluid-goes down concentration gradient

61
Q

Paracellular Ca reabsorption in thick ascending limb of Henles loop
-Driven by?

A

Positive transepithelial potential

62
Q

Paracellular Ca reabsorption in thick ascending limb of Henles loop-Driven by positive transepithelial potential
-What effects will loop diuretics have on this process?

A

Abolishes the positive transepithelial potential and the reabsorption of Na, K, Ca, Mg and NH2 decreases
-This is why loop diuretics are so powerful-gets rid of a lot of different electrolytes

63
Q

Reabsorption of which ions are particularly dependent on the positive transepithelial potential?

A

Ca and Mg

64
Q

Transcellular Ca reabsorption in distal tubular cells (explained in lecture)

A
  • Epithelial calcium channels are vitamin D dependent
  • So when PTH is released and vitamin D is activated it activates these channels to reabsorb Ca into the cell
  • Once in the cell, Ca binds to calbindin and is then reabsorbed into the capillary via Ca ATPase and/or Ca, Na exchanger
65
Q

Hypocalcemia-Parathyroid gland senses this

-What does parathyroid gland do?

A

-When parathyroid gland senses low Ca it releases PTH

66
Q

Patients on thiazide diuretics are at risk for?

A

Hypercalcemia

67
Q

Physiological control of tubular Ca reabsorption

-Where in the nephron is control exerted?

A

Control is exerted in the thick ascending limb and DCT

68
Q

Physiological control of tubular Ca reabsorption

-Reabsorption is stimulated by?

A

PTH, calcitriol (vit. D3), and calcitonin

69
Q

Physiological control of tubular Ca reabsorption

-Decreased plasma Ca induces cells parathyroid gland to?

A

secrete PTH

70
Q

Overall effect of PTH?

A

Increase EC Ca

71
Q

As plasma Ca increases, what happens to PTH?

A

Decreases

72
Q

As Plasma Ca increases, what happens to calcitonin (probably don’t need to know)?

A

Increases

73
Q

PTH and calcitriol flow chart

A

slide 46

74
Q

What can happen to patients with renal disease if it goes on long enough?

A

Since the renal tissue is damaged the kidney is unable to activate vitamin D and inhibits the body’s ability to reabsorb Ca via the tubule
This leads to increased PTH driven resorption of bone and thus the patient’s bones become fibrotic and diseased-secondary hyperparathyroidism

75
Q

Transcellular Ca reabsorption in distal tubular cells

-MOA of thiazide diuretics (from slide)?

A

-Inhibit the Na, Cl symporter in early DCT–>intracellular Na decreases–>enhances activity of Na, Ca exchanger creating an increased driving force for Ca reabsorption and Na excretion

76
Q

Mechanism of proximal tubular phosphate reabsorption

  • How does it get into the cell?
  • How does it get into the blood?
A
  • Most of it is by a sodium cotransporter-depends on sodium gradient-this gets the phosphate into the cell
  • Then it is sent into the blood by an anion counter transporter-anion goes from blood into the cell phosphate goes from cell into blood
77
Q

Proximal tubular phosphate reabsorption

-Reabsorption of phosphate is inhibited by?

A 
PTH-decreases Tm
Increases excretion (decreases absorption)
78
Q

Mg handling by nephron

-Bulk of the filtered Mg is reabsorbed in the?

A

Thick ascending limb (by paracellular movement)

79
Q

How is the transepithelial potential established and how does this apply to Mg reabsorption?

A

By potassium leak channels-positive charge builds up in the tubular urine and drives magnesium between the cells and helps it reabsorb (they repel each other b/c they are like charges)

80
Q

Effect of loop diuretics on the transepithelial potential and their MOA?

A

Increase flow? and decrease the transepithelial potential (pos charge)

81
Q

Renal control of phosphate

-In what part of the nephron is the majority of phosphate reabsorbed?

A

PCT

Renal Exam 2 (6 decks)

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