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Physiology > Renal Electrolyte Regulation > Flashcards

Renal Electrolyte Regulation Flashcards

1
Q

The concentration gradient for potassium is maintained by the , present on all cell membranes.

A

sodium-potassium ATPase

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2
Q

The distribution of potassium across cell membranes is called .

A

Internal Potassium Balance

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3
Q

Hyposmolarity can be a cause of (hypokalemia/hyperkalemia) .

A

Hypokalemia

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4
Q

ACIDOSIS can be a cause of (hypokalemia/hyperkalemia) .

A

HYPERKALEMIA

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5
Q

Beta-2 adrenergic agonists can cause (hypokalemia/hyperkalemia) .

A

Hypokalemia

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6
Q

Most of the total body potassium is located in the (extracellular/intracellular) fluid.

A

intracellular

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7
Q

One of the mechanisms underlying the association between the levels of potassium and the pH of intracellular or extracellular fluid relies on the across cell membranes.

A

Hydrogen Potassium Exchange

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8
Q

increases the number of sodium-potassium ATPases in the principal cells of the nephron.

A

Aldosterone

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9
Q

ALKALOSIS can be a cause of (hypokalemia/hyperkalemia)

A

HYPOKALEMIA

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10
Q

A decrease in blood potassium concentration is called .

A

Hypokalemia

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11
Q

The proximal convoluted tubule reabsorbs about % of the filtered potassium.

A

67%

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12
Q

Potassium (is/is not) freely filtered across the glomerular capillaries.

A

IS

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13
Q

Insulin stimulates potassium uptake by cells by increasing the activity of the .

A

sodium-potassium ATPase

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14
Q

Principal cells of the late distal tubule and collecting duct are responsible for potassium (reabsorption/secretion) through potassium channels.

A

Secretion

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15
Q

Prorenin conversion to renin in the juxtaglomerular cells can be stimulated by a decrease in mean arterial pressure or by beta 1 (antagonists/agonists) .

A

Agonists

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16
Q

Loop diuretics and thiazide diuretics, by inhibiting sodium reabsorption in the first part of the nephron, lead to increased sodium delivery to principal cells and consequently to (increased/decreased) potassium excretion.

A

Increased

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17
Q

The presence of large anions such as sulfate or bicarbonate in the lumen of the distal tubule and collecting duct (increases/decreases) potassium secretion.

A

Increases

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18
Q

Antidiuretic hormone activation of vasopressin 1 receptor (increases/decreases) vasoconstriction of arterioles and total peripheral resistance.

A

Increases

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19
Q

The (organ) is particularly sensitive to potassium levels

A

HEART

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20
Q

The single most important factor influencing potassium secretion into urine from principal cells is the concentration of in the extracellular fluid.

A

Potassium

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21
Q

An increase in blood potassium concentration is called .

A

Hyperkalemia

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22
Q

Cell lysis, as in burns, rhabdomyolysis, or chemotherapy, can be a cause of (hypokalemia/hyperkalemia) .

A

Hyperkalemia

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23
Q

Alpha adrenergic antagonists can cause (hypokalemia/hyperkalemia) .

A

Hypokalemia

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24
Q

Potassium, being a , is released during exercise from muscle cells to increase local blood flow to the skeletal muscle.

A

Vasodilator

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25
Q

Hyperosmolarity can be a cause of (hypokalemia/hyperkalemia) .

A

Hyperkalemia

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26
Q

A person is in potassium when the excretion of potassium equals intake of potassium

A

Balance

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27
Q

Activation of the renin-angiotensin II-aldosterone system by a decrease in mean arterial pressure will lead to a response that (increases/decreases) Na+ reabsorption, blood volume, cardiac output, and total peripheral resistance.

A

Increases

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28
Q

The and collecting duct are the parts of the nephron that adjust the potassium excretion to maintain potassium balance.

A

Late Distal Tubule

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29
Q

The secretion and synthesis of aldosterone is the result of angiotensin II activation of G protein-coupled angiotensin type receptors.

A

1

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30
Q

The renal mechanisms that allow to keep a constant extracellular potassium concentration are called .

A

External Potassium Balance

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31
Q

Aldosterone, by increasing the number of sodium channels on the luminal membrane of principal cells, increases the absorption of sodium and consequently the secretion of .

A

Potassium

32
Q

Hypoaldosteronism causes (increased/decreased) potassium secretion from principal cells.

A

Decreased

33
Q

Beta-2 adrenergic antagonists can cause (hypokalemia/hyperkalemia) .

A

Hyperkalemia

34
Q

Antidiuretic hormone activation of vasopressin 2 receptors on the principal cells of the renal increases water reabsorption and maintenance of body fluid osmolarity.

A

Collecting Ducts

35
Q

Insulin deficiency, as in type 1 diabetes, can be a cause of (hypokalemia/hyperkalemia) .

A

Hyperkalemia

36
Q

If potassium excretion is less than intake, a person is in potassium balance and hyperkalemia can occur.

A

Positive

37
Q

The magnitude of potassium secretion into urine by the principal cells is determined by the size of the gradient for potassium across the luminal membrane.

A

Electrochemical

38
Q

Excess of insulin can cause (hypokalemia/hyperkalemia) .

A

Hypokalemia

39
Q

Excretion of potassium from the nephron is (fixed/variable)

A

Variable

40
Q

Alpha adrenergic agonists can cause (hypokalemia/hyperkalemia) .

A

Hyperkalemia

41
Q

High sodium diets lead to increased sodium delivery to principal cells and consequently to (increased/decreased) potassium excretion.

A

Increased

42
Q

If potassium excretion surpasses potassium intake, a person is in potassium balance and hypokalemia can occur.

A

Negative

43
Q

Angiotensin II will stimulate Na+- H+ exchange in the renal (proximal/distal) tubules and increases the reabsorption of Na+ and HCO3- in order to increase extracellular fluid, blood volume and blood pressure.

A

Proximal

44
Q

When beta 2 agonists activate beta 2 adrenergic receptors, they cause an increase in the activity of the sodium-potassium pump, causing a shift of potassium (into/out of) the cell.

A

Into

45
Q

The extracellular concentration of potassium is (high/low)

A

Low

46
Q

Exercise can be a cause of (hypokalemia/hyperkalemia) , especially in people taking beta 2 adrenergic antagonists or with impaired renal function.

A

Hyperkalemia

47
Q

Renin-angiotensin II-aldosterone system is (activated/deactivated) when mechanoreceptors in the afferent arterioles of the kidney senses a decrease in renal perfusion pressure.

A

Activated

48
Q

Alpha-intercalated cells of the late distal tubule and collecting duct contain a(n) , the primary active transport mechanism used to reabsorb potassium from urine.

A

Hydrogen Potassium ATPase

49
Q

increases the number of potassium channels on the luminal membrane of principal cells in the nephron.

A

Aldosterone

50
Q

(Acidosis/alkalosis) decreases potassium excretion from principal cells of the distal convoluted tubule and collecting duct by reducing the activity of the sodium-potassium ATPase pump.

A

Acidosis

51
Q

The thick ascending limb of the loop of Henle reabsorbs % of the filtered load of potassium.

A

20

52
Q

Potassium (is/is not) part of the body’s buffer system.

A

IS

53
Q

Angiotensin II acts on the zona of the adrenal cortex to stimulate the secretion and synthesis of aldosterone.

A

Glomerulosa

54
Q

Respiratory acidosis and respiratory alkalosis typically (do/do not) cause potassium shifts.

A

Do NOT

55
Q

The alpha intercalated cells of the late distal tubule and collecting duct are responsible for potassium (reabsorption/secretion) .

A

REABSORPTION

56
Q

Phosphate is an important constituent of bones and also serves as a urinary buffer for .

A

Hydrogen ions

57
Q

About % of phosphate in the blood is protein bound.

A

10 %

58
Q

Phosphate reabsorption in the nephron (is/is not) saturable.

A

Is

59
Q

The hormone that regulates phosphate reabsorption in the proximal tubule is .

A

Parathyroid Hormone (PTH)

60
Q

Parathyroid hormone inhibits phosphate reabsorption by binding to a receptor on the (part of the nephron) .

A

PCT

61
Q

Of the filtered magnesium, % is then reabsorbed by the kidneys.

A

95%

62
Q

Around % of the filtered phosphate is reabsorbed by the proximal convoluted tubule.

A

70%

63
Q

5% of magnesium is reabsorbed in the (part of the nephron) .

A

Distal Tubule

64
Q

The major part of phosphate is localized in the , with the remainder divided between the intracellular and the extracellular compartments.

A

BONE MATRIX

65
Q

In the intracellular compartment, phosphate is a component of nucleic acids, high-energy molecules like and metabolic intermediates.

A

Adenosine Triphosphate

66
Q

% of the filtered magnesium is reabsorbed by the proximal tubule.

A

30%

67
Q

Increased urinary cyclic adenosine monophosphate and phosphaturia are signs of the action of (hormone) .

A

PTH

68
Q

% of plasma magnesium is bound to proteins.

A

20 %

69
Q

In the proximal convoluted tubule, phosphate is reabsorbed by (passive/active) transport.

A

Active

70
Q

Magnesium reabsorption by the (part of the nephron) is driven by the lumen-positive potential difference.

A

Thick Ascending Loop of Henle

71
Q

The phosphate not reabsorbed from the nephron serves as a urinary buffer for .

A

Hydrogen Ions

72
Q

% of the filtered phosphate is excreted.

A

15 %

73
Q

Of the phosphate that is not bound to plasma proteins, % of it is filtered across the glomerular capillaries.

A

90%

74
Q

The (part of the nephron) is the major site of magnesium absorption.

A

Thick Ascending Loop of Henle

75
Q

, by blocking sodium-phosphate cotransport in the proximal tubule, causes phosphaturia.

A

PTH

76
Q

% of the filtered phosphate is reabsorbed in the proximal straight tubule.

A

85%

Physiology (98 decks)

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