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Renal Electrolyte Regulation Flashcards

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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
Hyperosmolarity can be a cause of (hypokalemia/hyperkalemia) .
Hyperkalemia
26
A person is in potassium when the excretion of potassium equals intake of potassium
Balance
27
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.
Increases
28
The and collecting duct are the parts of the nephron that adjust the potassium excretion to maintain potassium balance.
Late Distal Tubule
29
The secretion and synthesis of aldosterone is the result of angiotensin II activation of G protein-coupled angiotensin type receptors.
1
30
The renal mechanisms that allow to keep a constant extracellular potassium concentration are called .
External Potassium Balance
31
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 .
Potassium
32
Hypoaldosteronism causes (increased/decreased) potassium secretion from principal cells.
Decreased
33
Beta-2 adrenergic antagonists can cause (hypokalemia/hyperkalemia) .
Hyperkalemia
34
Antidiuretic hormone activation of vasopressin 2 receptors on the principal cells of the renal increases water reabsorption and maintenance of body fluid osmolarity.
Collecting Ducts
35
Insulin deficiency, as in type 1 diabetes, can be a cause of (hypokalemia/hyperkalemia) .
Hyperkalemia
36
If potassium excretion is less than intake, a person is in potassium balance and hyperkalemia can occur.
Positive
37
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.
Electrochemical
38
Excess of insulin can cause (hypokalemia/hyperkalemia) .
Hypokalemia
39
Excretion of potassium from the nephron is (fixed/variable)
Variable
40
Alpha adrenergic agonists can cause (hypokalemia/hyperkalemia) .
Hyperkalemia
41
High sodium diets lead to increased sodium delivery to principal cells and consequently to (increased/decreased) potassium excretion.
Increased
42
If potassium excretion surpasses potassium intake, a person is in potassium balance and hypokalemia can occur.
Negative
43
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.
Proximal
44
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.
Into
45
The extracellular concentration of potassium is (high/low)
Low
46
Exercise can be a cause of (hypokalemia/hyperkalemia) , especially in people taking beta 2 adrenergic antagonists or with impaired renal function.
Hyperkalemia
47
Renin-angiotensin II-aldosterone system is (activated/deactivated) when mechanoreceptors in the afferent arterioles of the kidney senses a decrease in renal perfusion pressure.
Activated
48
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.
Hydrogen Potassium ATPase
49
increases the number of potassium channels on the luminal membrane of principal cells in the nephron.
Aldosterone
50
(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.
Acidosis
51
The thick ascending limb of the loop of Henle reabsorbs % of the filtered load of potassium.
20
52
Potassium (is/is not) part of the body’s buffer system.
IS
53
Angiotensin II acts on the zona of the adrenal cortex to stimulate the secretion and synthesis of aldosterone.
Glomerulosa
54
Respiratory acidosis and respiratory alkalosis typically (do/do not) cause potassium shifts.
Do NOT
55
The alpha intercalated cells of the late distal tubule and collecting duct are responsible for potassium (reabsorption/secretion) .
REABSORPTION
56
Phosphate is an important constituent of bones and also serves as a urinary buffer for .
Hydrogen ions
57
About % of phosphate in the blood is protein bound.
10 %
58
Phosphate reabsorption in the nephron (is/is not) saturable.
Is
59
The hormone that regulates phosphate reabsorption in the proximal tubule is .
Parathyroid Hormone (PTH)
60
Parathyroid hormone inhibits phosphate reabsorption by binding to a receptor on the (part of the nephron) .
PCT
61
Of the filtered magnesium, % is then reabsorbed by the kidneys.
95%
62
Around % of the filtered phosphate is reabsorbed by the proximal convoluted tubule.
70%
63
5% of magnesium is reabsorbed in the (part of the nephron) .
Distal Tubule
64
The major part of phosphate is localized in the , with the remainder divided between the intracellular and the extracellular compartments.
BONE MATRIX
65
In the intracellular compartment, phosphate is a component of nucleic acids, high-energy molecules like and metabolic intermediates.
Adenosine Triphosphate
66
% of the filtered magnesium is reabsorbed by the proximal tubule.
30%
67
Increased urinary cyclic adenosine monophosphate and phosphaturia are signs of the action of (hormone) .
PTH
68
% of plasma magnesium is bound to proteins.
20 %
69
In the proximal convoluted tubule, phosphate is reabsorbed by (passive/active) transport.
Active
70
Magnesium reabsorption by the (part of the nephron) is driven by the lumen-positive potential difference.
Thick Ascending Loop of Henle
71
The phosphate not reabsorbed from the nephron serves as a urinary buffer for .
Hydrogen Ions
72
% of the filtered phosphate is excreted.
15 %
73
Of the phosphate that is not bound to plasma proteins, % of it is filtered across the glomerular capillaries.
90%
74
The (part of the nephron) is the major site of magnesium absorption.
Thick Ascending Loop of Henle
75
, by blocking sodium-phosphate cotransport in the proximal tubule, causes phosphaturia.
PTH
76
% of the filtered phosphate is reabsorbed in the proximal straight tubule.
85%

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