Electrolyte Disorders Flashcards

boards and beyond (20 cards)

1
Q

Which of the following electrolyte abnormalities is most likely to be responsible for this patient’s presentation?

A

This patient’s ECG is remarkable for tall, “peaked” T-waves in the anterior and lateral precordial leads (V3-V6). Tall T-waves are a typical ECG finding in hyperkalemia and can occur with serum potassium greater than 5.5 mEq/L (normal 3.5-5).

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2
Q

How Abnormal levels of magnesium can affect both potassium and calcium. . Magnesium is required for the proper functioning of this protein. .

A

For calcium, severe magnesium depletion can result in improper functioning of the CaSR (calcium-sensing receptor) channel, a membrane protein receptor on the surface of chief cells in the parathyroid gland.

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3
Q

Abnormal functioning of this channel, as seen in hypomagnesaemia, causes

A

reduced PTH release leading to hypocalcemia

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4
Q

Slightly reduced magnesium acts similarly to calcium at the CaSR, triggering PTH release from the parathyroid glands.

A

This results in mild hypercalcemia rather than hypocalcemia.

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5
Q

Loop diuretics ……………….. (not activate) the Na-K-2Cl transporter in the thick ascending limb of the loop of Henle. This inhibition can lead to …………………………….

A

inhibit
hypocalcemia and hypomagnesemia

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6
Q

How is classified albuterol

A

beta-2 agonist

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7
Q

Large amounts of inhaled albuterol can cause

A

Hypokalemia

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8
Q

Drugs that cause excessive …………. or ……………. can result in hypokalemia. In addition, any state associated with …………… levels can cause hypokalemia due to increased renal potassium secretion

A

Diuresis , diarrhea
high aldosterone

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9
Q

This woman is experiencing perioral and acral (i.e. hand, foot, ear, nose) paresthesias, along with tetany (muscle twitching). These are common clinical manifestations of hypocalcemia.

A

hypocalcemi

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10
Q

Hypocalcemia has a variety of etiologies including .

A

hypoparathyroidism, renal failure, and certain medications.

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11
Q

Patients that undergo large blood transfusions are at risk

A

citrate-induced hypocalcemia.

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12
Q

.Magnesium normally………………. the ROMK (RenalOuterMedullaryPotassium) potassium channel in the renal collecting duct.

A

inhibits

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13
Q

Low levels of magnesium will remove the inhibition of these channels and therefore cause ……………………… of potassium into the urine.

A

Excess secretion

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14
Q

Malnutrition is part of the underlying cause of ………………………. in alcoholics

A

hypomagnesaemia

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15
Q

Proximal tubular cells in the kidney contain 1a-hydroxylase, an enzyme responsible for producing the active form of ………… Without active vitamin D, there will be poor absorption of ………… from the gastrointestinal tract.

A

vitamin D
calcium

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16
Q

In addition, poor renal function leads to inadequate excretion of phosphate. The end result is ……………………. As a result of low calcium, parathyroid hormone (PTH) levels will rise, but cannot restore calcium-phosphate homeostasis because of poor renal function.

A

hyperphosphatemic hypocalcemia

17
Q

Incidental hypercalcemia in a middle-aged female is most commonly caused by………………………………… . Phosphate levels may be low but often in primary hyperparathyroidism the serum phosphate is at the low end of the normal range as seen in this case.

Primary hyperparathyroidism is most commonly caused by a singular parathyroid adenoma (80%). Hyperplasia of all glands (15-20%) and carcinoma (<1%) are less likely causes. Patients that are good surgical candidates typically undergo removal of the hyperfunctioning gland.

A

hyperparathyroidism

18
Q

Primary hyperparathyroidism is the most common cause of “outpatient” hypercalcemia, meaning this diagnosis is most likely in ………………………………………………….

A

healthy, younger (i.e. not elderly) patients seen in an outpatient setting

19
Q

Primary hyperparathyroidism is most commonly caused by a singular

A

parathyroid adenoma (80%). Hyperplasia of all glands (15-20%) and carcinoma (<1%) are less likely causes.

20
Q

What CaSR is responsible ?

A

The CaSR is responsible for detecting low levels of calcium and triggering the release of PTH in response