Introduction to Regulation of K, Ca, Pi and Mg: DSA Flashcards

1
Q

State the normal ranges of plasma K+ concentration.

A

3.5-5.0 mEq/L

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2
Q

Describe K+ distribution in the body

A

Total in body: 3500 mEq K+ in the body

K+ is primary concentrated intracellularly (98%).

80% in muscle cells (150 mEq/L)

20% other cells

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3
Q

_____ difference in concentration of K+ between ICF and ECF

A

30-fold.

This is primarily d/t Na/K ATPase pump and NKCC2.

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4
Q

Hypokalemia

A

Plasma [K+] < ~3.7 mEq/L

D/t [vomiting, diarreah, too much insulin, not enough K, alkalosis]

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5
Q

Hyperkalemia

A

Plasma [K+] > ~5.2 mEq/L

More than 10 is lethal

D/t: Excessive intake, tissue release, shifts from ICF–>ECF (lk in acidosis, not enough insulin, tissue damage and hyperglycemia)

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6
Q

Pseudohyperkalemia

A

Artificially high plasma [K+] d/t lysis of RBC while blood is being drawn.

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7
Q

Identify the major routes of K+ loss from the body

A

We intake about 70mmol/day. Input=output.

  1. Gut via feces
    1. Output 10mmol/day
  2. Kidneys via urine
    1. Output 60mmol/day
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8
Q

Define the role of extracellular K+ in maintaining normal nerve and muscle function.

A

Regulating K+ is important to maintain RMP and membrane excitability.

Hyperkalemia hypopolarizes the membrane, causing the RMP to become less negative.

  • More excitable

Hypokalemia hyperpolarizes the membrane, causing the RMP to become more negative (hyperpolarized)

  • Less excitable
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9
Q

How do cardiac cells respond to hyperkalemia and hypokalemia?

A

Hyperkalemia–> cardiac cells actually become refractory (hyperpolarize), which induces bradycardia.

Hypokalemia–> the cells become over excitable, resulting in tachycardia and arrhythmia.

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10
Q

What are the classic signs of K+ abnormalities on the ECG?

A
  1. Low T wave–> hypo
  2. Tall peaked T wave–> hyper
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11
Q

What are the 4 roles of intracellular K+?

A
  1. Maintains cell volume
  2. Regulates intracellular pH
  3. Needed for some enzymes to function
  4. Needed for DNA/protein synthesis.
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12
Q

How does K+ maintain cell volume?

A

A loss of K intracellularly can be thought of as a simple loss in osmolality. This causes cell shrinkage to compensate. The opposite is true if potassium is gained.

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13
Q

How does K+ regulate intracellular pH?

A

Low K+–> low pH

High K+–> high pH

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14
Q

· Potassium establishes and maintains the cell membrane potential. Since a low plasma pH results in hypopolarization of skeletal muscle cells, it results in muscle weakness, paralysis, intestinal distention, and respiratory failure. On the other hand, hyperkalemia initially increases muscle excitability, but later causes muscle paralysis.

A
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15
Q

Low plasma potassium causes ________, and high plasma potassium causes _______

A

Low plasma potassium causes vasoconstriction, and high plasma potassium causes vasodilation

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16
Q

Normal range of dietary Ca2+ intake:

A

~1000 mg/day (adults)

17
Q

Major storage pools of Ca2+

A
  1. · Bone
  2. · Kidneys
  3. · GI tract
18
Q

Our body’s calcium pool is moderated by what?

A
  1. calcitonin
    1. Calcitonin opposes the effects of parathyroid hormone (PTH), which acts to increase the blood calcium level. Calcitonin lowers blood calcium levels by suppressing osteoclast activity in the bones and increasing the amount of calcium excreted in the urine.
  2. calcitriol & PTH
    1. PTH and calcitriol assist with resorption from bone, increasing Ca2+ levels in the blood.
19
Q

Thus, 3 ways Ca2+ can enter circulation:

A

1. Resorption from bone

2. Reabsorbed from the kidneys

3. Absorbed from the GI tract

20
Q

Major routes of Ca2+ loss from the body

A

· Most of the Ca2+ ingested in excreted as feces (~800 mg)

· 200 mg as urine

21
Q

Calcium can also act on the resting membrane potential of skeletal muscle cells.

How do?

A

Opposite of K+.

Hypocalcemia–> increases neuromuscular excitability by decreasing threshold to a more negative value.

  • Predisposes to hypocalcemic tetany/spasticity

Hypercalcemia–> decreases neuromuscular excitability by increasing threshold to a less negative value.

22
Q

Phosphorus dietary intake required.

A

~1500 mg

23
Q

Phosphate Body Pools

A

85% bone

24
Q

How is P lost?

A
  1. Feces
  2. Urine
  3. Distribed into bone
25
Q

What are the 4 regulators of phosphate metabolism

A

1. Dietary- amount we ingest

2. Calcitroil–>reabsorbs phosphate from the bone and absorption from intestines

3. PTH–> reabsorbs phosphate from the bone and indirectly increses absorption from GI tract via calcitriol

4. Renal tubular reabsorption: PTH increases phosphate excretion by the kidneys (opposite of calcium). Thus, it can be reasorbed via the kidkneez

26
Q

Mg Pools

A
  1. 50% bone
  2. 49% ICF (esp in muscle)
  3. 1% in ECF
27
Q

Total serum Mg2+

A

1.8 mEq/L (1.8-2.2)

28
Q

Free serum Mg2+

A

0.8- 1 mEq/L

29
Q

98% of K is intracellular while 2% is extracellular, this 30fold difference is due to the NaKATPase and NKCC2 transporters. How is the ICF K+ divided and what is the input and out put?

A

K+ is concentrated higher intracellular.

80% will be inside the muscle cells and 20% inside other cells.

We exrete most in urine (90%) and 10% in stool

30
Q

A majority of K+ is stored in

A
  1. muscle
  2. liver
  3. bone
  4. RBCs
31
Q

Hyperosmolality, alkalosis, B-catecholamines, and insulin all do what to K+ cell uptake?

A

increase

32
Q

A-catecholamines, acidosis, and cell damage all do what to K+ cell uptake?

A

decrease/impair

33
Q

Describe K+ in alkalosis/acidosis

A

Alkalosis–> low K+ in the ECF/ high K+ in the cell–> hypokalemic

Acidosis–> high K+ in the ECF/low K+ in the cell–> hyperkalemic