L1: Disorders of Potassium Balance Flashcards

1
Q

Where is potassium mainly stored?

A

intracellularly

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

After eating, what happens to the excess potassium entering your body?

A

cellular distribution - it is moved intracellularly

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

List the 5 key regulators of potassium cellular distribution - they influence the movement of K+ intracellularly?

A
  1. Insulin*
  2. Catecholamines*
  3. pH
  4. Cell Turnover
  5. Osmolality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do catecholamines regulate potassium cellular distribution?

A

stimulates Na+/K+ ATPase - drives K+ into cells

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

How does insulin regulate potassium cellular distribution? What is the effect of insulin after eating a meal?

A

stimulates Na+/K+ ATPase - drives K+ into cells

after a meal: moves K+, glucose and phosphate into the cell

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

How does pH regulate potassium cellular distribution? What happens in low and high pH?

A

via H+/K+ channel

Low pH: H+ pumped into cell, K+ pumped out
High pH: H+ pumped out of cell, K+ pumped in

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

How does cell turnover regulate potassium cellular distribution?

A
  • if cell breaks down, it releases K+

- in increased cell turnover, increased K+ intracellularly

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

How does osmolality affect potassium cellular distribution?

A
  • if hypertonic outside cell, water drawn out
  • water draws K+ out of cell with it

Result: low intracellular K+, high plasma K+ (hyperkalaemia)

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

What are 2 mechanisms by which potassium is regulated through in the body?

A
  1. Cellular Distribution

2. Renal Excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where is potassium reabsorbed and excreted in the nephron?

A

K+ reabsorbed in proximal tubule + loop of Henle

K+ excreted in cortical collecting duct

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

What are the 2 main principal cell types of the cortical collecting duct? What are the functions of each?

A
  1. Principal Cells - K+ excretion

2. Intercalated Cells - H+ excretion

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

Generally explain what occurs for K+ excretion in the cortical collecting duct.

A
  1. Na+ reabsorbed by ENaC channels
  2. Na+ pumped out of principal cell by Na+/K+ channel
  3. Cl- creates negative charge in tubular lumen
  4. K+ excreted into tubule
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are ENaC channels?

A

they are epithelial Na+ channels located in the cortical collecting duct

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

Potassium excretion in the principal cells of the collecting duct is regulated by what 2 processes?

A
  1. Tubular Flow

2. Aldosterone

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

What is defined as hypokalaemia? What is moderate hypokalaemia? What is severe hypokalaemia?

A

Hypokalaemia = < 3.5 mmol/L

Moderate Hypokalaemia = < 3.0 mmol/L

Severe Hypokalaemia = < 2.5 mmol/L

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

List 3 major causes of hypokalaemia

A
  1. Decreased Intake
  2. Intracellular Shift
  3. Increased Renal Excretion
17
Q

How can refeeding syndrome cause hypokalaemia?

A

there is insulin release which will draw K+ into cells

18
Q

What is primary hyperaldosteronism? What is another name for it?

A

aka Conn’s Syndrome

when adrenal glands produce too much aldosterone

19
Q

What is secondary hyperaldosteronism?

A

increase in aldosterone as a consequence of something else (e.g. diuretics, vomiting - loss of volume)

20
Q

Explain diuretic-induced hypokalaemia

A
  • diuretics inhibit Na+ reabsorption
  • increased Na+ (and water) in urine
  • increased urine output; decrease blood volume
  • aldosterone stimulated due to decrease blood volume (pressure0
  • aldosterone increases Na+ reabsorption and K+ excretion
21
Q

Explain vomit-induced hypokalaemia

A
  • vomit contains acid (increased excretion of acid)
  • leads to metabolic alkalosis
  • increase HCO3- in tubule
  • HCO3- creates a strong negative gradient
  • draws K+ into the tubule

aldosterone also stimulated (due to volume loss)
- causes Na+ reabsorption and K+ excretion

22
Q

List some of the consequences of hypokalaemia

A
  • muscle weakness/paralysis
  • ECG changes and arrhythmia
  • urinary concentrating deficits
  • hypertension and stroke
23
Q

On an ECG of a patient with hypokalaemia, what can be seen?

A

inverted T/U waves

24
Q

What is the preferred treatment for hypokalaemia

A

potassium (oral preferred over IV)

25
Q

What is considered hyperkalaemia?

A

K+ > 5.4 mmol/L

26
Q

What is the normal range of K+ in the blood?

A

3.5 - 5.0 mmol/L

27
Q

List 3 major causes of hyperkalaemia

A
  1. Increased Intake
  2. Extracellular Shift
  3. Decreased Renal Excretion
28
Q

List 4 causes that may lead to an extracellular shift and hyperkalaemia

A
  1. Hyperosmolality
  2. Cell Destruction
  3. Drugs
  4. Acidemia
29
Q

What are some drugs that can cause a K+ extracellular shift and lead to hyperkalaemia?

A

Beta Blockers
Digoxin
Succinylcholine

30
Q

What are 3 drugs that can inhibit the eNaC channel and lead to hyperkalaemia?

A
  1. Triamterene
  2. Amiloride
  3. Trimethoprim
31
Q

Hypoaldosteronism can cause hyperkalaemia. List some drugs that may cause hypoaldosteronism.

A
  • ACE inhibitors
  • Angiotensin Receptor Blockers
  • Renin Inhibitors
  • Heparin
  • Ketoconazole
  • Spironolactone
32
Q

What is the proposed mechanism of hyperkalaemia in Gordon’s Syndrome?

A

Chloride Shunt

- negative gradient not maintained so K+ does not get driven out

33
Q

What are the consequences of hyperkalaemia?

A
  • muscle weakness/paralysis
  • ECG changes and arrhythmia
  • decreased excitability of the heart* (+ decreased conductance)
34
Q

On an ECG of a patient with hyperkalaemia, what will be seen?

A

lengthening of the QRS complex

- lengthening can lead to flat lining

35
Q

In a patient with hyperkalaemia, what drugs are used to induce an intracellular K+ shift? [3]

A
  1. Digoxin Antidote (for Digoxin Toxicity)
  2. Albuterol/Salbutamol (Beta Agonist)**
  3. Insulin**
36
Q

In a patient with hyperkalaemia, what drugs are used to increase K+ renal excretion?

A
  1. Diuretics
  2. Fludrocortisone (aldosterone in drug form)
  3. Polystyrene Resins
  4. Dialysis
37
Q

What does Gordon’s Syndrome cause?

A

hyperkalaemia due to the presence of a chloride shunt

38
Q

If there is a lack of aldosterone, this can lead to….

A

hyperkalaemia