K Homeostasis

Question 1

Potassium enters and leaves the cells via three main routes;

Answer 1

the intestine,

the kidneys,

the membranes of all other cells

Question 2

Kidneys:
About 90% of the potassium filtered by the glomerulus is reabsorbed in the _______
The main control is at the distal tubules, the ______?, which is dependent on three factors;

Answer 2

proximal tubule
collecting ducts

The amount of sodium available for exchange
The circulating aldosterone concentration
The relative amounts of H⁺ and K⁺ in the tubular cells.

Question 3

The cell Membranes:
The Na⁺/K⁺ adenosine triphosphate pump
Potassium is also exchanged for H⁺
______ and ____ both increase K⁺ uptake by the cells
_____, increases loss of potassium into the ECF
______ receptors stimulation stimulates the Na⁺/K⁺ ATPase
Synthesis of the pump is also stimulated by ____
Drugs such as Digoxin also affect the pump.

Answer 3

Alkalosis & insulin

Acidosis

Β adrenergic

thyroxine

Question 4

Hypokalemia ≠ Potassium Depletion: Just because the blood level of potassium is low doesn’t necessarily mean the total amount of potassium in the body is low. The potassium might just be moving into cells from the blood.
Hyperkalemia ≠ Potassium Excess: Similarly, a high level of potassium in the blood doesn’t always mean there’s too much potassium in the body. The potassium might be moving out of cells into the blood.

Answer 4

potassium-hydrogen exchange:

Mechanism:

Cell Membrane Transport: In acidosis, there is an increased concentration of hydrogen ions (H+) in the blood.

Potassium-Hydrogen Exchange: To balance the excess H+ ions in the blood, the body uses a compensatory mechanism where H+ ions enter cells, and in exchange, potassium ions (K+) leave the cells and enter the blood. This process helps to temporarily buffer the acidity in the blood.

Net Effect: This shift reduces potassium uptake into cells, leading to an increase in extracellular potassium levels (hyperkalemia). Conversely, in alkalosis (low H+ concentration), potassium moves into cells, decreasing extracellular potassium levels (hypokalemia).

2. Insulin and Potassium Uptake

Insulin is a hormone that helps regulate blood sugar levels and also affects potassium distribution:

Mechanism:

Activation of Na+/K+-ATPase Pump: Insulin stimulates the Na+/K+-ATPase pump, an enzyme located in the cell membrane.

Pump Function: The Na+/K+-ATPase pump moves three sodium ions (Na+) out of the cell and two potassium ions (K+) into the cell using energy from ATP.

Net Effect: By enhancing the activity of this pump, insulin promotes the uptake of potassium from the blood into cells, lowering extracellular potassium levels. This mechanism is particularly important after meals, when insulin is released to manage the increase in blood glucose levels, and it helps prevent hyperkalemia.

3. Thymin (Thiamine) and Potassium Uptake

Thiamine (Vitamin B1) is essential for carbohydrate metabolism and may influence potassium levels indirectly through its role in energy production and cellular metabolism:

Question 5

Causes of Movement:
Hypokalemia:

Alkalosis (higher pH): Potassium moves into cells in exchange for hydrogen ions.
Insulin: Promotes potassium uptake by cells.
Beta-adrenergic stimulation: Such as during stress or with certain medications.
Hyperkalemia:

Acidosis (lower pH): Potassium moves out of cells in exchange for hydrogen ions.
Cell damage: Injury or breakdown of cells (like in trauma or muscle damage) releases potassium into the blood.
Lack of insulin: In conditions like diabetes, potassium can stay in the blood instead of moving into cells.

Question 6

Degrees of hyperkalemia are generally defined as follows:

Answer 6

Mild: 5.5-6.0mmol/L

Moderate: 6.1-7.0mmol/L

Severe: ≥7.0mmol/L

Question 7

A useful practical classification is to divide the causes of hyperkalemia into three groups: pseudohyperkalamia, increased potassium input into the ECF, and decreased renal excretion

Question 8

Hyperkalemia
Hyperkalemia means having too much potassium in the blood. It can have several causes, and the symptoms and treatment options vary.

Question 9

Hyperkalemia
Hyperkalemia means having too much potassium in the blood. It can have several causes, and the symptoms and treatment options vary.

Question 10

Causes of Hyperkalemia

Answer 10

Pseudohyperkalemia:

This isn’t true hyperkalemia but rather an error in test results, often due to:

Hemolysis: Breaking of red blood cells.

Leucocytosis: High white blood cell count.

Thrombocytosis: High platelet count.

Increased Potassium Intake/Load to ECF (Extracellular Fluid):

Exogenous (from outside the body):
Oral or IV therapy: Consuming too much potassium through supplements or treatments.
Endogenous (from inside the body):
Tissue necrosis: Death of body tissue (like in crush injuries, burns, or cancer).

Disturbed Potassium Distribution Between Cells and Blood:

Acidaemia: Low blood pH causing potassium to move out of cells.
Insulin deficiency: Common in diabetes, leading to potassium staying in the blood.
Drugs: Certain medications like digoxin or succinylcholine.
Hypertonicity: High levels of glucose or sodium.
Hyperkalemic periodic paralysis: A rare genetic disorder causing episodes of high potassium.

Question 11

Other causes of hyperkaldmia

Answer 11

Kidney Failure: Both acute and chronic kidney issues.

Drugs:

Potassium-sparing diuretics: Medications that reduce potassium excretion (amiloride, triamterene, spironolactone).

Prostaglandin inhibitors: Like indomethacin or ibuprofen.

ACE inhibitors: Such as captopril.

Heparin: An anticoagulant.

Mineralocorticoid Deficiency Syndromes:

Low cortisol and aldosterone: Conditions like Addison’s disease or adrenal hyperplasia.

Selective aldosterone deficiency: Conditions like hyporeninemic hypoaldosteronism, often worsened by drugs like indomethacin.

Question 12

What are the Clinical Features of Hyperkalemia

Answer 12

General Symptoms: Feeling tired or confused, muscle weakness, digestive issues like nausea and vomiting, and tingling sensations.

Serious Symptoms:

Cardiac arrhythmia: Irregular heartbeats.

Cardiac arrest: Heart stopping.

ECG Changes: Specific patterns like tall T-waves, wide QRS-complex, wide PR-interval, and sine waves.

Question 13

What are the different ways hyperkalemia can be managed?

Answer 13

Emergency Treatment: Needed if potassium levels are very high (above 7.0 mmol/L) or if there are significant ECG changes.

Calcium Gluconate: Given intravenously to protect the heart.

Glucose and Insulin: Given together intravenously to help move potassium into cells.

Sodium Bicarbonate: Used in severe acidosis to shift potassium into cells (usually via a central line).

Salbutamol: Inhaled to help lower blood potassium levels.

Resonium-A or Calcium Resonium: Oral medications that remove potassium from the body but take longer to work (at least 24 hours).

Question 14

Explain the treatment and mechanism in the previous answer

Answer 14

Treatments and Mechanisms

Calcium Gluconate

Why Used: To protect the heart.

Mechanism of Action: Calcium gluconate does not lower potassium levels but stabilizes the heart’s electrical activity, making it less likely to have dangerous arrhythmias caused by high potassium.

Glucose and Insulin

Why Used: To lower blood potassium levels.

Mechanism of Action: Insulin helps move potassium from the blood into the cells. Glucose is given to prevent blood sugar from dropping too low due to the insulin.

Sodium Bicarbonate

Why Used: To treat severe acidosis and lower blood potassium levels.

Mechanism of Action: Sodium bicarbonate makes the blood less acidic (raises pH), which causes potassium to move into the cells from the blood, thereby lowering the potassium level in the blood.

Salbutamol

Why Used: To lower blood potassium levels.

Mechanism of Action: Salbutamol is a beta-2 agonist (commonly used in asthma treatment) that stimulates beta-2 receptors, promoting the movement of potassium into cells, thereby lowering the potassium level in the blood.

Resonium-A or Calcium Resonium

Why Used: To remove potassium from the body.

Mechanism of Action: These are cation-exchange resins that bind potassium in the intestines. They exchange potassium for sodium or calcium and are then excreted from the body in the stool. This process takes longer to lower potassium levels compared to the other treatments (at least 24 hours).

Question 15

Causes and Pathophysiology
The main causes of hypokalemia are?

Answer 15

Loss from the Body: This is the most common mechanism. The kidneys are not very efficient at conserving potassium, so loss through urine is significant, especially when intake is low.
Decreased Intake: When not enough potassium is consumed.
Transcellular Shifts: Potassium moving from the blood into cells.
Extrarenal Loss: Losses from the body through routes other than the kidneys.
Renal Loss: Losses through the kidneys.

Question 16

List the specific causes

Answer 16

Specific Causes:

Decreased Intake:

Inappropriate intravenous therapy

Anorexia nervosa

Chronic alcoholism

Transcellular Shifts:

Insulin

Vitamin B12

Salbutamol

Barium toxicity

Hypokalemic periodic paralysis

Extrarenal Loss:

Vomiting

Diarrhea

Laxative abuse

Villous adenoma of the colon

Urine diversion to the gut

Renal Loss:

Metabolic alkalosis

Diuretic therapy

Mineralocorticoid excess syndromes

Renal tubular acidosis

Bartter’s syndrome

Gitelman’s syndrome

Magnesium depletion

Gentamicin therapy

Leukemia

Question 17

What are the Clinical Features

Answer 17

Muscle Weakness: Common symptom, along with fatigue and constipation.

Muscle Cramps and Tetany: More severe cases, especially if also low in calcium.

Polyuria: Increased urine production in chronic cases.

Cardiac Symptoms: Palpitations, arrhythmias, and specific ECG changes like prolonged PR interval, flat or depressed T waves, and prominent U waves.

Question 18

Explain the treatment of hypokalemia

Answer 18

Mild Hypokalemia: Treated with oral potassium supplements until levels normalize.

Common supplements:

Potassium chloride effervescent tablets (6.5 mmol K+ per tablet)

Slow-K (8 mmol K+ per tablet, as chloride)

Sando-K (12 mmol K+ per tablet, as bicarbonate and chloride)

Severe Hypokalemia: Requires intravenous potassium if oral intake is not possible. This needs to be done cautiously:

Avoid intravenous potassium if the patient has low urine output (oliguria).

The concentration of potassium in IV fluids should not exceed 40 mmol/L.

The rate of administration should not exceed 20 mmol/h, using an infusion pump

Question 19

Importance of Potassium

Answer 19

Potassium is a crucial electrolyte mainly found inside cells. It helps maintain the resting membrane potential and muscle contractions. The kidneys, gastrointestinal tract, and Na+/K+ ATPase pump regulate potassium levels. Any deviation can lead to hyperkalemia or hypokalemia, which can be serious if not promptly treated.

Question 20

Avoid Intravenous Potassium if the Patient Has Low Urine Output (Oliguria):

Reason: If the kidneys are not producing enough urine, giving IV potassium can be dangerous. The body may not be able to excrete the excess potassium, leading to hyperkalemia, which can be life-threatening.

Question 21

Rate of Administration Should Not Exceed 20 mmol/h, Using an Infusion Pump:

Reason: Infusion pumps provide precise control over the rate at which potassium is delivered. Administering potassium too quickly can lead to dangerous spikes in blood potassium levels, increasing the risk of cardiac arrhythmias and other complications. By limiting the rate to 20 mmol/h, the body has time to properly distribute and utilize the potassium.