CPY-L7 Potassium Disorders

Low potassium levels in the blood (K < 3.5).

High potassium levels in the blood.

Asymptomatic, but can lead to muscle weakness, excitability, and risk of arrhythmia.

Asymptomatic, but severe cases can present with muscle weakness, paralysis due to altered electrical signal, and progressive ECG abnormalities.

A real shortfall of potassium in the body.

Potassium moving between cells and blood, not a true loss of potassium, it is a temporary transfer.

Potassium loss through the kidneys.

High urine potassium signifies a renal loss of potassium.

Low urine potassium levels indicate a possible cause other than kidney issue.

Evaluating the cause of low potassium by assessing blood potassium, and analyzing the urine K levels to identify the source of loss.

A type of anemia caused by a deficiency in vitamins like B12, leading to abnormal red blood cell production.

A heightened need for energy, potentially due to medical conditions.

A test to analyze the amount of oxygen and carbon dioxide in the blood, often used to diagnose metabolic acidosis.

A condition where the body has too much acid in its blood.

Possible causes of metabolic acidosis, often due to loss of minerals.

CCT stands for Corrected Calcium. It is calculated by considering the patient's albumin level to adjust for potential inaccuracies in measuring total serum calcium.

CCT is only valid if the patient's serum albumin level is above 300 mg/dL and their serum sodium concentration is above 25 mmol/L.

A condition where potassium levels appear abnormally high in the blood, but it is not a true increase in potassium levels. It's caused by factors that release potassium from cells or artificially increase levels during the testing process.

Pseudohyperkalaemia can be caused by factors like delayed blood analysis, damage to the blood sample, certain blood cell conditions, and prolonged tourniquet use during blood draw.

A condition where plasma potassium levels are higher than serum potassium levels. This happens due to the sensitivity of the cell membranes of certain types of white blood cells to heparin, a common anticoagulant used in plasma samples.

A serious complication that occurs when large numbers of cancer cells quickly die off, releasing their intracellular contents into the bloodstream, including potassium. This can lead to hyperkalemia.

Urine potassium levels can help determine the cause of potassium imbalances. Urine K levels above 40 mmol/L often suggest a renal loss of potassium, while levels below 20mmol/L might indicate other underlying problems.

Anticoagulants are added to blood samples to prevent clotting. Different anticoagulants can impact the accuracy of potassium levels. For example, EDTA (purple tube) can cause false hyperkalemia while fluoride (grey tube) can lead to false hypokalemia.

A condition where the blood pH is abnormally high due to excessive bicarbonate (HCO3-) accumulation.

Loss of gastric acid (vomiting, nasogastric suction), diuretics usage, mineralocorticoid excess (Conn's Syndrome), severe hypokalemia (low potassium) and magnesium depletion.

Low potassium levels can contribute to metabolic alkalosis by activating the renin-angiotensin-aldosterone system (RAAS), leading to sodium retention and potassium loss.

Diuretics can lead to metabolic alkalosis by causing loss of sodium and chloride, which in turn activates RAAS, resulting in potassium loss and HCO3- retention.

Vomiting leads to loss of stomach acid, which is acidic, causing a relative increase in blood bicarbonate levels.

Symptoms include headache, dizziness, confusion, muscle weakness, arrhythmias, and tetany.

Diagnosis is made by measuring blood pH, bicarbonate levels, electrolytes, and arterial blood gas analysis.

Treatment focuses on correcting the underlying cause. It may involve fluid replacement, potassium supplementation, and acidifying agents.

A condition where the kidneys fail to properly regulate acid-base balance, leading to acidosis.

A condition where the distal tubules of the kidneys fail to excrete hydrogen ions.

A condition where the proximal tubules fail to reabsorb bicarbonate effectively, leading to its loss in the urine.

A condition characterized by deficient aldosterone or resistance to aldosterone, resulting in potassium retention and impaired excretion of hydrogen ions.

This type of metabolic alkalosis can be corrected by simply giving normal saline (NaCl) solution intravenously.

This type of metabolic alkalosis is not easily resolved with saline alone and requires further investigation and alternative treatments.

Urine chloride levels can help differentiate between saline-responsive and saline-resistant metabolic alkalosis. Low levels (<10 mmol/L) suggest saline responsiveness, while high levels (>20 mmol/L) indicate saline resistance.

A condition where there's too much mineralocorticoid, a type of hormone that regulates salt and water balance in the body. This can lead to high blood pressure and low potassium levels.

A specific mineralocorticoid hormone produced by the adrenal glands, responsible for regulating sodium and potassium levels in the body.

An excess of aldosterone in the body, leading to increased sodium retention and potassium loss. This often results in high blood pressure and low potassium.

Caused by a problem in the adrenal glands themselves, leading to overproduction of aldosterone.

An excess of aldosterone caused by another condition or disease outside of the adrenal glands.

A complex system in the body that regulates blood pressure, fluid balance, and electrolyte levels. It involves the production of renin, angiotensin, and aldosterone.

A specific type of paralysis triggered by high thyroid hormone levels and often associated with excessive eating or physical exertion.

Low magnesium levels in the blood.

A genetic disorder affecting the adrenal glands, leading to insufficient production of certain hormones and causing an excess of others, including aldosterone.

A genetic disorder that causes a heightened sensitivity to aldosterone, leading to increased sodium reabsorption and potassium loss.

A natural plant containing compounds that can mimic the effects of aldosterone, leading to mineralocorticoid excess.

An enzyme that converts inactive cortisone to the active hormone cortisol, reducing its effect as an aldosterone mimic.

A mechanism by which the body tries to compensate for excess aldosterone, preventing excessively high blood pressure and potassium loss.

A medication that blocks the action of aldosterone, used to treat high blood pressure, fluid buildup, and other conditions caused by mineralocorticoid excess.

TLS symptoms include electrolyte abnormalities, confusion or altered mental status, shortness of breath, chest pain, seizures, and even cardiac arrest.

Higher risk of TLS with aggressive cancers like leukemia and lymphoma, large tumor burden, rapid cancer cell death from treatment, and pre-existing kidney problems.

Treatments for TLS focus on hydration, preventing kidney damage, and correcting electrolyte imbalances. Medications like allopurinol help lower uric acid levels, and dialysis can be used if the kidneys are severely affected.

A condition where muscle cells break down, releasing their contents into the blood, leading to similar electrolyte imbalances as TLS, but also muscle damage and kidney problems.

Rhabdomyolysis symptoms include muscle pain and weakness, dark urine (myoglobinuria), elevated muscle enzymes like creatine kinase (CK), and kidney failure.

Treatment for rhabdomyolysis focuses on hydration, correcting electrolyte imbalances, and preventing kidney damage. Diuretics are used to help flush out myoglobin from the kidneys.

A group of inherited disorders affecting ion channels, which regulate the flow of electrolytes into and out of cells, causing various metabolic imbalances and health problems.

A genetic channelopathy affecting the thick ascending limb (TAL) of the nephron, leading to excessive salt and water loss in the urine, resulting in metabolic alkalosis and low potassium levels.

A genetic channelopathy affecting the distal convoluted tubule (DCT) of the nephron, causing salt and water loss, resulting in metabolic alkalosis and low potassium levels.

A genetic channelopathy causing overactivity of the sodium-chloride cotransporter (NCCT) in the DCT, leading to excessive sodium and chloride reabsorption, metabolic acidosis, and high potassium levels.

A genetic channelopathy causing a defective response to aldosterone in the collecting tubule (CCT), leading to sodium and water loss, metabolic acidosis, and high potassium levels.

Certain diuretics, like thiazides and loop diuretics, can affect electrolyte balance. Thiazides increase calcium levels and block the NCCT, reducing sodium reabsorption. Loop diuretics decrease calcium levels and block the NKCC2, also reducing sodium reabsorption.