Abnormally low potassium concentration in the blood. It may result from potassium loss by renal secretion or by the gastrointestinal route, as by vomiting or diarrhea. It may be manifested clinically by neuromuscular disorders ranging from weakness to paralysis, by electrocardiographic abnormalities (depression of the T wave and elevation of the U wave), by renal disease, and by gastrointestinal disorders. (Dorland, 27th ed)
A condition caused by the overproduction of ALDOSTERONE. It is characterized by sodium retention and potassium excretion with resultant HYPERTENSION and HYPOKALEMIA.
A group of disorders caused by defective salt reabsorption in the ascending LOOP OF HENLE. It is characterized by severe salt-wasting, HYPOKALEMIA; HYPERCALCIURIA; metabolic ALKALOSIS, and hyper-reninemic HYPERALDOSTERONISM without HYPERTENSION. There are several subtypes including ones due to mutations in the renal specific SODIUM-POTASSIUM-CHLORIDE SYMPORTERS.
An inherited renal disorder characterized by defective NaCl reabsorption in the convoluted DISTAL KIDNEY TUBULE leading to HYPOKALEMIA. In contrast with BARTTER SYNDROME, Gitelman syndrome includes hypomagnesemia and normocalcemic hypocalciuria, and is caused by mutations in the thiazide-sensitive SODIUM-POTASSIUM-CHLORIDE SYMPORTERS.
An autosomal dominant familial disorder characterized by recurrent episodes of skeletal muscle weakness associated with falls in serum potassium levels. The condition usually presents in the first or second decade of life with attacks of trunk and leg paresis during sleep or shortly after awakening. Symptoms may persist for hours to days and generally are precipitated by exercise or a meal high in carbohydrates. (Adams et al., Principles of Neurology, 6th ed, p1483)
Potassium or potassium compounds used in foods or as foods.
A condition due to decreased dietary intake of potassium, as in starvation or failure to administer in intravenous solutions, or to gastrointestinal loss in diarrhea, chronic laxative abuse, vomiting, gastric suction, or bowel diversion. Severe potassium deficiency may produce muscular weakness and lead to paralysis and respiratory failure. Muscular malfunction may result in hypoventilation, paralytic ileus, hypotension, muscle twitches, tetany, and rhabomyolysis. Nephropathy from potassium deficit impairs the concentrating mechanism, producing POLYURIA and decreased maximal urinary concentrating ability with secondary POLYDIPSIA. (Merck Manual, 16th ed)
A pathological condition that removes acid or adds base to the body fluids.
An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.
A group of genetic disorders of the KIDNEY TUBULES characterized by the accumulation of metabolically produced acids with elevated plasma chloride, hyperchloremic metabolic ACIDOSIS. Defective renal acidification of URINE (proximal tubules) or low renal acid excretion (distal tubules) can lead to complications such as HYPOKALEMIA, hypercalcinuria with NEPHROLITHIASIS and NEPHROCALCINOSIS, and RICKETS.
Na-Cl cotransporter in the convoluted segments of the DISTAL KIDNEY TUBULE. It mediates active reabsorption of sodium and chloride and is inhibited by THIAZIDE DIURETICS.
A tumor that secretes VASOACTIVE INTESTINAL PEPTIDE, a neuropeptide that causes VASODILATION; relaxation of smooth muscles; watery DIARRHEA; HYPOKALEMIA; and HYPOCHLORHYDRIA. Vipomas, derived from the pancreatic ISLET CELLS, generally are malignant and can secrete other hormones. In most cases, Vipomas are located in the PANCREAS but can be found in extrapancreatic sites.
Abnormally high potassium concentration in the blood, most often due to defective renal excretion. It is characterized clinically by electrocardiographic abnormalities (elevated T waves and depressed P waves, and eventually by atrial asystole). In severe cases, weakness and flaccid paralysis may occur. (Dorland, 27th ed)
A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.
Symptom complex due to ACTH production by non-pituitary neoplasms.
A benzenesulfonamide-phthalimidine that tautomerizes to a BENZOPHENONES form. It is considered a thiazide-like diuretic.
Urination of a large volume of urine with an increase in urinary frequency, commonly seen in diabetes (DIABETES MELLITUS; DIABETES INSIPIDUS).
Necrosis or disintegration of skeletal muscle often followed by myoglobinuria.
Tumors or cancer of the ADRENAL GLANDS.
Agents that promote the excretion of urine through their effects on kidney function.
A subclass of symporters found in KIDNEY TUBULES, DISTAL that are the major pathway for salt resorption. Inhibition of these symporters by BENZOTHIADIAZINES is the basis of action of some DIURETICS.
Disturbances in the ACID-BASE EQUILIBRIUM of the body.
Agents that inhibit SODIUM CHLORIDE SYMPORTERS. They act as DIURETICS. Excess use is associated with HYPOKALEMIA.
Disturbances in the body's WATER-ELECTROLYTE BALANCE.
A pteridinetriamine compound that inhibits SODIUM reabsorption through SODIUM CHANNELS in renal EPITHELIAL CELLS.
Excision of one or both adrenal glands. (From Dorland, 28th ed)
A powder that dissolves in water, which is administered orally, and is used as a diuretic, expectorant, systemic alkalizer, and electrolyte replenisher.
A nutritional condition produced by a deficiency of magnesium in the diet, characterized by anorexia, nausea, vomiting, lethargy, and weakness. Symptoms are paresthesias, muscle cramps, irritability, decreased attention span, and mental confusion, possibly requiring months to appear. Deficiency of body magnesium can exist even when serum values are normal. In addition, magnesium deficiency may be organ-selective, since certain tissues become deficient before others. (Harrison's Principles of Internal Medicine, 12th ed, p1936)
A benign neoplasm of the ADRENAL CORTEX. It is characterized by a well-defined nodular lesion, usually less than 2.5 cm. Most adrenocortical adenomas are nonfunctional. The functional ones are yellow and contain LIPIDS. Depending on the cell type or cortical zone involved, they may produce ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and/or ANDROSTENEDIONE.
A condition caused by prolonged exposure to excess levels of cortisol (HYDROCORTISONE) or other GLUCOCORTICOIDS from endogenous or exogenous sources. It is characterized by upper body OBESITY; OSTEOPOROSIS; HYPERTENSION; DIABETES MELLITUS; HIRSUTISM; AMENORRHEA; and excess body fluid. Endogenous Cushing syndrome or spontaneous hypercortisolism is divided into two groups, those due to an excess of ADRENOCORTICOTROPIN and those that are ACTH-independent.
Tumors or cancers of the ADRENAL CORTEX.
A group of CORTICOSTEROIDS primarily associated with water and electrolyte balance. This is accomplished through the effect on ION TRANSPORT in renal tubules, resulting in retention of sodium and loss of potassium. Mineralocorticoid secretion is itself regulated by PLASMA VOLUME, serum potassium, and ANGIOTENSIN II.
A widely used anti-inflammatory agent isolated from the licorice root. It is metabolized to GLYCYRRHETINIC ACID, which inhibits 11-BETA-HYDROXYSTEROID DEHYDROGENASES and other enzymes involved in the metabolism of CORTICOSTEROIDS. Therefore, glycyrrhizic acid, which is the main and sweet component of licorice, has been investigated for its ability to cause hypermineralocorticoidism with sodium retention and potassium loss, edema, increased blood pressure, as well as depression of the renin-angiotensin-aldosterone system.
A thiazide diuretic often considered the prototypical member of this class. It reduces the reabsorption of electrolytes from the renal tubules. This results in increased excretion of water and electrolytes, including sodium, potassium, chloride, and magnesium. It is used in the treatment of several disorders including edema, hypertension, diabetes insipidus, and hypoparathyroidism.
A genus of leguminous herbs or shrubs whose roots yield GLYCYRRHETINIC ACID and its derivative, CARBENOXOLONE.
A general term most often used to describe severe or complete loss of muscle strength due to motor system disease from the level of the cerebral cortex to the muscle fiber. This term may also occasionally refer to a loss of sensory function. (From Adams et al., Principles of Neurology, 6th ed, p45)
Excessive amount of sodium in the blood. (Dorland, 27th ed)
A lack of HYDROCHLORIC ACID in GASTRIC JUICE despite stimulation of gastric secretion.
A malignant form of polymorphic ventricular tachycardia that is characterized by HEART RATE between 200 and 250 beats per minute, and QRS complexes with changing amplitude and twisting of the points. The term also describes the syndrome of tachycardia with prolonged ventricular repolarization, long QT intervals exceeding 500 milliseconds or BRADYCARDIA. Torsades de pointes may be self-limited or may progress to VENTRICULAR FIBRILLATION.
A sterol usually substituted with radioactive iodine. It is an adrenal cortex scanning agent with demonstrated high adrenal concentration and superior adrenal imaging.
A hypermetabolic syndrome caused by excess THYROID HORMONES which may come from endogenous or exogenous sources. The endogenous source of hormone may be thyroid HYPERPLASIA; THYROID NEOPLASMS; or hormone-producing extrathyroidal tissue. Thyrotoxicosis is characterized by NERVOUSNESS; TACHYCARDIA; FATIGUE; WEIGHT LOSS; heat intolerance; and excessive SWEATING.
An analog of desoxycorticosterone which is substituted by a hydroxyl group at the C-18 position.
A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.
A hereditary or acquired form of generalized dysfunction of the PROXIMAL KIDNEY TUBULE without primary involvement of the KIDNEY GLOMERULUS. It is usually characterized by the tubular wasting of nutrients and salts (GLUCOSE; AMINO ACIDS; PHOSPHATES; and BICARBONATES) resulting in HYPOKALEMIA; ACIDOSIS; HYPERCALCIURIA; and PROTEINURIA.
A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN, leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM. The enzyme was formerly listed as EC 3.4.99.19.
Substances that dissociate into two or more ions, to some extent, in water. Solutions of electrolytes thus conduct an electric current and can be decomposed by it (ELECTROLYSIS). (Grant & Hackh's Chemical Dictionary, 5th ed)
A pathologic condition of acid accumulation or depletion of base in the body. The two main types are RESPIRATORY ACIDOSIS and metabolic acidosis, due to metabolic acid build up.
The internal portion of the kidney, consisting of striated conical masses, the renal pyramids, whose bases are adjacent to the cortex and whose apices form prominent papillae projecting into the lumen of the minor calyces.
A potassium sparing diuretic that acts by antagonism of aldosterone in the distal renal tubules. It is used mainly in the treatment of refractory edema in patients with congestive heart failure, nephrotic syndrome, or hepatic cirrhosis. Its effects on the endocrine system are utilized in the treatments of hirsutism and acne but they can lead to adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p827)
A heterogeneous group of hereditary and acquired disorders in which the KIDNEY contains one or more CYSTS unilaterally or bilaterally (KIDNEY, CYSTIC).
A benign epithelial tumor with a glandular organization.
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.

Impairment of skeletal muscle adenosine triphosphate-sensitive K+ channels in patients with hypokalemic periodic paralysis. (1/496)

The adenosine triphosphate (ATP)-sensitive K+ (KATP) channel is the most abundant K+ channel active in the skeletal muscle fibers of humans and animals. In the present work, we demonstrate the involvement of the muscular KATP channel in a skeletal muscle disorder known as hypokalemic periodic paralysis (HOPP), which is caused by mutations of the dihydropyridine receptor of the Ca2+ channel. Muscle biopsies excised from three patients with HOPP carrying the R528H mutation of the dihydropyridine receptor showed a reduced sarcolemma KATP current that was not stimulated by magnesium adenosine diphosphate (MgADP; 50-100 microM) and was partially restored by cromakalim. In contrast, large KATP currents stimulated by MgADP were recorded in the healthy subjects. At channel level, an abnormal KATP channel showing several subconductance states was detected in the patients with HOPP. None of these were surveyed in the healthy subjects. Transitions of the KATP channel between subconductance states were also observed after in vitro incubation of the rat muscle with low-K+ solution. The lack of the sarcolemma KATP current observed in these patients explains the symptoms of the disease, i.e., hypokalemia, depolarization of the fibers, and possibly the paralysis following insulin administration.  (+info)

C-terminal HERG mutations: the role of hypokalemia and a KCNQ1-associated mutation in cardiac event occurrence. (2/496)

BACKGROUND: The long-QT syndrome (LQTS) is a genetically heterogeneous disease in which 4 genes encoding ion-channel subunits have been identified. Most of the mutations have been determined in the transmembrane domains of the cardiac potassium channel genes KCNQ1 and HERG. In this study, we investigated the 3' part of HERG for mutations. METHODS AND RESULTS: New specific primers allowed the amplification of the 3' part of HERG, the identification of 2 missense mutations, S818L and V822 M, in the putative cyclic nucleotide binding domain, and a 1-bp insertion, 3108+1G. Hypokalemia was a triggering factor for torsade de pointes in 2 of the probands of these families. Lastly, in a large family, a maternally inherited G to A transition was found in the splicing donor consensus site of HERG, 2592+1G-A, and a paternally inherited mutation, A341E, was identified in KCNQ1. The 2 more severely affected sisters bore both mutations. CONCLUSIONS: The discovery of mutations in the C-terminal part of HERG emphasizes that this region plays a significant role in cardiac repolarization. Clinical data suggests that these mutations may be less malignant than mutations occurring in the pore region, but they can become clinically significant in cases of hypokalemia. The first description of 2 patients with double heterozygosity associated with a dramatic malignant phenotype implies that genetic analysis of severely affected young patients should include an investigation for >1 mutation in the LQT genes.  (+info)

Hypokalemia with syncope caused by habitual drinking of oolong tea. (3/496)

A 61-year-old woman developed hypokalemia, atrioventricular block and ventricular tachycardia with syncope after habitual drinking 2 to 3 liters of oolong tea per day. She had been suffering from rheumatoid arthritis and Sjogren's syndrome and her serum albumin was decreased (2.9 g/dl). Oolong tea contains caffeine at approximately 20 mg/dl. Great quantities of caffeine can induce hypokalemia. The serum protein binding caffeine is albumin. Accordingly, in patients with hypoalbuminemia, caffeine is apt to induce hypokalemia. This case suggested that great quantities of oolong tea, one of the so-called "healthy" drinks, result in serious symptoms for patients with hypoalbuminemia.  (+info)

Early prediction of neurological outcome after falls in children: metabolic and clinical markers. (4/496)

Falls are the foremost reason for non-fatal injuries and are second only to motor vehicle accidents in causing accidental death. The purpose of this study was to identify the clinical and metabolic predictors of the outcome of head injury caused by falls from a height. Medical records of 61 children who had been admitted to the paediatric intensive care unit from 1990 to 1993 after falling from a height were reviewed retrospectively. Outcomes were categorised as good, moderate, severe, and poor. Glasgow coma scores, pupillary responses, brain oedema, and midline shift are significantly associated with poor outcome (p < 0.05). Metabolic markers associated with poor outcome included hyperglycaemia and hypokalaemia. Children with a poor outcome had, at admission, significantly higher glucose concentrations compared with children with good outcomes (mean SD): 20.0 (7.1) v 9.31 (4.0) mmol/l, p < 0.01), and lower potassium concentrations compared with children with good, moderate, and severe outcomes (mean (SD): 2.8 (0.4) v 3.7 (0.4) mmol/l, p < 0.001, 3.5 (0.3) mmol/l, p < 0.01, and 3.41 (0.3) mmol/l, p < 0.05, respectively). These findings allow for an early allocation of effort and resources to children injured from such falls.  (+info)

Temporal responses of oxidative vs. glycolytic skeletal muscles to K+ deprivation: Na+ pumps and cell cations. (5/496)

When K+ output exceeds input, skeletal muscle releases intracellular fluid K+ to buffer the fall in extracellular fluid (ECF) K+. To investigate the mechanisms and muscle specificity of the K+ shift, rats were fed K+-deficient chow for 2-10 days, and two muscles at phenotypic extremes were studied: slow-twitch oxidative soleus and fast-twitch glycolytic white gastrocnemius (WG). After 2 days of low-K+ chow, plasma K+ concentration ([K+]) fell from 4.6 to 3.7 mM, and Na+-K+-ATPase alpha2 (not alpha1) protein levels in both muscles, measured by immunoblotting, decreased 36%. Cell [K+] decreased from 116 to 106 mM in soleus and insignificantly in WG, indicating that alpha2 can decrease before cell [K+]. After 5 days, there were further decreases in alpha2 (70%) and beta2 (22%) in WG, not in soleus, whereas cell [K+] decreased and cell [Na+] increased by 10 mM in both muscles. By 10 days, plasma [K+] fell to 2.9 mM, with further decreases in WG alpha2 (94%) and beta2 (70%); cell [K+] fell 19 mM in soleus and 24 mM in WG compared with the control, and cell [Na+] increased 9 mM in soleus and 15 mM in WG; total homogenate Na+-K+-ATPase activity decreased 19% in WG and insignificantly in soleus. Levels of alpha2, beta1, and beta2 mRNA were unchanged over 10 days. The ratios of alpha2 to alpha1 protein levels in both control muscles were found to be nearly 1 by using the relative changes in alpha-isoforms vs. beta1- (soleus) or beta2-isoforms (WG). We conclude that the patterns of regulation of Na+ pump isoforms in oxidative and glycolytic muscles during K+ deprivation mediated by posttranscriptional regulation of alpha2beta1 and alpha2beta2 are distinct and that decreases in alpha2-isoform pools can occur early enough in both muscles to account for the shift of K+ to the ECF.  (+info)

Severe muscle weakness due to hypokalemia as a manifestation of small-cell carcinoma. (6/496)

We describe the case of a 56-year-old man with severe muscle weakness due to heavy hypokalemia (serum potassium 1.44 mmol/l) associated with inappropriate kaliuria and alkalemia. Subsequent investigation revealed the presence of ectopic ACTH hypersecretion due to a small-cell lung carcinoma. A significant clinical/laboratory improvement was achieved following chemotherapy-induced regression of the primary tumor. The profound hypokalemia was probably the result of cortisol hypersecretion, which in concert with the ACTH-induced decreased 11beta-hydroxysteroid dehydrogenase activity can exhibit an increased mineralocorticoid activity. In addition, other ACTH-dependent mineralocorticoids may play a contributory role in the development of severe hypokalemia.  (+info)

The relationship between distal tubular proton secretion and dietary potassium depletion: evidence for up-regulation of H+ -ATPase. (7/496)

BACKGROUND: Dietary potassium depletion is associated with elevated plasma bicarbonate concentration and enhanced bicarbonate reabsorption in the distal tubule. The relationship between distal proton secretion and potassium status was investigated by in vivo microperfusion of the superficial distal tubule. METHODS: Experiments were performed on anaesthetized rats that had been maintained on either a low-potassium or control diet for 3-5 weeks prior to experimentation. The distal tubules were perfused at 10 nl/min with either a standard or a barium chloride-containing solution, and the late distal tubular transepithelial potential difference (Vte) and pH of the luminal fluid were recorded using a double-barrelled voltage and ion-sensitive microelectrode. RESULTS: In control rats, the Vte was -40.7+/-2.4 mV and the tubular fluid pH was 6.44+/-0.07; in potassium-depleted animals, the Vte was -15.0+/-1.4 mV and the pH was 6.76+/-0.03. The pH values in both groups of animals were significantly lower than would be predicted from the Vte and systemic pH for passive H+ distribution, indicating active proton secretion. Moreover, in hypokalaemic rats, this difference from predicted pH was significantly greater than in control animals (control = 0.27+/-0.06 vs. low-potassium = 0.46+/-0.03; P<0.01), suggesting enhanced active proton secretion. During perfusion with a solution containing BaCl2, the late distal tubule Vte became lumen positive in potassium-depleted rats, contrasting with an increased lumen negativity in potassium-replete controls. The barium-induced lumen-positive potential difference observed in the hypokalaemic rats was abolished by intravenous administration of acetazolamide. CONCLUSION: These data are consistent with enhanced electrogenic proton secretion (H+ -ATPase) during dietary potassium deprivation.  (+info)

Hypokalaemic paralysis revealing Sjogren syndrome in an elderly man. (8/496)

A 73 year old white man presented with life threatening hypokalaemic paralysis requiring admission to an intensive care unit. Biochemical investigations showed severe hypokalaemia with hyperchloraemic metabolic acidosis, a spot urine pH of 6.5, and a positive urinary anion gap, establishing the diagnosis of distal renal tubular acidosis. Autoimmune tests revealed Sjogren syndrome as the underlying cause of the distal renal tubular acidosis. Full recovery followed potassium and alkali replacement. This dramatic presentation of Sjogren syndrome has not previously been reported in an elderly man.  (+info)

Hypokalemia is a medical condition characterized by abnormally low potassium levels in the blood, specifically when the concentration falls below 3.5 milliequivalents per liter (mEq/L). Potassium is an essential electrolyte that helps regulate heart function, nerve signals, and muscle contractions.

Hypokalemia can result from various factors, including inadequate potassium intake, increased potassium loss through the urine or gastrointestinal tract, or shifts of potassium between body compartments. Common causes include diuretic use, vomiting, diarrhea, certain medications, kidney diseases, and hormonal imbalances.

Mild hypokalemia may not cause noticeable symptoms but can still affect the proper functioning of muscles and nerves. More severe cases can lead to muscle weakness, fatigue, cramps, paralysis, heart rhythm abnormalities, and in rare instances, respiratory failure or cardiac arrest. Treatment typically involves addressing the underlying cause and replenishing potassium levels through oral or intravenous (IV) supplementation, depending on the severity of the condition.

Hyperaldosteronism is a medical condition characterized by the overproduction of aldosterone, a hormone produced by the adrenal glands. Aldosterone helps regulate sodium and potassium balance and blood pressure by promoting sodium retention and potassium excretion in the kidneys.

There are two types of hyperaldosteronism: primary and secondary. Primary hyperaldosteronism is caused by an overproduction of aldosterone from an abnormality within the adrenal gland, such as a tumor (Conn's syndrome) or hyperplasia. Secondary hyperaldosteronism occurs when there is an excess production of renin, a hormone produced by the kidneys, which then stimulates the adrenal glands to produce more aldosterone. This can be caused by various conditions that affect kidney function, such as renal artery stenosis or heart failure.

Symptoms of hyperaldosteronism may include high blood pressure, low potassium levels (hypokalemia), muscle weakness, and frequent urination. Diagnosis typically involves measuring aldosterone and renin levels in the blood, as well as other tests to determine the underlying cause. Treatment depends on the type and cause of hyperaldosteronism but may include medications, surgery, or lifestyle changes.

Bartter syndrome is a rare genetic disorder that affects the kidneys' ability to reabsorb sodium and chloride, leading to an imbalance of electrolytes in the body. This condition is characterized by hypokalemia (low potassium levels), metabolic alkalosis (high pH levels in the blood), and normal or low blood pressure. It can also result in increased urine production, excessive thirst, and growth retardation in children. There are two major types of Bartter syndrome, based on the genes affected: type I caused by mutations in the SLC12A1 gene, and type II caused by mutations in the KCNJ1 gene. Type III is caused by mutations in the CLCNKB gene, while type IV is caused by mutations in the BSND or CLCNKB genes. Treatment typically involves supplementation of electrolytes, such as potassium and magnesium, as well as nonsteroidal anti-inflammatory drugs (NSAIDs) to help reduce sodium loss in the urine.

Gitelman Syndrome is a genetic disorder that affects the electrolyte and fluid balance in the body. It is characterized by low levels of potassium, magnesium, and chloride in the blood due to defects in the function of the distal convoluted tubule in the kidney. This results in increased urinary excretion of these ions.

The condition is caused by mutations in the SLC12A3 gene, which provides instructions for making a protein called thiazide-sensitive sodium chloride cotransporter (NCC). The NCC protein is responsible for reabsorbing sodium and chloride ions from the urine back into the bloodstream. In Gitelman Syndrome, the mutations in the SLC12A3 gene lead to reduced function of the NCC protein, resulting in increased excretion of sodium, chloride, potassium, and magnesium in the urine.

Symptoms of Gitelman Syndrome may include muscle weakness, cramps, spasms, fatigue, salt cravings, thirst, and decreased appetite. The condition is usually diagnosed in childhood or adolescence but can also present in adulthood. Treatment typically involves supplementation with potassium and magnesium to correct the electrolyte imbalances. In some cases, a medication called indapamide may be used to increase sodium reabsorption in the kidney and reduce potassium excretion.

Hypokalemic Periodic Paralysis (HPP) is a group of rare inherited disorders characterized by episodes of muscle weakness or paralysis, often associated with low potassium levels in the blood (hypokalemia). During an attack, muscles may become weak or fully paralyzed, typically affecting the legs and arms. The episodes can last from several hours to days. HPP is caused by genetic mutations that affect ion channels in muscle cells, leading to an imbalance of electrolytes and impaired muscle function. There are two main types: primary (or classic) HPP and secondary HPP. Primary HPP is further divided into thyrotoxic HPP and normokalemic HPP. Secondary HPP can be caused by various factors, such as medications or underlying medical conditions that cause hypokalemia.

Dietary Potassium is a mineral and an essential electrolyte that is required in the human body for various physiological processes. It is primarily obtained through dietary sources. The recommended daily intake of potassium for adults is 4700 milligrams (mg).

Potassium plays a crucial role in maintaining normal blood pressure, heart function, and muscle and nerve activity. It also helps to balance the body's fluids and prevent kidney stones. Foods that are rich in dietary potassium include fruits such as bananas, oranges, and melons; vegetables such as leafy greens, potatoes, and tomatoes; legumes such as beans and lentils; dairy products such as milk and yogurt; and nuts and seeds.

It is important to maintain a balanced intake of dietary potassium, as both deficiency and excess can have negative health consequences. A deficiency in potassium can lead to muscle weakness, fatigue, and heart arrhythmias, while an excess can cause hyperkalemia, which can result in serious cardiac complications.

Potassium deficiency, also known as hypokalemia, is a condition characterized by low levels of potassium (

Alkalosis is a medical condition that refers to an excess of bases or a decrease in the concentration of hydrogen ions (H+) in the blood, leading to a higher than normal pH level. The normal range for blood pH is typically between 7.35 and 7.45. A pH above 7.45 indicates alkalosis.

Alkalosis can be caused by several factors, including:

1. Metabolic alkalosis: This type of alkalosis occurs due to an excess of bicarbonate (HCO3-) in the body, which can result from conditions such as excessive vomiting, hyperventilation, or the use of certain medications like diuretics.
2. Respiratory alkalosis: This form of alkalosis is caused by a decrease in carbon dioxide (CO2) levels in the blood due to hyperventilation or other conditions that affect breathing, such as high altitude, anxiety, or lung disease.

Symptoms of alkalosis can vary depending on its severity and underlying cause. Mild alkalosis may not produce any noticeable symptoms, while severe cases can lead to muscle twitching, cramps, tremors, confusion, and even seizures. Treatment for alkalosis typically involves addressing the underlying cause and restoring the body's normal pH balance through medications or other interventions as necessary.

Potassium is a essential mineral and an important electrolyte that is widely distributed in the human body. The majority of potassium in the body (approximately 98%) is found within cells, with the remaining 2% present in blood serum and other bodily fluids. Potassium plays a crucial role in various physiological processes, including:

1. Regulation of fluid balance and maintenance of normal blood pressure through its effects on vascular tone and sodium excretion.
2. Facilitation of nerve impulse transmission and muscle contraction by participating in the generation and propagation of action potentials.
3. Protein synthesis, enzyme activation, and glycogen metabolism.
4. Regulation of acid-base balance through its role in buffering systems.

The normal serum potassium concentration ranges from 3.5 to 5.0 mEq/L (milliequivalents per liter) or mmol/L (millimoles per liter). Potassium levels outside this range can have significant clinical consequences, with both hypokalemia (low potassium levels) and hyperkalemia (high potassium levels) potentially leading to serious complications such as cardiac arrhythmias, muscle weakness, and respiratory failure.

Potassium is primarily obtained through the diet, with rich sources including fruits (e.g., bananas, oranges, and apricots), vegetables (e.g., leafy greens, potatoes, and tomatoes), legumes, nuts, dairy products, and meat. In cases of deficiency or increased needs, potassium supplements may be recommended under the guidance of a healthcare professional.

Renal tubular acidosis (RTA) is a medical condition that occurs when the kidneys are unable to properly excrete acid into the urine, leading to an accumulation of acid in the bloodstream. This results in a state of metabolic acidosis.

There are several types of RTA, but renal tubular acidosis type 1 (also known as distal RTA) is characterized by a defect in the ability of the distal tubules to acidify the urine, leading to an inability to lower the pH of the urine below 5.5, even in the face of metabolic acidosis. This results in a persistently alkaline urine, which can lead to calcium phosphate stones and bone demineralization.

Type 1 RTA is often caused by inherited genetic defects, but it can also be acquired due to various kidney diseases, drugs, or autoimmune disorders. Symptoms of type 1 RTA may include fatigue, weakness, muscle cramps, decreased appetite, and vomiting. Treatment typically involves alkali therapy to correct the acidosis and prevent complications.

Solute Carrier Family 12, Member 3 (SLC12A3) is a protein that belongs to the solute carrier family, which are membrane transport proteins involved in the movement of various substances across cell membranes. Specifically, SLC12A3 is a member of the electroneutral cation-chloride cotransporter (CCC) family and encodes for the protein known as downregulated in adenoma maturity alpha (DRA).

The DRA protein functions as an apical membrane transporter that mediates the coupled movement of sodium, chloride, and bicarbonate ions across epithelial cells. It is primarily expressed in the colon, where it plays a critical role in maintaining electrolyte homeostasis by facilitating the absorption of sodium and chloride ions from the intestinal lumen into the bloodstream.

Mutations in the SLC12A3 gene have been associated with several human diseases, including congenital chloride diarrhea (CLD), a rare autosomal recessive disorder characterized by chronic watery diarrhea due to excessive loss of sodium and chloride ions.

A vipoma, also known as a verner morrison syndrome or a non-insulin-secreting pancreatic tumor, is a rare medical condition characterized by the excessive production and secretion of vasoactive intestinal peptides (VIP) from a functional neuroendocrine tumor in the pancreas. This leads to a series of symptoms known as watery diarrhea, hypokalemia, and acidosis (WDHA) syndrome due to the effects of VIP on the gastrointestinal system. Symptoms include severe watery diarrhea, dehydration, electrolyte imbalances, and low blood pressure. Treatment typically involves surgical removal of the tumor, along with supportive care to manage symptoms and correct electrolyte abnormalities.

Hyperkalemia is a medical condition characterized by an elevated level of potassium (K+) in the blood serum, specifically when the concentration exceeds 5.0-5.5 mEq/L (milliequivalents per liter). Potassium is a crucial intracellular ion that plays a significant role in various physiological processes, including nerve impulse transmission, muscle contraction, and heart rhythm regulation.

Mild to moderate hyperkalemia might not cause noticeable symptoms but can still have harmful effects on the body, particularly on the cardiovascular system. Severe cases of hyperkalemia (potassium levels > 6.5 mEq/L) can lead to potentially life-threatening arrhythmias and heart failure.

Hyperkalemia may result from various factors, such as kidney dysfunction, hormonal imbalances, medication side effects, trauma, or excessive potassium intake. Prompt identification and management of hyperkalemia are essential to prevent severe complications and ensure proper treatment.

Aldosterone is a hormone produced by the adrenal gland. It plays a key role in regulating sodium and potassium balance and maintaining blood pressure through its effects on the kidneys. Aldosterone promotes the reabsorption of sodium ions and the excretion of potassium ions in the distal tubules and collecting ducts of the nephrons in the kidneys. This increases the osmotic pressure in the blood, which in turn leads to water retention and an increase in blood volume and blood pressure.

Aldosterone is released from the adrenal gland in response to a variety of stimuli, including angiotensin II (a peptide hormone produced as part of the renin-angiotensin-aldosterone system), potassium ions, and adrenocorticotropic hormone (ACTH) from the pituitary gland. The production of aldosterone is regulated by a negative feedback mechanism involving sodium levels in the blood. High sodium levels inhibit the release of aldosterone, while low sodium levels stimulate its release.

In addition to its role in maintaining fluid and electrolyte balance and blood pressure, aldosterone has been implicated in various pathological conditions, including hypertension, heart failure, and primary hyperaldosteronism (a condition characterized by excessive production of aldosterone).

Ectopic ACTH syndrome is a medical condition characterized by the excessive production of adrenocorticotropic hormone (ACTH) from a source outside of the pituitary gland, typically from a tumor in another part of the body. The most common sources of ectopic ACTH are small-cell lung carcinomas, but it can also occur with other types of tumors such as thymic carcinoids, pancreatic islet cell tumors, and bronchial carcinoids.

The excessive production of ACTH leads to an overproduction of cortisol from the adrenal glands, resulting in a constellation of symptoms known as Cushing's syndrome. These symptoms can include weight gain, muscle weakness, thinning of the skin, easy bruising, mood changes, and high blood pressure, among others.

Ectopic ACTH syndrome is typically more severe than pituitary-dependent Cushing's syndrome, and it may be more difficult to diagnose and treat due to the underlying tumor causing the excessive ACTH production. Treatment usually involves removing the tumor or controlling its growth, as well as managing the symptoms of Cushing's syndrome with medications that block cortisol production or action.

Chlorthalidone is a diuretic medication, which is a type of drug that helps the body get rid of excess salt and water by increasing urine production. It is a type of sulfonamide, and it works by blocking the reabsorption of sodium and chloride in the distal convoluted tubules of the kidneys, which leads to increased excretion of these ions and water in the urine.

Chlorthalidone is used to treat hypertension (high blood pressure) and edema (fluid retention) associated with various medical conditions, such as heart failure, cirrhosis, and kidney disease. It may be used alone or in combination with other medications to achieve better blood pressure control.

Like all medications, chlorthalidone can cause side effects, including electrolyte imbalances, dehydration, dizziness, headache, muscle cramps, and gastrointestinal disturbances. It is important to take this medication as directed by a healthcare provider and to report any bothersome or persistent symptoms promptly.

Polyuria is a medical term that describes the production of large volumes of urine, typically defined as exceeding 2.5-3 liters per day in adults. This condition can lead to frequent urination, sometimes as often as every one to two hours, and often worsens during the night (nocturia). Polyuria is often a symptom of an underlying medical disorder such as diabetes mellitus or diabetes insipidus, rather than a disease itself. Other potential causes include kidney diseases, heart failure, liver cirrhosis, and certain medications. Proper diagnosis and treatment of the underlying condition are essential to manage polyuria effectively.

Rhabdomyolysis is a medical condition characterized by the breakdown and degeneration of skeletal muscle fibers, leading to the release of their intracellular contents into the bloodstream. This can result in various complications, including electrolyte imbalances, kidney injury or failure, and potentially life-threatening conditions if not promptly diagnosed and treated.

The process of rhabdomyolysis typically involves three key components:

1. Muscle injury: Direct trauma, excessive exertion, prolonged immobilization, infections, metabolic disorders, toxins, or medications can cause muscle damage, leading to the release of intracellular components into the bloodstream.
2. Release of muscle contents: When muscle fibers break down, they release various substances, such as myoglobin, creatine kinase (CK), lactate dehydrogenase (LDH), aldolase, and potassium ions. Myoglobin is a protein that can cause kidney damage when present in high concentrations in the bloodstream, particularly when it is filtered through the kidneys and deposits in the renal tubules.
3. Systemic effects: The release of muscle contents into the bloodstream can lead to various systemic complications, such as electrolyte imbalances (particularly hyperkalemia), acidosis, hypocalcemia, and kidney injury or failure due to myoglobin-induced tubular damage.

Symptoms of rhabdomyolysis can vary widely depending on the severity and extent of muscle damage but may include muscle pain, weakness, swelling, stiffness, dark urine, and tea-colored or cola-colored urine due to myoglobinuria. In severe cases, patients may experience symptoms related to kidney failure, such as nausea, vomiting, fatigue, and decreased urine output.

Diagnosis of rhabdomyolysis typically involves measuring blood levels of muscle enzymes (such as CK and LDH) and evaluating renal function through blood tests and urinalysis. Treatment generally focuses on addressing the underlying cause of muscle damage, maintaining fluid balance, correcting electrolyte imbalances, and preventing or managing kidney injury.

Adrenal gland neoplasms refer to abnormal growths or tumors in the adrenal glands. These glands are located on top of each kidney and are responsible for producing hormones that regulate various bodily functions such as metabolism, blood pressure, and stress response. Adrenal gland neoplasms can be benign (non-cancerous) or malignant (cancerous).

Benign adrenal tumors are called adenomas and are usually small and asymptomatic. However, some adenomas may produce excessive amounts of hormones, leading to symptoms such as high blood pressure, weight gain, and mood changes.

Malignant adrenal tumors are called adrenocortical carcinomas and are rare but aggressive cancers that can spread to other parts of the body. Symptoms of adrenocortical carcinoma may include abdominal pain, weight loss, and hormonal imbalances.

It is important to diagnose and treat adrenal gland neoplasms early to prevent complications and improve outcomes. Diagnostic tests may include imaging studies such as CT scans or MRIs, as well as hormone level testing and biopsy. Treatment options may include surgery, radiation therapy, chemotherapy, or a combination of these approaches.

Diuretics are a type of medication that increase the production of urine and help the body eliminate excess fluid and salt. They work by interfering with the reabsorption of sodium in the kidney tubules, which in turn causes more water to be excreted from the body. Diuretics are commonly used to treat conditions such as high blood pressure, heart failure, liver cirrhosis, and kidney disease. There are several types of diuretics, including loop diuretics, thiazide diuretics, potassium-sparing diuretics, and osmotic diuretics, each with its own mechanism of action and potential side effects. It is important to use diuretics under the guidance of a healthcare professional, as they can interact with other medications and have an impact on electrolyte balance in the body.

Sodium chloride symporters are membrane transport proteins that actively co-transport sodium and chloride ions into a cell. They are also known as sodium-chloride cotransporters or NCCs. These transporters play a crucial role in regulating the electrolyte balance and water homeostasis in various tissues, particularly in the kidney's distal convoluted tubule.

The primary function of sodium chloride symporters is to reabsorb sodium and chloride ions from the filtrate in the nephron back into the bloodstream. By doing so, they help maintain the body's sodium concentration and control water balance through osmosis.

Mutations in the gene encoding for the NCC can lead to various kidney disorders, such as Gitelman syndrome or Bartter syndrome type III, which are characterized by electrolyte imbalances, low blood pressure, and metabolic alkalosis.

An acid-base imbalance refers to a disturbance in the normal balance of acids and bases in the body, which can lead to serious health consequences. The body maintains a delicate balance between acids and bases, which is measured by the pH level of the blood. The normal range for blood pH is between 7.35 and 7.45, with a pH below 7.35 considered acidic and a pH above 7.45 considered basic or alkaline.

Acid-base imbalances can occur due to various factors such as lung or kidney disease, diabetes, severe infections, certain medications, and exposure to toxins. The two main types of acid-base imbalances are acidosis (excess acid in the body) and alkalosis (excess base in the body).

Acidosis can be further classified into respiratory acidosis (caused by impaired lung function or breathing difficulties) and metabolic acidosis (caused by an accumulation of acid in the body due to impaired kidney function, diabetes, or other conditions).

Alkalosis can also be classified into respiratory alkalosis (caused by hyperventilation or excessive breathing) and metabolic alkalosis (caused by excessive loss of stomach acid or an excess intake of base-forming substances).

Symptoms of acid-base imbalances may include confusion, lethargy, shortness of breath, rapid heartbeat, nausea, vomiting, and muscle weakness. If left untreated, these conditions can lead to serious complications such as coma, seizures, or even death. Treatment typically involves addressing the underlying cause of the imbalance and may include medications, oxygen therapy, or fluid and electrolyte replacement.

Sodium chloride symporter inhibitors are a class of pharmaceutical agents that block the function of the sodium chloride symporter (NCC), which is a protein found in the kidney's distal convoluted tubule. The NCC is responsible for reabsorbing sodium and chloride ions from the filtrate back into the bloodstream, helping to regulate electrolyte balance and blood pressure.

Sodium chloride symporter inhibitors work by selectively binding to and blocking the NCC, preventing it from transporting sodium and chloride ions across the cell membrane. This leads to increased excretion of sodium and chloride in the urine, which can help lower blood pressure in patients with hypertension.

Examples of sodium chloride symporter inhibitors include thiazide diuretics such as hydrochlorothiazide and chlorthalidone, which have been used for many years to treat hypertension and edema associated with heart failure and liver cirrhosis. These medications work by reducing the amount of sodium and fluid in the body, which helps lower blood pressure and reduce swelling.

It's worth noting that while sodium chloride symporter inhibitors can be effective at treating hypertension, they can also cause side effects such as electrolyte imbalances, dehydration, and increased urination. As with any medication, it's important to use them under the guidance of a healthcare provider and to follow dosing instructions carefully.

Water-electrolyte imbalance refers to a disturbance in the balance of water and electrolytes (such as sodium, potassium, chloride, and bicarbonate) in the body. This imbalance can occur when there is an excess or deficiency of water or electrolytes in the body, leading to altered concentrations in the blood and other bodily fluids.

Such imbalances can result from various medical conditions, including kidney disease, heart failure, liver cirrhosis, severe dehydration, burns, excessive sweating, vomiting, diarrhea, and certain medications. Symptoms of water-electrolyte imbalance may include weakness, fatigue, muscle cramps, seizures, confusion, and in severe cases, coma or even death. Treatment typically involves addressing the underlying cause and correcting the electrolyte and fluid levels through appropriate medical interventions.

Triamterene is a potassium-sparing diuretic (a type of "water pill") that is used to treat fluid retention (edema) and high blood pressure. It works by preventing your body from absorbing too much salt and keeps your potassium levels from getting too low.

The medical definition of Triamterene, according to the National Library of Medicine's MedlinePlus, is: "A medication that helps to reduce the amount of fluid in the body by increasing the amount of urine produced. It is used to treat high blood pressure and edema (fluid retention)."

Triamterene is available only with a prescription and is typically taken by mouth in the form of a tablet, usually two or three times a day after meals. Common side effects include headache, dizziness, and stomach upset. It is important to follow your healthcare provider's instructions carefully when taking this medication, as it can have serious interactions with other medications and may cause an imbalance of electrolytes in the body if not used properly.

Adrenalectomy is a surgical procedure in which one or both adrenal glands are removed. The adrenal glands are small, triangular-shaped glands located on top of each kidney that produce hormones such as cortisol, aldosterone, and adrenaline (epinephrine).

There are several reasons why an adrenalectomy may be necessary. For example, the procedure may be performed to treat tumors or growths on the adrenal glands, such as pheochromocytomas, which can cause high blood pressure and other symptoms. Adrenalectomy may also be recommended for patients with Cushing's syndrome, a condition in which the body is exposed to too much cortisol, or for those with adrenal cancer.

During an adrenalectomy, the surgeon makes an incision in the abdomen or back and removes the affected gland or glands. In some cases, laparoscopic surgery may be used, which involves making several small incisions and using specialized instruments to remove the gland. After the procedure, patients may need to take hormone replacement therapy to compensate for the loss of adrenal gland function.

Potassium citrate is a medication and dietary supplement that contains potassium and citrate. Medically, it is used to treat and prevent kidney stones, as well as to manage metabolic acidosis in people with chronic kidney disease. Potassium citrate works by increasing the pH of urine, making it less acidic, which can help to dissolve certain types of kidney stones and prevent new ones from forming. It is also used as an alkalizing agent in the treatment of various conditions that cause acidosis.

In addition to its medical uses, potassium citrate is also found naturally in some fruits and vegetables, such as oranges, grapefruits, lemons, limes, and spinach. It is often used as a food additive and preservative, and can be found in a variety of processed foods and beverages.

It's important to note that taking too much potassium citrate can lead to high levels of potassium in the blood, which can be dangerous. Therefore, it is important to follow the dosage instructions carefully and talk to your doctor before taking this medication if you have any medical conditions or are taking any other medications.

Magnesium deficiency, also known as hypomagnesemia, is a condition characterized by low levels of magnesium in the blood. Magnesium is an essential mineral that plays a crucial role in many bodily functions, including muscle and nerve function, heart rhythm, bone strength, and immune system regulation.

Hypomagnesemia can occur due to various factors, such as poor dietary intake, malabsorption syndromes, chronic alcoholism, diabetes, certain medications (such as diuretics), and excessive sweating or urination. Symptoms of magnesium deficiency may include muscle cramps, tremors, weakness, heart rhythm abnormalities, seizures, and mental status changes.

It is important to note that mild magnesium deficiency may not cause any symptoms, and the diagnosis typically requires blood tests to measure magnesium levels. Treatment for hypomagnesemia usually involves oral or intravenous magnesium supplementation, along with addressing the underlying causes of the deficiency.

An adrenocortical adenoma is a benign tumor that arises from the cells of the adrenal cortex, which is the outer layer of the adrenal gland. These tumors can produce and release various hormones, such as cortisol, aldosterone, or androgens, depending on the type of cells they originate from.

Most adrenocortical adenomas are nonfunctioning, meaning that they do not secrete excess hormones and may not cause any symptoms. However, some functioning adenomas can produce excessive amounts of hormones, leading to a variety of clinical manifestations. For example:

* Cortisol-secreting adenomas can result in Cushing's syndrome, characterized by weight gain, muscle wasting, thin skin, easy bruising, and mood changes.
* Aldosterone-producing adenomas can cause Conn's syndrome, marked by hypertension (high blood pressure), hypokalemia (low potassium levels), and metabolic alkalosis.
* Androgen-secreting adenomas may lead to hirsutism (excessive hair growth) or virilization (development of male secondary sexual characteristics) in women.

The diagnosis of an adrenocortical adenoma typically involves imaging tests, such as CT or MRI scans, and hormonal evaluations to determine if the tumor is functioning or not. Treatment usually consists of surgical removal of the tumor, especially if it is causing hormonal imbalances or growing in size.

Cushing syndrome is a hormonal disorder that occurs when your body is exposed to high levels of the hormone cortisol for a long time. This can happen due to various reasons such as taking high doses of corticosteroid medications or tumors that produce cortisol or adrenocorticotropic hormone (ACTH).

The symptoms of Cushing syndrome may include:

* Obesity, particularly around the trunk and upper body
* Thinning of the skin, easy bruising, and purple or red stretch marks on the abdomen, thighs, breasts, and arms
* Weakened bones, leading to fractures
* High blood pressure
* High blood sugar
* Mental changes such as depression, anxiety, and irritability
* Increased fatigue and weakness
* Menstrual irregularities in women
* Decreased fertility in men

Cushing syndrome can be diagnosed through various tests, including urine and blood tests to measure cortisol levels, saliva tests, and imaging tests to locate any tumors. Treatment depends on the cause of the condition but may include surgery, radiation therapy, chemotherapy, or adjusting medication dosages.

Adrenal cortex neoplasms refer to abnormal growths (tumors) in the adrenal gland's outer layer, known as the adrenal cortex. These neoplasms can be benign or malignant (cancerous). Benign tumors are called adrenal adenomas, while cancerous tumors are called adrenocortical carcinomas.

Adrenal cortex neoplasms can produce various hormones, leading to different clinical presentations. For instance, they may cause Cushing's syndrome (characterized by excessive cortisol production), Conn's syndrome (caused by aldosterone excess), or virilization (due to androgen excess). Some tumors may not produce any hormones and are discovered incidentally during imaging studies for unrelated conditions.

The diagnosis of adrenal cortex neoplasms typically involves a combination of imaging techniques, such as CT or MRI scans, and hormonal assessments to determine if the tumor is functional or non-functional. In some cases, a biopsy may be necessary to confirm the diagnosis and differentiate between benign and malignant tumors. Treatment options depend on the type, size, location, and hormonal activity of the neoplasm and may include surgical excision, radiation therapy, chemotherapy, or a combination of these approaches.

Mineralocorticoids are a class of steroid hormones that primarily regulate electrolyte and fluid balance in the body. The most important mineralocorticoid is aldosterone, which is produced by the adrenal gland in response to signals from the renin-angiotensin system. Aldosterone acts on the distal tubules and collecting ducts of the nephrons in the kidneys to increase the reabsorption of sodium ions (Na+) and water into the bloodstream, while promoting the excretion of potassium ions (K+) and hydrogen ions (H+) into the urine. This helps maintain blood pressure and volume, as well as ensuring a proper balance of electrolytes in the body. Other mineralocorticoids include cortisol and corticosterone, which have weak mineralocorticoid activity and play a more significant role as glucocorticoids, regulating metabolism and immune response.

Glycyrrhizic acid is a compound derived from the root of the licorice plant (Glycyrrhiza glabra). It has been defined medically as a triterpene glycoside with anti-inflammatory and expectorant properties. It is known to inhibit the enzyme 11-beta-hydroxysteroid dehydrogenase, which can lead to increased levels of cortisol in the body, potentially causing side effects such as hypertension and hypokalemia if consumed in large amounts or over an extended period.

In some medical contexts, glycyrrhizic acid may be used for its potential benefits, including its ability to suppress viral replication and inflammation. However, due to the risk of side effects, it is often used in modified forms or at reduced concentrations.

Hydrochlorothiazide is a diuretic drug, which means it helps the body get rid of extra salt and water by increasing the amount of urine that is produced. The medical definition of Hydrochlorothiazide is:

A thiazide diuretic drug used to treat hypertension and edema associated with heart failure, liver cirrhosis, and kidney disorders. It works by inhibiting the reabsorption of sodium and chloride ions in the distal convoluted tubule of the nephron, which increases water excretion and decreases blood volume and pressure. Hydrochlorothiazide may be used alone or in combination with other antihypertensive agents. It is also used to treat conditions such as diabetes insipidus, renal tubular acidosis, and hypercalcemia.

The usual starting dose of hydrochlorothiazide for adults is 25 mg to 50 mg once a day, which may be increased gradually depending on the patient's response. The maximum recommended daily dose is 100 mg. Common side effects of hydrochlorothiazide include increased urination, headache, dizziness, and muscle cramps.

"Glycyrrhiza" is the medical term for the licorice plant (Glycyrrhiza glabra), which belongs to the legume family. The root of this plant contains glycyrrhizin, a sweet-tasting compound that has been used in traditional medicine for various purposes such as treating coughs, stomach ulcers, and liver disorders. However, excessive consumption of glycyrrhizin can lead to serious side effects like high blood pressure, low potassium levels, and even heart problems. Therefore, it is important to use licorice products under the guidance of a healthcare professional.

Paralysis is a loss of muscle function in part or all of your body. It can be localized, affecting only one specific area, or generalized, impacting multiple areas or even the entire body. Paralysis often occurs when something goes wrong with the way messages pass between your brain and muscles. In most cases, paralysis is caused by damage to the nervous system, especially the spinal cord. Other causes include stroke, trauma, infections, and various neurological disorders.

It's important to note that paralysis doesn't always mean a total loss of movement or feeling. Sometimes, it may just cause weakness or numbness in the affected area. The severity and extent of paralysis depend on the underlying cause and the location of the damage in the nervous system.

Hypernatremia is a medical condition characterized by an abnormally high concentration of sodium (na+) in the blood, specifically a serum sodium level greater than 145 mEq/L. Sodium is an essential electrolyte that helps regulate water balance in and around your cells. It's crucial for many body functions, including the maintenance of blood pressure, regulation of nerve and muscle function, and regulation of fluid balance.

Hypernatremia typically results from a deficit of total body water relative to solute, which can be caused by decreased water intake, increased water loss, or a combination of both. Common causes include dehydration due to severe vomiting or diarrhea, excessive sweating, burns, kidney diseases, and the use of certain medications such as diuretics.

Symptoms of hypernatremia can range from mild to severe and may include thirst, muscle weakness, lethargy, irritability, confusion, seizures, and in extreme cases, coma or even death. Treatment typically involves correcting the underlying cause and gradually rehydrating the individual with intravenous fluids to restore normal sodium levels.

Achlorhydria is a medical condition characterized by the absence or near-absence of hydrochloric acid in the stomach. Hydrochloric acid is a digestive fluid that helps to break down food, particularly proteins, and also creates an acidic environment that prevents harmful bacteria from growing in the stomach.

Achlorhydria can be caused by various factors, including certain medications, autoimmune disorders, aging, or surgical removal of the stomach. Symptoms of achlorhydria may include indigestion, bloating, abdominal pain, and malabsorption of nutrients. If left untreated, it can lead to complications such as anemia, vitamin B12 deficiency, and increased risk of gastrointestinal infections.

It is important to note that achlorhydria can be diagnosed through various tests, including a gastric acid analysis or a pH test. Treatment for achlorhydria may involve supplementing with hydrochloric acid or other digestive enzymes, modifying the diet, and addressing any underlying conditions.

Torsades de Pointes is a type of polymorphic ventricular tachycardia, characterized by a distinct pattern on the electrocardiogram (ECG) where the QRS complexes appear to twist around the isoelectric line. This condition is often associated with a prolonged QT interval, which can be congenital or acquired due to various factors such as medications, electrolyte imbalances, or heart diseases. Torsades de Pointes can degenerate into ventricular fibrillation, leading to sudden cardiac death if not promptly treated.

I'm sorry for any confusion, but "Adosterol" is not a recognized term in medical or scientific literature. It's possible that there may be a spelling mistake or it could be a term used only within a specific context, such as a code name in a research study. If you have more information about where this term was used, I might be able to provide a more accurate response. However, without additional context, I can't provide a medical definition for "Adosterol".

Thyrotoxicosis is a medical condition that results from an excess of thyroid hormones in the body, leading to an overactive metabolic state. It can be caused by various factors such as Graves' disease, toxic adenoma, Plummer's disease, or excessive intake of thyroid hormone medication. Symptoms may include rapid heart rate, weight loss, heat intolerance, tremors, and increased sweating, among others. Thyrotoxicosis is not a diagnosis itself but a manifestation of various underlying thyroid disorders. Proper diagnosis and management are crucial to prevent complications and improve quality of life.

18-Hydroxydesoxycorticosterone is a steroid hormone that is produced by the adrenal gland. It is an intermediate in the biosynthesis of aldosterone, which is the major hormone responsible for regulating sodium and potassium balance in the body. 18-Hydroxydesoxycorticosterone itself has minimal biological activity, but it is converted to aldosterone by the enzyme aldosterone synthase.

The medical relevance of 18-Hydroxydesoxycorticosterone lies in its role as a precursor to aldosterone and its potential use as a marker for certain adrenal gland disorders. For example, increased production of 18-Hydroxydesoxycorticosterone has been observed in some cases of primary hyperaldosteronism, which is a condition characterized by excessive aldosterone production leading to high blood pressure and low potassium levels. Measuring the levels of this hormone can help diagnose and manage such conditions.

Furosemide is a loop diuretic medication that is primarily used to treat edema (fluid retention) associated with various medical conditions such as heart failure, liver cirrhosis, and kidney disease. It works by inhibiting the sodium-potassium-chloride cotransporter in the ascending loop of Henle in the kidneys, thereby promoting the excretion of water, sodium, and chloride ions. This increased urine output helps reduce fluid accumulation in the body and lower blood pressure.

Furosemide is also known by its brand names Lasix and Frusid. It can be administered orally or intravenously, depending on the patient's condition and the desired rate of diuresis. Common side effects include dehydration, electrolyte imbalances, hearing loss (in high doses), and increased blood sugar levels.

It is essential to monitor kidney function, electrolyte levels, and fluid balance while using furosemide to minimize potential adverse effects and ensure appropriate treatment.

Fanconi syndrome is a medical condition that affects the proximal tubules of the kidneys. These tubules are responsible for reabsorbing various substances, such as glucose, amino acids, and electrolytes, back into the bloodstream after they have been filtered through the kidneys.

In Fanconi syndrome, there is a defect in the reabsorption process, causing these substances to be lost in the urine instead. This can lead to a variety of symptoms, including:

* Polyuria (excessive urination)
* Polydipsia (excessive thirst)
* Dehydration
* Metabolic acidosis (an imbalance of acid and base in the body)
* Hypokalemia (low potassium levels)
* Hypophosphatemia (low phosphate levels)
* Vitamin D deficiency
* Rickets (softening and weakening of bones in children) or osteomalacia (softening of bones in adults)

Fanconi syndrome can be caused by a variety of underlying conditions, including genetic disorders, kidney diseases, drug toxicity, and heavy metal poisoning. Treatment typically involves addressing the underlying cause, as well as managing symptoms such as electrolyte imbalances and acid-base disturbances.

Renin is a medically recognized term and it is defined as:

"A protein (enzyme) that is produced and released by specialized cells (juxtaglomerular cells) in the kidney. Renin is a key component of the renin-angiotensin-aldosterone system (RAAS), which helps regulate blood pressure and fluid balance in the body.

When the kidney detects a decrease in blood pressure or a reduction in sodium levels, it releases renin into the bloodstream. Renin then acts on a protein called angiotensinogen, converting it to angiotensin I. Angiotensin-converting enzyme (ACE) subsequently converts angiotensin I to angiotensin II, which is a potent vasoconstrictor that narrows blood vessels and increases blood pressure.

Additionally, angiotensin II stimulates the adrenal glands to release aldosterone, a hormone that promotes sodium reabsorption in the kidneys and increases water retention, further raising blood pressure.

Therefore, renin plays a critical role in maintaining proper blood pressure and electrolyte balance in the body."

Electrolytes are substances that, when dissolved in water, break down into ions that can conduct electricity. In the body, electrolytes are responsible for regulating various important physiological functions, including nerve and muscle function, maintaining proper hydration and acid-base balance, and helping to repair tissue damage.

The major electrolytes found in the human body include sodium, potassium, chloride, bicarbonate, calcium, magnesium, and phosphate. These electrolytes are tightly regulated by various mechanisms, including the kidneys, which help to maintain their proper balance in the body.

When there is an imbalance of electrolytes in the body, it can lead to a range of symptoms and health problems. For example, low levels of sodium (hyponatremia) can cause confusion, seizures, and even coma, while high levels of potassium (hyperkalemia) can lead to heart arrhythmias and muscle weakness.

Electrolytes are also lost through sweat during exercise or illness, so it's important to replace them through a healthy diet or by drinking fluids that contain electrolytes, such as sports drinks or coconut water. In some cases, electrolyte imbalances may require medical treatment, such as intravenous (IV) fluids or medication.

Acidosis is a medical condition that occurs when there is an excess accumulation of acid in the body or when the body loses its ability to effectively regulate the pH level of the blood. The normal pH range of the blood is slightly alkaline, between 7.35 and 7.45. When the pH falls below 7.35, it is called acidosis.

Acidosis can be caused by various factors, including impaired kidney function, respiratory problems, diabetes, severe dehydration, alcoholism, and certain medications or toxins. There are two main types of acidosis: metabolic acidosis and respiratory acidosis.

Metabolic acidosis occurs when the body produces too much acid or is unable to eliminate it effectively. This can be caused by conditions such as diabetic ketoacidosis, lactic acidosis, kidney failure, and ingestion of certain toxins.

Respiratory acidosis, on the other hand, occurs when the lungs are unable to remove enough carbon dioxide from the body, leading to an accumulation of acid. This can be caused by conditions such as chronic obstructive pulmonary disease (COPD), asthma, and sedative overdose.

Symptoms of acidosis may include fatigue, shortness of breath, confusion, headache, rapid heartbeat, and in severe cases, coma or even death. Treatment for acidosis depends on the underlying cause and may include medications, oxygen therapy, fluid replacement, and dialysis.

The kidney medulla is the inner portion of the renal pyramids in the kidney, consisting of multiple conical structures found within the kidney. It is composed of loops of Henle and collecting ducts responsible for concentrating urine by reabsorbing water and producing a hyperosmotic environment. The kidney medulla has a unique blood supply and is divided into an inner and outer zone, with the inner zone having a higher osmolarity than the outer zone. This region of the kidney helps regulate electrolyte and fluid balance in the body.

Spironolactone is a prescription medication that belongs to a class of drugs known as potassium-sparing diuretics. It works by blocking the action of aldosterone, a hormone that helps regulate sodium and potassium balance in your body. This results in increased urine production (diuresis) and decreased salt and fluid retention.

Spironolactone is primarily used to treat edema (fluid buildup) associated with heart failure, liver cirrhosis, or kidney disease. It's also prescribed for the treatment of high blood pressure and primary hyperaldosteronism, a condition where the adrenal glands produce too much aldosterone.

Furthermore, spironolactone is used off-label to treat conditions such as acne, hirsutism (excessive hair growth in women), and hormone-sensitive breast cancer in postmenopausal women.

It's important to note that spironolactone can cause increased potassium levels in the blood (hyperkalemia) and should be used with caution in patients with kidney impairment or those taking other medications that affect potassium balance. Regular monitoring of electrolyte levels, including potassium and sodium, is essential during spironolactone therapy.

Cystic kidney diseases are a group of genetic disorders that cause fluid-filled sacs called cysts to form in the kidneys. These cysts can vary in size and can grow over time, which can lead to damage in the kidneys and affect their function. There are two main types of cystic kidney diseases: autosomal dominant polycystic kidney disease (ADPKD) and autosomal recessive polycystic kidney disease (ARPKD).

ADPKD is the most common type and is characterized by the presence of numerous cysts in both kidneys. It is usually diagnosed in adulthood, but it can also occur in children. The cysts can cause high blood pressure, kidney stones, urinary tract infections, and eventually kidney failure.

ARPKD is a rare, inherited disorder that affects both the kidneys and liver. It is characterized by the presence of numerous cysts in the kidneys and abnormalities in the bile ducts of the liver. ARPKD is usually diagnosed in infancy or early childhood and can cause serious complications such as respiratory distress, kidney failure, and liver fibrosis.

Other types of cystic kidney diseases include nephronophthisis, medullary cystic kidney disease, and glomerulocystic kidney disease. These conditions are also inherited and can cause kidney damage and kidney failure.

Treatment for cystic kidney diseases typically involves managing symptoms such as high blood pressure, pain, and infections. In some cases, surgery may be necessary to remove large cysts or to treat complications such as kidney stones. For individuals with advanced kidney disease, dialysis or a kidney transplant may be necessary.

An adenoma is a benign (noncancerous) tumor that develops from glandular epithelial cells. These types of cells are responsible for producing and releasing fluids, such as hormones or digestive enzymes, into the surrounding tissues. Adenomas can occur in various organs and glands throughout the body, including the thyroid, pituitary, adrenal, and digestive systems.

Depending on their location, adenomas may cause different symptoms or remain asymptomatic. Some common examples of adenomas include:

1. Colorectal adenoma (also known as a polyp): These growths occur in the lining of the colon or rectum and can develop into colorectal cancer if left untreated. Regular screenings, such as colonoscopies, are essential for early detection and removal of these polyps.
2. Thyroid adenoma: This type of adenoma affects the thyroid gland and may result in an overproduction or underproduction of hormones, leading to conditions like hyperthyroidism (overactive thyroid) or hypothyroidism (underactive thyroid).
3. Pituitary adenoma: These growths occur in the pituitary gland, which is located at the base of the brain and controls various hormonal functions. Depending on their size and location, pituitary adenomas can cause vision problems, headaches, or hormonal imbalances that affect growth, reproduction, and metabolism.
4. Liver adenoma: These rare benign tumors develop in the liver and may not cause any symptoms unless they become large enough to press on surrounding organs or structures. In some cases, liver adenomas can rupture and cause internal bleeding.
5. Adrenal adenoma: These growths occur in the adrenal glands, which are located above the kidneys and produce hormones that regulate stress responses, metabolism, and blood pressure. Most adrenal adenomas are nonfunctioning, meaning they do not secrete excess hormones. However, functioning adrenal adenomas can lead to conditions like Cushing's syndrome or Conn's syndrome, depending on the type of hormone being overproduced.

It is essential to monitor and manage benign tumors like adenomas to prevent potential complications, such as rupture, bleeding, or hormonal imbalances. Treatment options may include surveillance with imaging studies, medication to manage hormonal issues, or surgical removal of the tumor in certain cases.

Hypertension is a medical term used to describe abnormally high blood pressure in the arteries, often defined as consistently having systolic blood pressure (the top number in a blood pressure reading) over 130 mmHg and/or diastolic blood pressure (the bottom number) over 80 mmHg. It is also commonly referred to as high blood pressure.

Hypertension can be classified into two types: primary or essential hypertension, which has no identifiable cause and accounts for about 95% of cases, and secondary hypertension, which is caused by underlying medical conditions such as kidney disease, hormonal disorders, or use of certain medications.

If left untreated, hypertension can lead to serious health complications such as heart attack, stroke, heart failure, and chronic kidney disease. Therefore, it is important for individuals with hypertension to manage their condition through lifestyle modifications (such as healthy diet, regular exercise, stress management) and medication if necessary, under the guidance of a healthcare professional.

The word hypokalemia comes from hypo- 'under' + kalium 'potassium' + -emia 'blood condition'. Mild hypokalemia is often without ... Potassium bicarbonate is preferred when correcting hypokalemia associated with metabolic acidosis. Severe hypokalemia (. ... defined as hypokalemia. Hypokalemia leads to characteristic ECG changes (PR prolongation, ST-segment and T-wave depression, U- ... The hypokalemia is thought to be from the combination of the diuretic effect of caffeine and copious fluid intake, although it ...
Hypokalemia, a deficiency of potassium in the plasma, can be fatal if severe. Common causes are increased gastrointestinal loss ... Diets low in potassium can lead to hypertension and hypokalemia. Supplements of potassium are most widely used in conjunction ... ISBN 978-0-7817-9469-5. Visveswaran, Kasi (2009). "hypokalemia". Essentials of Nephrology (2nd ed.). BI Publications. p. 257. ...
See Hypokalemia.) Na+ - sodium ions have a similar role to potassium ions. (See Sodium deficiency.) Mn2+- manganese ions are ...
A severe shortage of potassium in body fluids may cause a potentially fatal condition known as hypokalemia. Hypokalemia ... Mumoli N, Cei M (2008). "Licorice-induced hypokalemia". Int. J. Cardiol. 124 (3): e42-4. doi:10.1016/j.ijcard.2006.11.190. PMID ... In rare cases, habitual consumption of large amounts of black licorice has resulted in hypokalemia. Licorice contains a ...
Mohr JA, Clark RM, Waack TC, Whang R (August 1979). "Nafcillin-associated hypokalemia". JAMA. 242 (6): 544. doi:10.1001/jama. ... Hypokalemia Nausea and vomiting Diarrhea, often due to suppression of normal gastrointestinal bacteria, which, on occasion, ... although one retrospective study found greater rates of hypokalemia and acute kidney injury in patients taking nafcillin ...
Hypokalemia often results. The completely immobile patient is at increased risk of bed sores as well as infection from ...
Stage 1 is characterized by no symptoms but mild hypokalemia. Stage 2 is characterized with symptoms and mild hypokalemia. ... "Hypokalemia - PubMed Health". Ncbi.nlm.nih.gov. Retrieved 6 February 2013. Lin, H. W.; Chau, T.; Lin, C. S.; Lin, S. H. (2009 ... The effects of hypokalemia can include fatigue, muscle weakness, or paralysis. The severity of the hypokalemic state can be ... Stage 3 is characterized by only moderate to severe hypokalemia. Cytokines are somnogenic and are likely key mediators of sleep ...
Fluid retention may also lead to dilutional anemia (in 10 to 15% of patients). Hypokalemia may also result. Symptoms of fluid ...
"Hypokalaemia". Yanowitz, Frank G. "VII. Atrial Enlargement". ECG Learning Center. Archived from the original on 2010-03-29. ... A P wave with increased amplitude can indicate hypokalemia. It can also indicate right atrial enlargement. A P wave with ...
Hypokalemia is a potassium deficiency. It is defined by the level of potassium in the blood; levels 3.5 and 5.0 mmoL are ... And so it was concluded that extreme cola consumption can lead to hypokalemia. Symptoms caused by an increased consumption of ... There are many case reports on the relationship between hypokalemia and sugar sweetened beverages such as cola-based drinks. ... Packer, C. D. (June 1, 2009). "Cola-induced hypokalaemia: a super-sized problem". International Journal of Clinical Practice. ...
ISBN 978-1-4557-2865-7. Viera AJ, Wouk N (September 2015). "Potassium Disorders: Hypokalemia and Hyperkalemia". American Family ...
In medical terms, low potassium is called hypokalemia. When a pouch is constructed small amounts of ileum are lost to the ... "Low Potassium Level Causes (Hypokalemia)". Lightner, A. L.; Shogan, B. D.; Mathis, K. L.; Larson, D. W.; Duchalais, E.; ...
Blachley, Jon D.; Knochel, James P. (1980). "Tobacco Chewer's Hypokalemia: Licorice Revisited". New England Journal of Medicine ... hypokalaemia, weight gain or loss, and hypertension. Liquorice root with bark Inflorescence of G. glabra Various liquorice ...
Hypokalemia (low blood potassium) occurs occasionally; the risk of hypokalemia is higher in persons who are magnesium deficient ...
1975; 231: 734-5. Micturition syncope, hypokalemia, and atrial fibrillation. Kounis NG, Kenmure AC. JAMA 1976; 236: 954 " ...
In states of hypokalemia (a state of potassium deficiency), concurrent magnesium deficiency results in a state of hypokalemia ... Conversely, magnesium deficiency alone is not likely to cause a state of hypokalemia. Sgk1 kinase has also been reported to ... Huang CL, Kuo E (October 2007). "Mechanism of hypokalemia in magnesium deficiency". Journal of the American Society of ...
Thus hypomagnesemia results in an increased excretion of potassium in kidney, resulting in a hypokalaemia. This condition is ... Intravenous magnesium sulfate (MgSO4) can be given in response to heart arrhythmias to correct for hypokalemia, preventing pre- ... Huang CL, Kuo E (October 2007). "Mechanism of hypokalemia in magnesium deficiency". Journal of the American Society of ... the hypomagnesemia is accompanied by other defects in electrolyte handling such as hypocalciuria and hypokalemia. The genes ...
Muscle cramps can also be a symptom or complication of pregnancy; kidney disease; thyroid disease; hypokalemia, hypomagnesemia ... called hypokalemia), or magnesium (called hypomagnesemia). Some skeletal muscle cramps do not have a known cause. Motor neuron ...
Rastegar A, Soleimani M, Rastergar A (December 2001). "Hypokalaemia and hyperkalaemia". Postgraduate Medical Journal. 77 (914 ...
"Effect of cetamolol on epinephrine-induced hypokalemia". Journal of Clinical Pharmacology. 28 (8): 751-6. doi:10.1002/j.1552- ...
Wilson, Brent; Paul, Panchajanya; Mehta, Sunny; Coffey, Barbara (February 2013). "Hypokalemia Secondary to Bupropion Sustained ...
Maini AA, Maxwell-Scott H, Marks DJ (February 2014). "Severe alkalosis and hypokalemia with stanozolol misuse". The American ...
This causes a lower total body concentration of potassium and potentially, hypokalemia. Hypokalemia affects polarization of ... In the presence of hypokalemia even a mildly elevated aldosterone should be considered inappropriately high. A high-normal or ... When a cause is not readily apparent, and especially when hypokalemia is identified, hyperaldosteronism should be considered. ... Potential complications include hemorrhage and postoperative hypokalemia. With complete removal of the tumor, prognosis is ...
Brown, M. J.; Brown, D. C.; Murphy, M. B. (8 December 1983). "Hypokalemia from Beta-Receptor Stimulation by Circulating ...
Several cases of severe hypokalemia have been reported. Meropenem rapidly reduces serum concentrations of valproic acid. As a ...
Yamada was hospitalised for hypokalemia. From around this time, he became ill and was repeatedly hospitalised and discharged ...
These include hypokalemia, arrythmia and acute cardiac arrest. Chelation therapy - removal of metals from the body by ...
It occurs with hypokalemia due to vomiting or diarrhea. The ultrastructural changes of reversible cell injury include: Blebbing ...
Urinary fractional excretion potassium is high or inappropriately normal in the context of hypokalaemia, and high levels of ... Primary aldosteronism will cause metabolic alkalosis and hypokalaemia, but hypertension will be present and serum renin will be ... Diagnosis of Gitelman syndrome can be confirmed after eliminating other common pathological sources of hypokalemia and ... Gitelman HJ, Graham JB, Welt LG (1966). "A new familial disorder characterized by hypokalemia and hypomagnesemia". Transactions ...
Gitelman HJ, Graham JB, Welt LG (1966). "A new familial disorder characterized by hypokalemia and hypomagnesemia". Trans Assoc ... The clinical findings characteristic of Bartter syndrome is hypokalemia, metabolic alkalosis, and normal to low blood pressure ... On the other hand, sustained hypokalemia and hyperreninemia can cause progressive tubulointerstitial nephritis, resulting in ... hypokalemia), increased blood pH (alkalosis), and normal to low blood pressure. There are two types of Bartter syndrome: ...
  • Normal potassium levels in humans are between 3.5 and 5.0 mmol/L (3.5 and 5.0 mEq/L) with levels below 3.5 mmol/L defined as hypokalemia. (wikipedia.org)
  • Hypokalemia is generally defined as a serum potassium level of less than 3.5 mEq/L (3.5 mmol/L). Moderate hypokalemia is a serum level of 2.5-3.0 mEq/L, and severe hypokalemia is a level of less than 2.5 mEq/L. (medscape.com)
  • However, within 2 weeks of discontinuation of therapy, hypokalemia (3.0 mmol/L) returned with concurrent normal serum sodium and chloride levels. (vin.com)
  • From profound hypokalemia to life-threatening hyperkalemia: a case of barium sulfide poisoning. (cdc.gov)
  • Severe hypokalemia, with serum potassium concentrations of 2.5-3 meq/L (Nl: 3.5-5.0 meq/L), may cause muscle weakness, myalgia, tremor, and muscle cramps (owing to disturbed function of skeletal muscle), and constipation (from disturbed function of smooth muscle). (wikipedia.org)
  • With more severe hypokalemia, flaccid paralysis and hyporeflexia may result. (wikipedia.org)
  • Reports exist of rhabdomyolysis occurring with profound hypokalemia with serum potassium levels less than 2 meq/L. Respiratory depression from severe impairment of skeletal muscle function is found in some people. (wikipedia.org)
  • Severe hypokalemia may manifest as bradycardia with cardiovascular collapse. (medscape.com)
  • Severe hypokalemia leads to heart arrhythmias, muscle weakness, and cardiomyopathy that can be fatal. (personalabs.com)
  • For example, diabetic ketoacidosis , a severe and even life-threatening complication of diabetes causing your blood to become too acidic, can be tied to hypokalemia. (personalabs.com)
  • cardiac hyperexcitability may occur with severe hypokalemia. (msdmanuals.com)
  • Primary aldosteronism associated with severe rhabdomyolysis due to profound hypokalemia. (medscape.com)
  • Individuals that have severe hypokalemia and are experiencing symptoms may need to be hospitalized. (canadadrugstore.com)
  • Hypokalemia can lead to an irregular heartbeat , which may lead to death in severe cases. (medicalnewstoday.com)
  • Severe hypokalemia induced by barium toxicity can cause ventricular dysrhythmias (1-7). (cdc.gov)
  • While chronic disorders included in the list of low potassium causes have an indirect connection to hypokalemia, some disorders can have a profound impact in terms of severity. (personalabs.com)
  • is a rare autosomal dominant disorder characterized by transient episodes of profound hypokalemia thought to be due to sudden abnormal shifts of potassium into cells. (msdmanuals.com)
  • Within 1-4 hours of ingestion, profound hypokalemia and generalized muscle weakness can develop which may progress to paralysis of the limbs and respiratory muscles. (cdc.gov)
  • Mild hypokalemia is often without symptoms, although it may cause elevation of blood pressure, and can provoke the development of an abnormal heart rhythm. (wikipedia.org)
  • Symptoms that are present are often from the underlying cause of the hypokalemia rather than the hypokalemia itself. (medscape.com)
  • The symptoms of hypokalemia are nonspecific and predominantly are related to muscular or cardiac function. (medscape.com)
  • Mild hypokalemia often does not cause symptoms. (canadadrugstore.com)
  • Mild hypokalemia is a condition which does not often show any signs or symptoms. (canadadrugstore.com)
  • Most people suffering from mild cases of hypokalemia may not notice the symptoms but most cases of hypokalemia present with several other signs of being ill. (simplyhealth.io)
  • Though hypokalemia is not an independent illness, one of the most common symptoms if the ailment is low blood pressure. (simplyhealth.io)
  • What are the signs and symptoms of hypokalemia? (medicinenet.com)
  • The most important use of potassium is to treat the symptoms of hypokalemia (low potassium), which include weakness, lack of energy, muscle cramps, stomach disturbances, an irregular heartbeat, and an abnormal EKG (electrocardiogram, a test that measures heart function). (stlukes-stl.com)
  • Metabolic alkalosis can be due to extreme sodium absorption, which disrupts potassium levels and leads to hypokalemia. (personalabs.com)
  • Excess of aldosterone leads to hypertension (because of the sodium retention) and hypokalemia because of excess potassium secretion and consequent urinary loss. (medicine-opera.com)
  • Blood pressure medications such as loop diuretics (e.g. furosemide) and thiazide diuretics (e.g. hydrochlorothiazide) commonly cause hypokalemia. (wikipedia.org)
  • Other medications such as the antifungal amphotericin B or the cancer drug cisplatin can also cause long-term hypokalemia. (wikipedia.org)
  • Hypokalemia can be due to certain disorders, medications or drugs, chronic alcohol abuse, intense physical activity, and nutritional deficiency. (personalabs.com)
  • Numerous conditions and certain medications can trigger hypokalemia such as Piperacillin/Tazobactam, Flucloxacillin, Cephalexin and Vancomycin. (endocrine-abstracts.org)
  • Intracellular shifts as well as certain medications can also cause hypokalemia. (msdmanuals.com)
  • Hypokalemia is usually caused by medications or other conditions, but can also develop if there is an intracellular shift of your body's potassium. (simplyhealth.io)
  • I've been asked about licorice and hypokalemia. (medicine-opera.com)
  • How does excess licorice consumption cause hypertension and hypokalemia? (pearls4peers.com)
  • The association between consistent licorice ingestion, hypertension and hypokalaemia: as systematic review and meta-analysis. (pearls4peers.com)
  • For instance, Bartter Syndrome, a genetic renal tubular disorder, promotes hypokalemia and other electrolyte abnormalities. (personalabs.com)
  • Other ways that GRA may cause hypertension and hypokalemia include inhibition of 5 β-reductase in the liver, an enzyme that metabolizes aldosterone and direct stimulation of mineralocorticoid receptors, though overall these mechanisms may not be as important as the effect of GRA on cortisol metabolism in renal tissue. (pearls4peers.com)
  • Pathogenesis of hypokalemia in autosomal dominant hypocalcemia type 1. (medscape.com)
  • Patients are often asymptomatic, particularly those with mild hypokalemia. (medscape.com)
  • Meropenem can cause refractory hypokalemia that could result in ileus, muscle weakness, rhabdomyolysis or respiratory failure. (endocrine-abstracts.org)
  • Diuretic abuse among athletes and people with eating disorders may present with hypokalemia due to urinary potassium loss. (wikipedia.org)
  • KAPLAN, NORMAN M. / Attenuation of Diuretic‐Induced Hypokalemia by Amiloride, a Potassium‐Sparing Agent . (utmb.edu)
  • Hypokalemia, like hypophosphatemia, could be a complication associated with refeeding in patients with cancer. (scielo.br)
  • Measurement of urine potassium is essential to establishment of the pathophysiologic mechanism of hypokalemia and, thus, to determination of the differential diagnosis. (medscape.com)
  • These transport mechanisms play a role in familial hypokalemia-hypomagnesemia or Gitelman syndrome. (medscape.com)
  • Moreover, eating disorders like bulimia nervosa and anorexia nervosa can also lead to hypokalemia. (personalabs.com)
  • Hypokalemia: A Marker of Covert Bulimia Nervosa. (qxmd.com)
  • Greenfeld D, Mickley D, Quinlan DM, Roloff P. Hypokalemia in outpatients with eating disorders. (medscape.com)
  • An increase in the pH of the blood (alkalosis) can cause temporary hypokalemia by causing a shift of potassium out of the plasma and interstitial fluids into the urine via a number of interrelated mechanisms. (wikipedia.org)
  • Hypokalemia may result from inadequate potassium intake, increased potassium excretion, or a shift of potassium from the extracellular to the intracellular space. (medscape.com)
  • Meropenem-associated hypokalemia is believed to be due to the increased urinary potassium excretion, but it is not confirmed yet whether this is aldosterone-mediated or not. (endocrine-abstracts.org)
  • A low level of magnesium in the blood can also cause hypokalemia. (wikipedia.org)
  • We hypothesized that in humans, WNK bodies occur as well in hypokalemia. (mdc-berlin.de)
  • However, electrocardiogram (ECG) findings in combined hypercalcaemia and hypokalaemia have rarely been described. (annals.edu.sg)
  • Which of the following ECG findings indicates hypokalemia? (examobjective.com)
  • Hypokalemia contributes to the progression of chronic kidney disease, while a definitive pathophysiogical theory to explain this remains to be established. (mdc-berlin.de)
  • Objective To evaluate serum potassium levels and rates of hypokalaemia in patients treated with liquorice-containing Japanese traditional Kampo-medicines Yokukansan (YK) and Yokukansan-ka-chinpihange (YKCH). (bmj.com)
  • Hypokalemia can be caused by decreased intake of potassium but is usually caused by excessive losses of potassium in the urine or from the gastrointestinal (GI) tract. (msdmanuals.com)
  • Hypokalemia usually happens when the body loses too much potassium in the urine or intestines. (stlukes-stl.com)
  • The aim of this study was to investigate the eventual presence of hypokalemia during the early phase of refeeding in patients with cancer. (scielo.br)
  • This is the first report to identify the risk factors for hypokalaemia as an initial symptom of pseudoaldosteronism in patients treated with YK preparations containing small amounts of glycyrrhiza (1.5 g/day). (bmj.com)
  • Patients with both unilateral macro-adenoma and hypokalemia are more prone to acquire postoperative BP normalization. (degruyter.com)
  • In a study of hemodialysis patients, only 0.6%, 0.5%, and 0.9% hypokalemia events occurred at 1, 2, and 3 months after initiating patiromer treatment. (renalandurologynews.com)
  • An electrocardiogram which was recorded when the hypercalcaemia was associated with hypokalaemia showed absence of the ST segment, prolonged T wave, a shortened QTac interval and prominent U waves. (annals.edu.sg)
  • Administration of Meropenem was associated with persistent and difficult to correct hypokalemia despite the absence of other possible aetiologies. (endocrine-abstracts.org)
  • Hypokalemia is one of the most common water-electrolyte imbalances. (wikipedia.org)
  • Additionally, when hypokalemia develops, kidney function also gets significantly disrupted. (personalabs.com)
  • Hypokalemia is a condition that develops when a person is suffering from a potassium deficiency in their bloodstream. (simplyhealth.io)
  • Hypokalemia is one of the commonly encountered electrolyte derangements in clinical practice. (endocrine-abstracts.org)
  • [ 1 ] Hypokalemia is a potentially life-threatening imbalance that may be iatrogenically induced. (medscape.com)
  • 5-Minute Clinical Consult , www.unboundmedicine.com/5minute/view/Diagnosaurus/114276/all/Hypokalemia. (unboundmedicine.com)
  • Viagra is indicated for the treatment of erectile dysfunction in men lasix hypokalemia . (onlinehome.us)
  • Being that it is not an independent illness, the main condition will require treatment in order to resolve hypokalemia. (simplyhealth.io)
  • Hypokalemia was present in the early stages of high-calorie refeeding. (scielo.br)
  • Hypokalemia is a low level of potassium (K+) in the blood serum. (wikipedia.org)
  • Hypokalemia is a condition where the body's blood potassium levels are far too low. (canadadrugstore.com)
  • Hypokalemia is observed with low total body potassium and a low intracellular concentration of potassium. (wikipedia.org)
  • Hypokalemia is a condition in which your body has low potassium levels. (personalabs.com)

No images available that match "hypokalemia"