Hypokalaemia Health Dictionary

A condition in which the kidneys are unable to excrete normal amounts of acid made by the body.

The blood is more acidic than normal, and the urine less acidic.

Causes include kidney damage due to disease, drugs, or a genetic disorder; but in many cases the cause is unknown.

The acidosis may result in osteomalacia, kidney stones (see calculus, urinary tract), nephrocalcinosis, and hypokalaemia (an abnormally low level of potassium in the blood).... renal tubular acidosis

This is a colourless, odourless, tasteless, nonirritating gas formed on incomplete combustion of organic fuels. Exposure to CO is frequently due to defective gas, oil or solid-fuel heating appliances. CO is a component of car exhaust fumes and deliberate exposure to these is a common method of suicide. Victims of ?res often suffer from CO poisoning. CO combines reversibly with oxygen-carrying sites of HAEMOGLOBIN (Hb) molecules with an a?nity 200 to 300 times greater than oxygen itself. The carboxyhaemoglobin (COHb) formed becomes unavailable for oxygen transportation. In addition the partial saturation of the Hb molecule results in tighter oxygen binding, impairing delivery to the tissues. CO also binds to MYOGLOBIN and respiratory cytochrome enzymes. Exposure to CO at levels of 500 parts per million (ppm) would be expected to cause mild symptoms only and exposure to levels of 4,000 ppm would be rapidly fatal.

Each year around 50 people in the United Kingdom are reported as dying from carbon monoxide poisoning, and experts have suggested that as many as 25,000 people a year are exposed to its effects within the home, but most cases are unrecognised, unreported and untreated, even though victims may suffer from long-term effects. This is regrettable, given that Napoleon’s surgeon, Larrey, recognised in the 18th century that soldiers were being poisoned by carbon monoxide when billeted in huts heated by woodburning stoves. In the USA it is estimated that 40,000 people a year attend emergency departments suffering from carbon monoxide poisoning. So prevention is clearly an important element in dealing with what is sometimes termed the ‘silent killer’. Safer designs of houses and heating systems, as well as wider public education on the dangers of carbon monoxide and its sources, are important.

Clinical effects of acute exposure resemble those of atmospheric HYPOXIA. Tissues and organs with high oxygen consumption are affected to a great extent. Common effects include headaches, weakness, fatigue, ?ushing, nausea, vomiting, irritability, dizziness, drowsiness, disorientation, incoordination, visual disturbances, TACHYCARDIA and HYPERVENTILATION. In severe cases drowsiness may progress rapidly to COMA. There may also be metabolic ACIDOSIS, HYPOKALAEMIA, CONVULSIONS, HYPOTENSION, respiratory depression, ECG changes and cardiovascular collapse. Cerebral OEDEMA is common and will lead to severe brain damage and focal neurological signs. Signi?cant abnormalities on physical examination include impaired short-term memory, abnormal Rhomberg’s test (standing unsupported with eyes closed) and unsteadiness of gait including heel-toe walking. Any one of these signs would classify the episode as severe. Victims’ skin may be coloured pink, though this is very rarely seen even in severe incidents. The venous blood may look ‘arterial’. Patients recovering from acute CO poisoning may suffer neurological sequelae including TREMOR, personality changes, memory impairment, visual loss, inability to concentrate and PARKINSONISM. Chronic low-level exposures may result in nausea, fatigue, headache, confusion, VOMITING, DIARRHOEA, abdominal pain and general malaise. They are often misdiagnosed as in?uenza or food poisoning.

First-aid treatment is to remove the victim from the source of exposure, ensure an e?ective airway and give 100-per-cent oxygen by tight-?tting mask. In hospital, management is largely suppportive, with oxygen administration. A blood sample for COHb level determination should be taken as soon as practicable and, if possible, before oxygen is given. Ideally, oxygen therapy should continue until the COHb level falls below 5 per cent. Patients with any history of unconsciousness, a COHb level greater than 20 per cent on arrival, any neurological signs, any cardiac arrhythmias or anyone who is pregnant should be referred for an expert opinion about possible treatment with hyperbaric oxygen, though this remains a controversial therapy. Hyperbaric oxygen therapy shortens the half-life of COHb, increases plasma oxygen transport and reverses the clinical effects resulting from acute exposures. Carbon monoxide is also an environmental poison and a component of cigarette smoke. Normal body COHb levels due to ENDOGENOUS CO production are 0.4 to

0.7 per cent. Non-smokers in urban areas may have level of 1–2 per cent as a result of environmental exposure. Smokers may have a COHb level of 5 to 6 per cent.... carbon monoxide (co)

One of a number of drugs known as CARDIAC GLYCOSIDES. They increase the contractility of heart muscle, depress the conducting tissue while increasing myocardial excitability, and increase activity of the VAGUS nerve. Digoxin is usually given orally for the treatment of atrial FIBRILLATION and heart failure. The adverse effects of overdosage (which occur more commonly in people with HYPOKALAEMIA, the elderly, and those with renal failure – see KIDNEYS, DISEASES OF) are vomiting, DYSRHYTHMIA, muscle weakness, and visual disturbances. The ELECTROCARDIOGRAM (ECG) has a characteristic appearance.... digoxin

The leaves of various species of Cassia senna. It is one of the most active of the simple laxative drugs (see LAXATIVES). Senna is excreted in the urine, giving it a dark red or yellow colour. In the case of nursing mothers, some of the drug is excreted in the milk and may affect the infant. A standardised preparation of senna, Senokot®, is widely used for the management of constipation in children and old people. A side-e?ect of senna is HYPOKALAEMIA; like other laxatives, it should not be used too often.... senna

Spasms and twitching of the muscles, most commonly in the hands and feet, although the muscles of the face, larynx, or spine may also be affected. The spasms are caused by a biochemical disturbance and are painless at first; if the condition persists, the spasms tend to become increasingly painful. Muscle damage may result if the underlying cause is not treated. The most common underlying cause is hypocalcaemia. Other causes include hypokalaemia, hyperventilation during a panic attack, or, more rarely, hypoparathyroidism.... tetany

abnormalities seen with chronic hypokalaemia (usually K+ <3.0 mmol/l) and manifest by impaired urine-concentrating ability and reduced capacity to excrete sodium. Histological changes include cytoplasmic vacuolation of the renal tubules and medullary fibrosis.... hypokalaemic nephropathy

Substances which increase urine and solute production by the KIDNEYS. They are used in the treatment of heart failure, HYPERTENSION, and sometimes for ASCITES secondary to liver failure. They may work by extra-renal or renal mechanisms.

The potential side-effects of diuretics are HYPOKALAEMIA, DEHYDRATION, and GOUT (in susceptible individuals).

Extra-renal mechanisms (a) Inhibiting release of antidiuretic hormone (e.g. water, alcohol); (b) increased renal blood ?ow (e.g. dopamine in renal doses).

Renal mechanisms (a) Osmotic diuretics act by ‘holding’ water in the renal tubules and preventing its reabsorption (e.g. mannitol); (b) loop diuretics prevent sodium, and therefore water, reabsorption (e.g. FRUSEMIDE); (c) drugs acting on the cortical segment of the Loop of Henle prevent sodium reabsorption, but are ‘weaker’ than loop diuretics (e.g. THIAZIDES); (d) drugs acting on the distal tubule prevent sodium reabsorption by retaining potassium

(e.g. spironalactone).... diuretics

Gossypium herbaceum L. German: Baumwollenbaum. French: Cotonnier en arbre. Italian: Cotone arbusto. Arabian: Kuttun. Indian: Karpas. Iranian: Pambah. Dried root bark. Cotton fibre leaves.

Constituents: mucilage, flavonoids, fixed oil, resin, tannin.

Action: abortifacient. Parturient. Traditional male contraceptive (unproven). Oxytocic, (fresh gathered). Uses. For procuring abortion. Claimed to contract the womb after the action of Ergot, but safer. Alabama Indian squaws made a tea of the freshly-gathered roots to ease pains of childbirth. For absent or painful menstruation. Pain in ovaries. Morning sickness. Reduces sperm count and sexual urge in the male. Reference. Rats were made temporarily infertile without change of mating behaviour, without reducing the male hormone (testosterone) and without heart abnormalities. (Dr Yun-feng-Ren, People’s Republic of China)

Not used in pregnancy. Hypokalaemia may follow overdose. Preparations. Liquid Extract, BPC (1934). Dose, 2-4ml. Tincture BPC (1934). Dose 30-60 drops. ... cotton root

Failure of the left ventricle to receive blood from the pulmonary circulation and to maintain efficient output of incoming blood to the arterial system. Failure to do so leads to congestion of blood in the lungs followed by fluid retention. If uncorrected, leads to kidney disturbance, low blood pressure, cyanosis (blueness of the skin). Onset may be tragically sudden.

Failure of the left ventricle may occur in cases of pericarditis, disease of the aortic valve, nephritis or high blood pressure.

Left ventricular failure is often of sudden onset, urgent, and may manifest as “cardiac asthma”.

Causes: blood clot, anaemia, thyroid disorder, coronary disease, congenital effects, drug therapy (beta blockers, etc), and to fevers that make heavy demands on the left ventricle.

Symptoms: breathlessness, wheezing, sweating, unproductive cough, faintness, bleeding from the lungs, palpitation. Cardiac asthma at night: feels he needs air; better upright than lying flat. Exertion soon tires. Sensation as if heart would stop. Blueness of lips and ears from hold-up in circulation of the blood through the lungs. Frequent chest colds. Awakes gasping for breath. Always tired. Cold hands and feet. Symptoms abate as compensation takes place. ‘Cream and roses’ complexion. The failure of left ventricle soon drags into failure of the right ventricle.

Right ventricular failure leads to congestive heart failure, with raised venous pressure in neck veins and body generally, causing oedema, ascites and liver engorgement.

Treatment. Agents to strengthen, support, and eliminate excess fluids from the body. BHP (1983) advises four main remedies: Hawthorn, Motherwort, Broom and Lily of the Valley. The latter works in a digitaloid manner, strengthening the heart, contracting the vessels, and lessening congestion in the lungs. Tinctures. Hawthorn 2; Stone root 1. Lily of the Valley 1. Dose: 15-45 drops thrice daily.

Broom tea. 2 teaspoons flowers, or 2-3 teaspoons tops and flowers, in cup water brought to boil and simmered one minute. 1 cup freely.

To remove fluid retention in the lungs, diuretics are indicated; chief among which is Dandelion root because of its high potassium content to prevent hypokalaemia. Dandelion coffee. As urinary excretion increases, patient improves.

Vitamin E. Not to be taken in left ventricular disorders.

Diet. See entry: DIET – HEART AND CIRCULATION.

UK Research. Researchers found that left ventricular failure was reduced by a quarter when patients were given magnesium intravenously for the first 24 hours after admission to the coronary care unit. They conclude that it should be given before any other heart therapy is commenced, and that patients should receive regular infusions if no other drug treatment is used. (The Lancet, 2.4.1994). This supports the use of magnesium sulphate (Epsom’s salts) by a past generation of herbal practitioners for the condition. ... heart – left ventricular failure (lvf)

Drugs that help remove excess water from the body by increasing the amount lost as urine. They are used in the treatment of various disorders, which include severe premenstrual syndrome, hypertension, heart failure, the eye condition glaucoma, nephrotic syndrome, and cirrhosis of the liver.

Types of diuretic drug differ markedly in their speed and mode of action. Thiazide diuretics cause a moderate increase in urine production. Loop diuretics are fast-acting, powerful drugs. They are often used as an emergency treatment for heart failure. Potassium-sparing diuretics are used along with thiazide and loop diuretics, both of which may cause the body to lose too much potassium. Carbonic anhydrase inhibitors block the action of the enzyme carbonic anhydrase, which affects the amount of bicarbonate ions in the blood; these drugs increase urine output moderately but are effective only for short periods of time. Osmotic diuretics are used to maintain urine output following serious injury or major surgery.

Diuretic drugs may cause chemical imbalances in the blood.

Hypokalaemia (low blood levels of potassium) is usually treated with potassium supplements or potassium-sparing diuretic drugs.

A diet rich in potassium may be helpful.

Some diuretics raise the blood level of uric acid, increasing the risk of gout.

Certain diuretics increase the blood glucose level, which can cause or worsen diabetes mellitus.... diuretic drugs

A mineral needed to help maintain normal heart rhythm, regulate the body’s water balance, conduct nerve impulses, and contract muscles. Dietary sources of potassium include lean meat, whole grains, green leafy vegetables, beans, and various fruits, such as apricots, dates, and peaches.

A low level of potassium in the blood is known as hypokalaemia. It is usually a result of loss of fluids through diarrhoea and/or vomiting, and causes fatigue, drowsiness, dizziness, and muscle weakness. In more severe cases, there may be abnormal heart rhythms and muscle paralysis.

Excess potassium in the blood is known as hyperkalaemia and is much less common than hypokalaemia. It may be due to excessive intake of potassium supplements, severe kidney failure, Addison’s disease, or prolonged treatment with potassium-sparing in a similar way to nitrates, and widens both arteries and veins. Possible side effects include flushing, nausea, vomiting, and dizziness.... potassium

n. intestinal obstruction, usually obstruction of the small intestine (ileum). Clinical symptoms include abdominal pain and distension, vomiting, and absolute constipation. Paralytic or adynamic ileus is functional obstruction of the ileum due to loss of intestinal movement (peristalsis), which may be caused by abdominal surgery (see laparotomy); spinal injuries; electrolyte abnormalities, particularly of potassium (hypokalaemia); peritonitis; or ischaemia. Treatment consists of intravenous administration of fluid and removal of excess stomach secretions by nasogastric tube until peristalsis returns (the ‘drip and suck’ approach). If possible, the underlying condition is treated. Mechanical ileus may be caused by gallstones entering the bowel through a fistula or widened bile duct (gallstone ileus); tumour; *intussusception; intestinal *volvulus; foreign bodies; thickened *meconium in newborn babies (meconium ileus); or parasitic infestation, for example with the threadworm Enterobius vermicularis (verminous ileus).... ileus

disease of the *tubulointerstitium of the kidney. Acute interstitial nephritis (AIN) represents in many cases an allergic reaction to drugs (especially ampicillin, cephalexin, NSAIDs, allopurinol, and frusemide). AIN can also be associated with acute infections and autoimmune disease. Thirst and polyuria may be prominent, and renal function severely affected. In allergic cases, the use of steroids hastens recovery after the allergen has been removed. Chronic interstitial nephritis (CIN) is associated with progressive scarring of the tubulointerstitium, often with lymphocyte infiltration. Primary causes of CIN include gout, radiation nephropathy, sarcoidosis, *analgesic nephropathy, reflux nephropathy, chronic hypokalaemia and hypercalcaemia, and *Aristolochia-associated nephropathies. Management of CIN involves removal of the precipitating cause, where identified, and control of hypertension.... interstitial nephritis

a rare autosomal *dominant condition characterized by hypertension associated with hypokalaemia, metabolic alkalosis, and low levels of plasma *renin and *aldosterone. The hypertension often starts in infancy and is due to excess resorption of sodium and excretion of potassium by the renal tubules. The syndrome is caused by a single genetic mutation on chromosome 16, which results in dysregulation of a sodium channel in the distal convoluted tubule. Treatment is with a low salt diet and a potassium-sparing diuretic that directly blocks the sodium channel, such as amiloride or triamterene. [G. G. Liddle (1921–89), US endocrinologist]... liddle’s syndrome

(NDI) a condition characterized by *polyuria and *polydipsia and due to failure of the renal tubules to respond, or to respond fully, to *vasopressin. One form of congenital NDI is caused by an X-linked (see sex-linked) dominant mutation of the gene encoding the vasopressin V2 receptor. A rarer form of congenital NDI is an autosomal recessive condition associated with genetic mutations in the gene encoding AQP-2 water channels (see aquaporin). Acquired NDI is much commoner than the congenital form and usually less severe. It is present in most patients with advancing chronic renal failure, is a feature of certain electrolyte disorders (hypokalaemia, hypercalcaemia), and can complicate chronic lithium treatment.... nephrogenic diabetes insipidus