hypokalaemia

[la jaja]

terme en anglais trouvé sur une chatterie d'Asians.

quelqu'un pourrait me traduire et me dire à quoi ça correspond ?????

[quézal]

moi je connais le terme' hypocalcémie', je ne sais pas si ça a un rapport...: dans quel contexte tu as lu ça ???

[jena]

An abnormally low concentration of potassium ions in the blood.

[la jaja]

ba ba ba ba ba Jéna !!!!! t'es culturée toa : Miçi !

Quézal : c'était une chatterie étrangère qui parlait de ça sur ses Burmeses européens.

par contre, chuis un peu frustrée là, parce que je ne sais pas à quoi mène un déficit de potassium, en dehors des problèmes musculaires :

[quézal]

Jaja oui, je viens de voir ça sur Wiki..dia; effectivement ils disent que les Burmèses peuvent être touchés par ce souci ...les éléveurs de Bubu doivent être au courant

d'après ce que je comprends: myalgie et arythmie...apparemment ça peut être un facteur héréditaire... pour le reste, mes souvenirs de langue de Shakespeare sont très très lointains, et on étudiait pas la bio en anglais de toute façon.... :

[la jaja]

mdr Quézal, on était en train de lire la mm chose !!!! je comprends bien mieux pourquoi ma véto voulait absolument le taux de potassium :

en revanche, c'est un problème de santé que je découvre chez le bubu qui est interessant à savoir.

[quézal]

:::

[jena]

pourquoi jaja ,tu doutais de mon intelligence:::::

[jena]

encors un sujet qui fache???::: nonnnnnn

[mavidouchat]

Hypokaliémie, c'est une baisse de potassium dans le sang ... : Mais cela n'a rien de spécifique ... ça peut avoir plein de causes, diarhées, vomissements, médicaments, problème rénal etc ...

[quézal]

Mavidouchat: appremment les sujets Burmeses y sont sensibles, du moins certaines lignées si je comprends bien



y'a pas d'éleveurs de bubu , alors????

[jena]

tu connais l'anglais , depatouille toi::


HYPOKALAEMIA

DEFINITION

A serum potassium concentration less than 3.5 mmol/L (mEq/L).

A serum potassium concentration of less than 2 mmol/L is regarded as
severe hypokalaemia.

TOXIC CAUSES

Hypokalaemia in acute poisonings a consequence of one the following
mechanisms:

Secondary to shift of potassium from extracellular to intracellular
space
Competitive blockade of K+ channels
Barium
Chloroquine
Increased Na+/K+ ATPase activity
Beta 2 agonists (e.g. albuterol/salbutamol, terbutaline,
epinephrine)
Caffeine
Insulin
Theophylline,
Toxic metabolic alkalosis or respiratory alkalosis

Secondary to increased renal losses of potassium
Chronic glucocorticoid administration
Chronic toluene abuse
Liquorice and carbenoxolone
Potassium-losing diuretics

Secondary to increased gastrointestinal losses of potassium
Any acute poisoning associated with protracted vomiting or
diarrhoea.

Secondary to increased potassium loss in sweat
Cholinergic syndrome with severe sweating

NON-TOXIC CASES

Secondary to shift of potassium from extracellular to intracellular
space
Insulinoma
Metabolic or respiratory alkalosis
Total parenteral nutrition

Secondary to increased gastrointestinal losses of potassium
Anorexia nervosa/bulimia
Diarrhoea
Prolonged gastric suction
Toxic megacolon

Villous adenoma of colon
Vomiting, protracted
Zollinger-Ellison syndrome

Secondary to increased renal losses of potassium
Cushing's syndrome
Hyperaldosteronism, primary or secondary
Increased urinary flow (postobstructive diuresis, large
IV infusions)
Magnesium deficiency
Renal tubular acidosis

Inadequate dietary intake of potassium
Alcoholism
Anorexia nervosa
Intravenous infusion of potassium-free fluid
Malnutrition

CLINICAL FEATURES

At serum potassium concentrations between 2.5 and 3.5 mmol/L the
patient may be asymptomatic or experience mild symptoms, including
weakness and muscle fatigue. As serum potassium concentration falls
below 2.5 mmol/L, clinical manifestations may progress to include
severe muscle weakness, ileus, respiratory paralysis and atrial and
ventricular arrhythmias. The patient with severe hypokalaemia is at
risk of sudden death from respiratory or cardiac arrest (ventricular
tachycardia).

Hypokalaemia alters the resting membrane potential and slows
repolarisation. These changes are reflected in the electrocardiogram
by depression of ST segments, flattening of the T wave, and prominence
of the U wave (rarely). The absence of a visible T wave and the
presence of a U wave may mimic QT prolongation.

DIFFERENTIAL DIAGNOSIS

Arrhythmias: Hypoxia, use of digitalis or other drugs, myocardial
injury, and other electrolyte disturbances (hypomagnesaemia).
Muscle weakness: Myasthenia gravis, botulism, and central or
peripheral neurological disease.

RELEVANT INVESTIGATIONS

Serum potassium
Serum sodium, chloride, and bicarbonate
Renal function tests (urea, creatinine)
ECG
Arterial blood gas analysis
Urine potassium concentration (24 hour collection)

TREATMENT

Treatment is determined by the acuity and mechanism of the
intoxication, as well as the serum potassium, the severity of
symptoms, and the presence or absence of ECG abnormalities. For
patients with hypokalaemia due to chronic diuretic use or prolonged
severe gastrointestinal or renal potassium losses, the total body
potassium deficit may be as large as 300 to 500 mEq. On the other
hand, hypokalaemia due to intracellular shift of potassium is
associated with relatively small total body potassium deficit and may
not warrant aggressive replacement.

Mild hypokalaemia can usually be managed with oral potassium
supplements. Moderate-to-severely symptomatic patients require, in
addition to management of the underlying condition, continuous cardiac
monitoring and intravenous potassium supplementation. Specific
management of acute complications such as cardiorespiratory arrest,
ventricular arrhythmias, respiratory failure and rhabdomyolyis is also
indicated.

Mild hypokalaemia (3 to 3.5 mmol/L)
Oral potassium supplementation of 30 to 100 mmols/day is
adequate.
Elixir: 10% elixir provides 20 mmols/tablespoon; 2 to 3
tablespoons/day is usually sufficient. Best tolerated when
diluted with juice and taken with meals.
Tablets: Wax matrix tablets contain 6 to 8 mmols/tablet and may
be better tolerated than the liquid form.

Moderate hypokalaemia (2.5 to 3 mmol/L)
Oral potassium replacement as for mild hypokalaemia, if
tolerated. In symptomatic patients, and those unable to take
oral potassium, administer up to 10 mmol of potassium per hour
intravenously, with continuous cardiac monitoring and frequent
monitoring (e.g. every 4 hours) of the serum potassium
concentration.

Moderately severe hypokalaemia (2 to 2.5 mmol/L)
Oral potassium replacement as for mild hypokalaemia, if
tolerated. In addition, administer up to 15 mmol of potassium per
hour intravenously, with continuous cardiac monitoring and
frequent monitoring (e.g. every 4 hours) of the serum potassium
concentration.

Severe hypokalaemia (2 mmol/L)
Oral potassium replacement as for mild hypokalaemia, if
tolerated. In addition, administer up to 20 mmol of potassium per
hour intravenously, with continuous cardiac monitoring and
frequent monitoring (e.g. every 4 hours) of the serum potassium
concentration. In very severe cases, infusion rates as high as
30 mmol/hour have been used, but caution should be exercised
because of the potential for cardiotoxicity, especially if the
potassium is administered via a central catheter.

Pediatric dosing of potassium is based on the body weight, duration
and mechanism of hypokalaemia, and the potassium level. In general,
dosing should not exceed 0.25 mmol/kg per hour.

Hypokalaemia associated with beta-2 adrenergic stimulation may be
treated with beta-adrenergic blockers (eg, propranolol, esmolol).
Caution should be used if the patient has a history of asthma.

CLINICAL COURSE AND MONITORING

Continuous monitoring of cardiac rhythm together with careful
monitoring of serum potassium and other electrolyte concentrations,
acid-base status, and renal function is indicated until severe
hypokalaemia and the underlying cause are controlled.

Over-zealous infusion of potassium in the acute phase of hypokalaemia
secondary to potassium channel blockade or beta-2-adrenergic
stimulation may result in rebound hyperkalaemia during recovery.

LONG-TERM COMPLICATIONS

Hypoxic brain and other organ injury may occur as a result of cardiac
or respiratory arrest secondary to hypokalaemia.

Acute renal failure may be associated with rhabdomyolysis secondary to
hypokalaemia.

[quézal]

merçi Jena, chuis drôlement bien avancée là!!:::

[Baltique]

Et bien Jaja, c'est la première fois que j'entends parler de çà chez les burmèses européens. :

Le taux de potassium est très important dans l'équilibre ionique du sang et pour le rythme cardiaque et dans l'équilibre calcium / potassium. Asuivre :

[Baltique]

Jena, comment on fait un copier / coller ? merci