This document discusses alterations in potassium metabolism, including hypokalemia and hyperkalemia. It covers the physiological considerations of potassium regulation in the body, with 98% located intracellularly and serum levels normally between 3.5-5 mEq/L. Rapid regulation of potassium involves the sodium-potassium pump and hormones like insulin and catecholamines. Causes, clinical presentations, and treatments are described for both hypokalemia and hyperkalemia. Hypokalemia can result from excessive losses or intracellular shifts, while hyperkalemia involves a positive potassium balance or rapid extracellular shifts. Treatments aim to correct the underlying cause, stabilize cardiac function, shift potassium intracellularly, and promote excretion.

1. UNIVERSIDAD TECNICA DE MACHALA
ACADEMIC UNIT OF CHEMICAL
SCIENCES AND HEALTH
MEDICINE SCHOOL
ENGLISH
ALTERATIONS OF
POTASSIUM
METABOLISM
STUDENTS
William Cruz
Kevin Herrera
Jorge Pacheco
Angie Chamba
Sonia Quijilema
TEACHER:
Mgs. Barreto Huilcapi Lina Maribel
CLASS:
EIGHTH SEMESTER ‘’A’’
Machala, El Oro
2018

2. ALTERATIONS OF POTASSIUM METABOLISM
Physiological considerations.- Potassium is the most abundant cation in the human
organism, with a total of 4000 mEq (4000 mmol). Located mostly (98%) in the
intracellular space and only 60 mEq are in the extracellular. The serum potassium
concentration is maintained between 3.5-5 mEq / L (3.5-5 mmol / L).
Rapid regulation.- The force retaining potassium inside the cell is the
transmembrane negative charge, maintained by the Na-K-ATPase pump of the cell
membrane, which exchanges three sodium ions for two of potassium ions. Insulin and
catecholamines are the two main hormones that regulate the entry of potassium into
the cell through the activation of the Na-K-ATPase pump.
The alteration of the extracellular pH influences the transcellular distribution of
potassium. A pH decrease of 0.1 U produces an increase of about 0.5 mEq / L (0.5
mmol / L) in the serum potassium and a rise in pH of 0.1 U induces a similar
reduction.
Slow regulation.- The intake of potassium in the diet is variable and requires
mechanisms that regulate homeostasis. The kidney removes 90-95% of the potassium
ingested in the diet, and the rest is eliminated by the digestive tract. Renal adaptation
to sustained potassium overload is relatively slow and needs 6-12 h to normalize
serum potassium levels, while the kidney's response to dietary potassium restriction is
still slower and is not fully activated until after After 7-10 days. Even then, urinary
potassium losses are usually greater than 20 mEq / day.
Potassium and neuromuscular excitability. - Involved in the activation
mechanisms of excitable tissues, such as the heart, skeletal muscle and smooth
muscle. The main clinical manifestations associated with potassium disorders are
secondary to alterations in transmembrane electrical phenomena in excitable tissues
that result in cardiac conduction disorders and neuromuscular function.
HYPOKALEMIA

3. Concept.- Hypokalemia is considered to be serum potassium levels below 3.5 mEq /
L (3.5 mmol / L). Hypokalemia should be differentiated from the potassium deficit.
Etiology.- The majority of hypokalemia are usually due to excessive intestinal and /
or renal losses or to the massive entry of potassium into the cell. The renal losses of
potassium differ in three groups of different clinical entities:
a) hypokalemia with arterial hypertension.
b) hypokalemia with normotension arterial
c) drug-induced hypokalemia.
WITHIN EACH ONE WE FIND:
 Hypokalemia associated with arterial hypertension: Primary
aldosteronism, vasculorrenal hypertension, 11-b-hydroxysteroid
dehydrogenase deficiency, Cushing's syndrome, congenital adrenal
hyperplasia, Liddle's syndrome and familial hypokalemic periodic paralysis.
 Hypokalemia with normal blood pressure: Kidney tubular acidosis types I
(distal) and II (proximal) and Bartter syndrome (hereditary).
 Drug-induced hypokalemia: loop diuretics (furosemide, bumetanide),
thiazides, indapamide, mannitol and acetazolamide; the mineralocorticoids
and glucocorticoids; carbenicillin and other penicillins; amphotericin B; the
aminoglycosides, cisplatin, foscarnet and alcohol.
Clinical picture.- With muscle potassium concentrations between 2 and 2.5 mEq / L
(2 and 2.5 mmol / L) muscle weakness appears. The arreflexica paralysis appears in
situations of severe hypokalemia as well as constipation, paralytic ileus and
respiratory failure. In the heart, hypokalemia produces electrophysiological disorders:
flattening of T waves and the appearance of U waves. Severe hypokalemia (serum
potassium below 2 mEq / L [2 mmol / L]) inhibits the reabsorption of chlorine in the
ascending portion of the loop of Henle and causes urinary losses of this, with
hypochloremic metabolic alkalosis. Chronic hypokalemia can develop vacuolization
of the proximal tubule and interstitial fibrosis.
Treatment.- Consists of the administration of potassium salts, in addition to
correcting the disorder responsible for hypokalemia. If there are digestive disorders or

4. neuromuscular manifestations, especially cardiac, administration by intravenous route
is advisable; the total amount of potassium administered in a day will be less than 200
mEq. For oral administration, organic potassium salts, such as gluconate or citrate,
are more convenient.
HYPERKALEMIA
Concept.- Defined by serum potassium levels greater than 5 mEq / L (5mmol / L), it
is the most serious of the electrolyte alterations, due to the risk of causing fatal
ventricular arrhythmias quickly. Before any hyperkalemia, the first thing is to rule out
the existence of a pseudohyperkalemia.
Etiology.- The true hyperkalemia is produced by a positive balance of potassium
(defect of elimination or excess of contribution) or by a rapid exit of potassium from
the intracellular space to the extracellular one.
Clinical picture.- It manifests in the form of neuromuscular and cardiac alterations.
Paresthesias, muscle weakness, flaccid paralysis and respiratory arrest can occur in
the neuromuscular system. The initial electrocardiographic alteration associated with
hyperkalemia is the appearance of peaked T waves, which emerge with K
concentrations of 6.5 mEq / L.
Treatment.- Severe hyperkalemia with electrocardiographic alterations constitutes a
critical situation, requiring immediate treatment such as: myocardial stabilization,
transfer of potassium from the extracellular to the intracellular space and the
elimination of potassium from the body by diuretics.
a) Myocardial stabilization.- the administration of calcium gluconate i.v (10-30
mL of a 20% solution in a min) does not modify the serum potassium but
improves the ECG immediately.
b) Transfer of potassium from the extracellular space to the intracellular space.-
(insulin, B2-agonists and sodium bicarbonate). Insulin is the fastest way to
decrease serum potassium; its effect is observed 15 minutes after
administration. B2-agonists administered by inhalation or i.v produce a rapid
entry of potassium into the cell, allowing transient control of hyperkalemia.

5. Sodium bicarbonate, at a rate of 40-150 mEq via i.v, passes potassium into the
cells in an interval of 3-4 h.
c) Elimination of potassium from the organism by diuretics - especially those of
asa (furosemide) increase the urinary excretion of potassium in patients with
preserved renal function. Hemodialysis or peritoneal dialysis are effective
methods of eliminating body potassium and correcting hyperkalemia.
BIBLIOGRAPHIC REFERENCE:
Campistol Plana, J., "Alterations of potassium metabolism", Farreras, V. Rozman, C,
Internal Medicine, Barcelona-Spain, Elsevier, 2016, Vol. 1, p., 782-787