Hypokalemia history and symptoms: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
|||
| Line 10: | Line 10: | ||
==== Medication History ==== | ==== Medication History ==== | ||
* | *[[Diuretic]]s (loop and thiazides) | ||
*Beta agonists | *[[Beta-agonists]] | ||
*Chloroquine | *[[Chloroquine]] | ||
*Theophylline | *[[Theophylline]] | ||
*Insulin | *[[Insulin]] | ||
*Corticosteroids | *[[Corticosteroids]] | ||
*Licorice | *[[Licorice]] | ||
*Nephrotoxic drugs (platinum-based chemotherapy, aminoglycosides) | *[[Nephrotoxic drugs]] (platinum-based chemotherapy, [[aminoglycosides]]) | ||
* | *[[Laxative]]s | ||
==== Past Medical History ==== | ==== Past Medical History ==== | ||
*Uncontrolled diabetes | *Uncontrolled [[diabetes]] | ||
*Hyperthyroidism | *[[Hyperthyroidism]] | ||
*Pernicious anemia | *[[Pernicious anemia]] | ||
*COPD (treated with Beta agonists and theophylline) | *[[COPD]] (treated with Beta agonists and theophylline) | ||
*Cushing’s disease | *[[Cushing’s disease]] | ||
*Periodic paralysis | *Periodic [[paralysis]] | ||
*Ileostomy/short bowel | *[[Ileostomy]]/[[short bowel]] | ||
*Primary hyperaldosteronism | *[[Primary hyperaldosteronism]] | ||
*Liddle syndrome | *[[Liddle syndrome]] | ||
*Bartter and Gitelman syndrome | *[[Bartter syndrome|Bartter]] and [[Gitelman syndrome]] | ||
*Prolonged starvation | *Prolonged [[starvation]] | ||
*Cancer | *[[Cancer]] | ||
*Renal tubular acidosis type I and type II | *[[Renal tubular acidosis]] type I and type II | ||
=== Symptoms === | === Symptoms === | ||
| Line 52: | Line 52: | ||
==== Renal ==== | ==== Renal ==== | ||
*[[Nephrogenic diabetes insipidus]] due to decreased concentrating ability. As a consequence, the patient presents with [[polyuria]] and polydipsia | *[[Nephrogenic diabetes insipidus]] due to decreased concentrating ability. As a consequence, the patient presents with [[polyuria]] and [[polydipsia]] | ||
*Increased bicarbonate reabsorption | *Increased bicarbonate reabsorption | ||
*Increased ammonia formation which may precipitate [[hepatic encephalopathy]] in cirrhotic patients | *Increased ammonia formation which may precipitate [[hepatic encephalopathy]] in cirrhotic patients | ||
Revision as of 14:17, 27 February 2013
|
Hypokalemia Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Hypokalemia history and symptoms On the Web |
|
American Roentgen Ray Society Images of Hypokalemia history and symptoms |
|
Risk calculators and risk factors for Hypokalemia history and symptoms |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Assistant Editor(s)-In-Chief: Jack Khouri
History and Symptoms
History
A detailed history can help depict the cause of hypokalemia.
Dietary History
Malnutrition: lack of meat and fruit intake
Medication History
- Diuretics (loop and thiazides)
- Beta-agonists
- Chloroquine
- Theophylline
- Insulin
- Corticosteroids
- Licorice
- Nephrotoxic drugs (platinum-based chemotherapy, aminoglycosides)
- Laxatives
Past Medical History
- Uncontrolled diabetes
- Hyperthyroidism
- Pernicious anemia
- COPD (treated with Beta agonists and theophylline)
- Cushing’s disease
- Periodic paralysis
- Ileostomy/short bowel
- Primary hyperaldosteronism
- Liddle syndrome
- Bartter and Gitelman syndrome
- Prolonged starvation
- Cancer
- Renal tubular acidosis type I and type II
Symptoms
The severity of symptoms depends on the degree of hypokalemia, but keep in mind that there is marked individual variability.
Constitutional
- Fatigue
- Weakness
- Vomiting
- Constipation
- Muscle cramps and paralysis (the lower extremity muscles are most commonly involved) which may involve the intestine and cause ileus
- Respiratory muscle weakness leading to respiratory failure.
Cardiac
- Hypertension
- Arrhythmias including premature atrial and ventricular complexes, paroxysmal atrial or junctional tachycardia and even ventricular tachycardia or fibrillation
- Heart block
- Digoxin therapy, CAD and left ventricular hypertrophy potentiate hypokalemia effects on the heart
Renal
- Nephrogenic diabetes insipidus due to decreased concentrating ability. As a consequence, the patient presents with polyuria and polydipsia
- Increased bicarbonate reabsorption
- Increased ammonia formation which may precipitate hepatic encephalopathy in cirrhotic patients
- Decreased sodium reabsorption resulting in hyponatremia