Excessive intake
Excessive intake of potassium is not a primary cause of hyperkalemia because the human body usually can adapt to the rise in the potassium levels by increasing the excretion of potassium into urine through aldosterone hormone secretion and increasing the number of potassium secreting channels in kidney tubules. Acute hyperkalemia in infants is also rare even though their body volume is small, with accidental ingestion of potassium salts or potassium medications. Hyperkalemia usually develops when there are other co-morbidities such as hypoaldosteronism and chronic kidney disease. Pseudohyperkalemia
Pseudohyperkalemia occurs when the measured potassium level is falsely elevated. This condition is usually suspected when the patient is clinically well without any ECG changes. Mechanical trauma during blood drawing can cause potassium leakage out of the red blood cells due to haemolysis of the blood sample. Repeated fist clenching during the blood draw can cause a transient rise in potassium levels. Prolonged length of blood storage can also increase serum potassium levels. Hyperkalemia may become apparent when a persons platelet concentration is more than 500,000/microL in a clotted blood sample (serum blood sample). Potassium leaks out of platelets after clotting has occurred. A high white cell count (greater than 120,000/microL) in people with chronic lymphocytic leukemia increases the fragility of red blood cells, thus causing pseudohyperkalemia during blood processing. This problem can be avoided by processing serum samples, because clot formation protects the cells from haemolysis during processing.
Many KP bumps contain an ingrown hair that has coiled. This is a result of the keratinized skins "capping off" the hair follicle, preventing the hair from exiting. The hair grows encapsulated inside the follicle. KP is more common in patients affected by atopic diseases such as allergic rhinitis and atopic dermatitis. KP subtypes are occasionally part of genetically inherited syndromes associated with intellectual disability, neuro-cardio-facial-cutaneous syndromes, RASopathies, ectodermal dysplasias, and certain myopathies. Diagnosis
Physicians can often diagnose KP simply by examining the skin without specialized tests, but a dermatologist can use dermoscopy to confirm the diagnosis and assess if a person with KP is responding to treatment. Physicians often consider family history and the presence of symptoms when making the diagnosis. Those with this condition are generally encouraged to contact a physician if the bumps are bothersome and do not improve with over-the-counter lotions. Differential diagnosis
Several medications that can cause a skin eruption similar to KP include cyclosporine, BRAF inhibitors, and tyrosine kinase inhibitors. Classification
The several different types of KP include KP rubra (red, inflamed bumps, which can be on arms, head, legs), KP alba (rough, bumpy skin with no irritation), KP rubra faceii (reddish rash on the cheeks), KP atrophicans, keratosis follicularis spinulosa decalvans, atrophoderma vermiculatum, KP atrophicans faciei, erythromelanosis follicularis faciei et colli, and papular profuse precocious KP.KP is commonly described in association with other dry-skin conditions, such as ichthyosis vulgaris, dry skin, and atopic dermatitis, including those of asthma and allergies.