Hyperphosphatemia

Hyperphosphatemia Symptoms
Increased amounts of phosphate in the system can have a serious effect on the persons nervous and cardiovascular system:

Central Nervous system effect: altered mental status, delirium, obtundation, coma, convulsions and seizures, muscle cramping or tetany, neuromuscular hyperexcitability and paresthesia. Cardiovascular system effect: hypotension, heart failure, and prolongation of the QT interval (ECG). Eyes: Cataracts. Hyperphosphatemia cases do not necessarily need hospitalization, not unless the condition was identified while in admission. But this condition needs to be constantly assessed when complications arise such as hypocalcemic tetany or massive extraosseous deposition of calcium phosphate crystals.

Hyperphosphatemia Causes
Phosphorus is an essential element of the cellular system. Phosphorus plays a balance between the intracellular and extracellular compartments and to our tissues and bones. Hyperphosphatemia is commonly caused by the alteration of our renal system causing the decrease of renal excretion of phosphate. Marked elevation of phosphorus is due to these factors:

Renal insufficiency acute or chronic. Renal insufficiency or renal failure is one of the common causes of hyperphosphatemia. The kidneys role is to adequately filter out the toxins and waste products from our blood. Since the normal functioning of the renal system is not attained, it filters out the excess phosphate of our body. Cellular injury trauma, burns, shock are some of the causes of hyperphosphatemia. Poison excessive intake of biphosphonate and vitamin D intoxication can cause this condition. Acidosis diabetic and alcoholic acidosis are one of the root causes of the marked elevation of phosphate in the system. Hypoparathyroidism The low levels of the parathyroid hormone cause this condition. Normally, the PTH acts as an inhibitor for renal reabsorption. When PTH is not enough in the body, there is more reabsorption of phosphate thus resulting to hyperphosphatemia. Tumor lysis syndrome This condition is often caused by cytotoxic therapy. The mechanism of this condition is the rapid cell turnover causing increase release of phosphate and other elements such as potassium, purines, and cell proteins. Those who are at risk for hyperphosphatemia are the following patients who have these conditions: Renal disease Those who may have past or recent sessions of hemodialysis. Cancer Bone tumor is a risk factor of the condition. Chemotherapy treatment can also alter the levels of phosphorus. Medications Taking oral potassium phosphate, antacid use and biphosphonate therapy makes a person at risk for this condition.

Hypermagnesemia
Symptoms
Weakness, nausea and vomiting Impaired breathing Decreased respirations Hypotension Hypercalcemia Arrhythmia and Asystole Decreased or absent deep tendon reflexes Bradycardia

Arrhythmia and asystole are possible cardiac complications of hypermagnesemia. Magnesium acts as physiologic calcium blocker, which results in electrical conduction abnormalities.

Hypermagnesemia in renal failure

Causes

Intake
Although a rare cause of hyperphosphatemia, excessive intake of phosphate can cause hyperphosphatemia. Foods that are high in phosphate are soda, chocolate, biscuits (from the supermarket), ketchup, frozen pizza and hot dogs. Massive intake of these foods can result in hyperphosphatemia, especially if kidney function is not ideal.

Vitamin D
One function of vitamin D is to help absorption of phosphate by the gastrointestinal system and then secretion by the kidneys. As a result, large amounts of vitamin D could cause hyperphosphatemia if phosphate builds up in the gastrointestinal system. In general, these levels of vitamin D intake can only occur by taking too many vitamin supplements, as there are no foods with enough vitamin D to easily cause vitamin D intoxication.

Kidney Failure
One of the main roles that the kidneys have is processing and excreting waste through the production of urine. When the kidneys fail, the compounds that the kidneys normally excrete, such as phosphate, begin to build up in the bloodstream. This condition can eventually lead to hyperphosphatemia.

Hypoparathyroidism
The parathyroid is a gland that is located very near the thyroid gland, and it is responsible for secreting the parathyroid hormone. If the parathyroid becomes damaged via trauma or an autoimmune disease, decreased parathyroid hormone will result. One of the functions of parathyroid hormone is to make the kidney secrete phosphate, so hypoparathyroidism can lead to hyperphosphatemia.

Cell Lysis
Cells contain large amounts of phosphate. When a large number of cells die suddenly and are broken down, this releases the phosphate into the bloodstream. Some conditions that can cause this massive release of phosphate are rhabdomyolysis (where muscle cells are suddenly broken down) and tumor lysis syndrome (a result of killing tumors with radiation and chemotherapy). This can also lead to hyperphosphatemia.

Hypophosphatemia
Common causes of hypophosphatemia [edit]

Refeeding syndrome This causes a demand for phosphate in cells due to the action of Hexokinase, an enzyme that attaches phosphate to glucose to begin metabolism of this. Also, production of ATP when cells are fed and recharge their energy supplies, requires phosphate. Respiratory alkalosis Any alkalemic condition moves phosphate out of the blood into cells. This includes most common respiratory alkalemia (a higher than normal blood pH from low carbon dioxide levels in the blood), which in turn is caused by any hyperventilation (such as may result from sepsis, fever, pain, anxiety, drug withdrawal, and many other causes). This phenomenon is seen because in respiratory alkalosis carbon dioxide (CO2) decreases in the extracellular space, causing intracellular CO2 to freely diffuse out of the cell. This drop in intracellular CO2 causes a rise in cellular pH which has a stimulating effect on glycolysis. Since the process of glycolysis requires phosphate (the end product is adenosine triphosphate), the result is a massive uptake of phosphate into metabolically active tissue (such as muscle) from the serum. It is interesting to note, however, that this effect is not seen in metabolic alkalosis, for in such cases the cause of

the alkalosis is increased bicarbonate rather than decreased CO2. Bicarbonate, unlike CO2, has poor [1] diffusion across the cellular membrane and therefore there is little change in intracellular pH.

Alcohol abuse Alcohol impairs phosphate absorption. Alcoholics are usually also malnourished with regard to minerals. In addition, alcohol treatment is associated with refeeding, and the stress of alcohol withdrawal may create respiratory alkalosis, which exacerbates hypophosphatemia (see above). Malabsorption This includes GI damage, and also failure to absorb phosphate due to lack of vitamin D, or chronic use of phosphate binders such as sucralfate, aluminum-containing antacids, and (more rarely) calcium-containing antacids.

Primary hypophosphatemia is the most common cause of nonnutritional rickets. Laboratory findings include lownormal serum calcium, moderately low serum phosphate, elevated serum alkaline phosphatase, and low serum [2] 1,25 dihydroxy-vitamin D levels, hyperphosphaturia, and no evidence of hyperparathyroidism. Other rarer causes include

Certain blood cancers such as lymphoma or leukemia Hereditary causes Hepatic failure Tumor-induced osteomalacia

Major signs and symptoms [edit]

Muscle dysfunction and weakness. This occurs in major muscles, but also may manifest as: diplopia, low cardiac output, dysphagia, and respiratory depression due to respiratory muscle weakness. Mental status changes. This may range from irritability to gross confusion, delirium, and coma. White cell dysfunction, causing worsening of infections. Instability of cell membranes due to low ATP levels: this may cause rhabdomyolysis with increased CPK, and also hemolytic anemia. Large pulp chambers in their teeth.

Hypomagnesemia
Signs and symptoms [edit]
Deficiency of magnesium causes weakness, muscle cramps, cardiac arrhythmia, increased irritability of the nervous system with tremors, athetosis, jerking, nystagmus and an extensor plantar reflex. In addition, there may be confusion, disorientation, hallucinations, depression, [citation needed] epileptic fits, hypertension, tachycardia and tetany.

Causes [edit]
Magnesium deficiency is not uncommon in hospitalized patients. Elevated levels of magnesium (hypermagnesemia), however, are nearly always iatrogenic. Ten to twenty percent of all hospitalpatients and 60 [citation needed] 65% of patients in the intensive care unit (ICU) have hypomagnesemia. Hypomagnesemia is underdiagnosed, as testing for serum magnesium levels is not routine. Low levels of magnesium in blood may mean that there is not enough magnesium in the diet, the intestines are not absorbing enough magnesium, or the kidneys are excreting too much magnesium. Deficiencies may be due to the following conditions:

Drugs [edit]

Alcoholism. Hypomagnesemia occurs in 30% of alcohol abusers and in 85% of delirium tremens inpatients, [citation needed] due to malnutrition and chronic diarrhea. Alcohol stimulates renal excretion of magnesium, which is also increased because of alcoholic and diabetic ketoacidosis, hypophosphatemia and hyperaldosteronism resulting from liver disease. Also,

hypomagnesemia is related to thiamine deficiency because magnesium is needed for transforming thiamine into thiamine pyrophosphate.

Medications [edit]

Loop and thiazide diuretic use (the most common cause of hypomagnesemia)
[2]

Antibiotics (i.e. aminoglycoside, amphotericin, pentamidine, gentamicin, tobramycin, viomycin) block [citation needed] resorption in the loop of Henle. 30% of patients using these antibiotics have hypomagnesemia. Long term use of proton pump inhibitors such as omeprazole. Other drugs.
[3][4]

Digitalis, displaces magnesium into the cell. Digitalis causes an increased intracellular concentration of sodium, which in turn increases intracellular calcium by passively decreasing the action of the sodiumcalcium exchanger in the sarcolemma. The increased intracellular calcium gives a positive inotropic effect.
[2]

Adrenergics, displace magnesium into the cell Cisplatin, stimulates renal excretion Ciclosporin, stimulates renal excretion Mycophenolate mofetil

Metabolic Abnormalities [edit]

Insufficient selenium,
[5]

vitamin D, sunlight exposure or vitamin B6

Gastrointestinal causes: the distal tractus digestivus secretes high levels of magnesium. Therefore, secretory diarrhea can cause hypomagnesemia. Thus, Crohn's disease, ulcerative colitis,Whipple's disease and celiac sprue can all cause hypomagnesemia. Gitelman/Bartter Syndromes Renal magnesium loss in Bartter's syndrome, necrosis (ATN) and kidney transplant
[6]

postobstructive diuresis, diuretic phase of acute tubular

Diabetes Mellitus: 38% of diabetic outpatient clinic visits involve hypomagnesemia, probably through renal loss because of glycosuria or ketoaciduria.

Other [edit]

Acute myocardial infarction: within the first 48 hours after a heart attack, 80% of patients have hypomagnesemia. This could be the result of an intracellular shift because of an increase in catecholamines. Malabsorption Acute pancreatitis Hydrogen fluoride poisoning Massive transfusion (MT) is a lifesaving treatment of hemorrhagic shock, but can be associated with [7] significant complications.

Hyperchloremia
Hyperchloremia Causes
1. Artifact (low Anion Gap) 2. Metabolic and Endocrine

High sodium level in blood Diabetes insipidus or diabetic coma Hyperparathyroidism Metabolic Acidosis

Type I Renal Tubular Acidosis Type II Renal Tubular Acidosis (lightwood syndrome) Hypernatremia 3. Gastrointestinal Vomiting Prolonged Diarrhea Dehydration Kidney diseases Loss of pancreatic secretion Ureteral colonic anastomosis Ileal loops 4. Brain stem injury resulting in neurogenic hyperventilation 5. Medications

Androgens Estrogens Corticosteroids Diuretics (carbonic anhydrase inhibitors)

Hyperchloremia Symptoms
Often, no symptoms are found. Some include :-

Excess fluid loss or dehydration (diarrhea, vomiting) High blood sugar Kussmauls breathing (deep and rapid breathing) Dyspnea Intense thirst Weakness Tachypnea Hypertension Pitting edema Diminished cognitive ability Possible coma

hypocholeremia
Hypochloremia Causes
Metabolic Alkalosis

Diarrhea Vomiting Respiratory losses Gastric suction (NG Suction) Hyponatremia

Adrenal Insufficiency (Addisons Disease) Renal Failure Edematous states Congestive Heart Failure Pseudohyponatremia Salt-losing nephritis Excessive IV fluids during hospitalization Excessive sweating Burns

Other Causes
Dietary changes (low sodium diet) Medications:

Loop and Thiazide Diuretics Aldosterone ACTH Corticosteroids Bicarbonates Laxatives Genetic diseases Cystic fibrosis Bartters syndrome (is a group of several disorders due to impaired salt reabsorption in the thick ascending Henles loop)

Hypochloremia Symptoms

Excess fluid loss or dehydration (diarrhea, vomiting) Low serum chloride levels Muscle hypertonicity (Spasticity) Tetany Shallow, depressed breathing Hyponatremia Muscle weakness Muscle twitching Sweating High fever