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Disturbance
s
Magnesium
Deficiency/Hypomagnesemia
Causes:
1. decreased dietary magnesium
intake
2. gastrointestinal magnesium losses
3. defects in redistribution of
magnesium
extracellular to intracellular
4. renal magnesium loss
Epidemiology
Muscular weakness
Tremors
Seizure
Paresthesias
Tetany
Positive Chvostek sign and Trousseau sign
Vertical and horizontal nystagmus
Diagnosis
1. The majority of patients with clinical manifestations
of magnesium deficiency have hypomagnesemia.
Measurement of serum magnesium is relatively easy,
and it has become the method of choice to estimate
magnesium content, although its use in evaluating
total body stores is limited.
2. Magnesium assessment can also be made via red
cell, mononuclear cell, or skeletal muscle intracellular
content; 24-hour urinary excretion; fractional
excretion (FE) of magnesium; and intracellular free
magnesium ion concentration with fluorescent dye or
nuclear magnetic resonance spectroscopy.
Hypermagnesemia
A condition that arises from
abnormally elevated magnesium
levels in the blood
Causes:
1.renal failure
2.excessive intake
3.excessive tissue breakdown (eg;
hemolysis)
4.Hypothyroidism, adrenal
insufficiency, milk-alkali
syndrome, Addisons Disease
Epidemiology
1. Occurs quite rarely
2. Mostly in patients of renal failure
Diagnosis
1. Composition of electrolytes in blood, including
potassium, magnesium, and calcium levels
2. BUN and creatinine levels
. To assess the kidneys ability to excrete excess magnesium
CHLORIDE
PHYSIOLOGICAL FUNCTION
prominent negatively charged ion of the blood, where it
represents 70% of the bodys total negative ion content
chloride combines with hydrogen in the stomach to
make hydrochloric acid
maintain electrical neutrality across the stomach
membrane
The exchange of chloride and bicarbonate, between
red blood cells and the plasma helps to govern the pH
balance and transport of carbon dioxide, a waste
product of respiration
Chlorine
Disturbances
Hyperchloremia
indicated by a high level of chloride in
the blood
Causes:
Loss of body fluids from prolonged vomiting,
diarrhea, sweating or high fever (dehydration).
High levels of blood sodium.
Kidney failure, or kidney disorders
Diabetes insipidus or diabetic coma
Drugs such as: androgens, corticosteroids,
estrogens, and certain diuretics.
At risk
Diagnosis
1. Serum chloride levels > 106 mEq/L confirm the
diagnosis.
2. Serum pH is under 7.35
3. Serum carbon dioxide levels < 22 mEq/L.
4. Sometimes, a chloride test can be done on a
sample of the total urine collected over a 24hour period (24-hour urine sample). This finds
out how much chloride is excreted in the urine.
Refer to an endocrinologist
6. Treatment
a) Sodium bicarbonate I.V infusion to raise the
bicarbonate level in blood and for permitting
renal excretion of chloride anion, as chloride and
bicarbonate compete to combine with sodium.
b) Lactated Ringers solution which is administered
in mind cases of hyperchloremia. In liver, this
gets converted to bicarbonate, thereby
increasing the base bicarbonate for correcting
the acidosis caused.
c) Low sodium diet, the excess chloride ions may
combine with sodium to form hypernatremia.
Hypochloremia
anelectrolyte disturbancein which
there is an abnormally low level of
thechlorideion in the blood. (The
normal serum range for chloride is 97 to
107mEq/L.)
Causes
1. Loss of body fluids from prolonged vomiting, diarrhea,
sweating or high fevers.
2. Drugs such as: bicarbonate, corticosteroids, diuretics,
and laxatives.
3. Dietary changes (low sodium diet)-Hyponatremia
4. Medications:
. Loop and Thiazide Diuretics
. Aldosterone
. ACTH
. Corticosteroids
. Bicarbonates
. Laxatives
5. Genetic diseases
Cystic fibrosis
Bartters syndrome(is a group of several
disorders due to impaired salt reabsorption in the
thick ascending Henles loop)
At risk
Diagnosis
1.
2.
3.
4.
6. Dietary modifications
Consume sodium and potassium rich diet, as hypochloremia
causes deficiency of these nutrients.