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Diagnosis of contraction alkalosis is made by correlating laboratory data with clinical history and examination. Metabolic alkalosis in the presence of decreased effective circulatory volume, loop diuretic use, or other causes of intravascular depletion such as profound diarrhea should raise suspicion for contraction alkalosis as a likely etiology in the absence of other causes.
Factors that may induce or sustain [2] hyperventilation include: physiological stress, anxiety or panic disorder, high altitude, head injury, stroke, respiratory disorders such as asthma, pneumonia, or hyperventilation syndrome, [5] cardiovascular problems such as pulmonary embolisms, anemia, an incorrectly calibrated medical respirator, [1] [3 ...
It can also be caused by administration of diuretics [2] and endocrine disorders such as Cushing's syndrome. Compensatory mechanism for metabolic alkalosis involve slowed breathing by the lungs to increase serum carbon dioxide, [2] a condition leaning toward respiratory acidosis. As respiratory acidosis often accompanies the compensation for ...
The diagnosis of respiratory alkalosis is done via test that measure the oxygen and carbon dioxide levels (in the blood), chest x-ray and a pulmonary function test of the individual. [ 1 ] The Davenport diagram is named after Horace W Davenport a teacher and physiologist which allows theoreticians and teachers to graphically describe acid base ...
Hypocalcemia is a medical condition characterized by low calcium levels in the blood serum. [5] The normal range of blood calcium is typically between 2.1–2.6 mmol/L (8.8–10.7 mg/dL, 4.3–5.2 mEq/L), while levels less than 2.1 mmol/L are defined as hypocalcemic. [1] [3] [6] Mildly low levels that develop slowly often have no symptoms.
Hypovolemia then leads to metabolic alkalosis (increase in blood pH) by stimulating bicarbonate reabsorption in order to maintain extracellular volume. [5] [10] In summary, the symptoms of alkalosis is the net result of over-consumption of absorbable alkali, hypercalcemia-induced hypovolemia, and impaired glomerular filtration rate. [5]
Gitelman syndrome; Other names: Primary renal tubular hypokalemic hypomagnesemia with hypocalciuria: A model of transport mechanisms in the distal convoluted tubule.Sodium chloride (NaCl) enters the cell via the apical thiazide-sensitive NCC and leaves the cell through the basolateral Cl − channel (ClC-Kb), and the Na + /K +-ATPase.
infrequent and low volume urination; dry mucous membranes (e.g. a dry tongue) poor capillary refill (e.g. when the patient's fingertip is pressed, the skin turns white, but upon release, the skin does not return to pink as fast as it should - usually >2 seconds) decreased skin turgor (e.g. the skin remains "tented" when it is pinched) a weak pulse