TAILIEUCHUNG - Chapter 048. Acidosis and Alkalosis (Part 12)

Metabolic Alkalosis Associated with ECFV Expansion, Hypertension, and HyperaIncreased aldosterone levels may be the result of autonomous primary adrenal overproduction or of secondary aldosterone release due to renal overproduction of renin. Mineralocorticoid excess increases net acid excretion and may result in metabolic alkalosis, which may be worsened by associated K + deficiency. ECFV expansion from salt retention causes hypertension. The kaliuresis persists because of mineralocorticoid excess and distal Na + absorption causing enhanced K+ excretion, continued K+ depletion with polydipsia, inability to concentrate the urine, and polyuria. Liddle's syndrome (Chap. 278) results from increased activity of the collecting duct Na+. | Chapter 048. Acidosis and Alkalosis Part 12 Metabolic Alkalosis Associated with ECFV Expansion Hypertension and Hyperaldosteronism Increased aldosterone levels may be the result of autonomous primary adrenal overproduction or of secondary aldosterone release due to renal overproduction of renin. Mineralocorticoid excess increases net acid excretion and may result in metabolic alkalosis which may be worsened by associated K deficiency. ECFV expansion from salt retention causes hypertension. The kaliuresis persists because of mineralocorticoid excess and distal Na absorption causing enhanced K excretion continued K depletion with polydipsia inability to concentrate the urine and polyuria. Liddle s syndrome Chap. 278 results from increased activity of the collecting duct Na channel ENaC and is a rare inherited disorder associated with hypertension due to volume expansion manifested as hypokalemic alkalosis and normal aldosterone levels. Symptoms With metabolic alkalosis changes in central and peripheral nervous system function are similar to those of hypocalcemia Chap. 346 symptoms include mental confusion obtundation and a predisposition to seizures paresthesia muscular cramping tetany aggravation of arrhythmias and hypoxemia in chronic obstructive pulmonary disease. Related electrolyte abnormalities include hypokalemia and hypophosphatemia. newpage Metabolic Alkalosis Treatment This is primarily directed at correcting the underlying stimulus for HCO3-generation. If primary aldosteronism renal artery stenosis or Cushing s syndrome is present correction of the underlying cause will reverse the alkalosis. H loss by the stomach or kidneys can be mitigated by the use of proton pump inhibitors or the discontinuation of diuretics. The second aspect of treatment is to remove the factors that sustain the inappropriate increase in HCO3- reabsorption such as ECFV contraction or K deficiency. Although K deficits should be repaired NaCl therapy is usually sufficient to reverse .

• Y học thường thức
• Acidosis and Alkalosis
• bệnh học và điều trị
• bài giảng bệnh học
• tài liệu học ngành y
• Harrisons Internal Medicine
• Respiratory acidosis
• Respiratory alkalosis
• Metabolic acidosis
• Arterial blood gas interpretation
• Metabolic alkalosis
• Compensatory mechanisms
• BMC Pharmacology and Toxicology
• Airway surface liquid pH
• Airway blood flow
• Blood gases
• Case examples
• medical books
• pharmacology
• epidemiologic
• Obstetrics
• anatomy
• Preventing Morbidity
• Multidisciplinary Care
• Handbook of blood gas
• Base interpretation
• Buffer systems
• Carbon dioxide levels
• Gas exchange
• The non invasive monitoring
• Clinical approach
• Diagnose acid–base disorders
• Drinking binge yesterday