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Anonymous users2024-02-07Exhalation refers to the weakening of alveolar ventilation and ventilation function, which can not fully excrete the CO2 produced in the body, resulting in blood P
Increased CO2, causing hypercapnia. Oxynal alkali is the excessive production of CO2 in the body, which leads to a decrease in PACO2 and eventually causes low-carbon alkalemia. Acidophoacidosis.
Acid substitute) refers to an increase in extracellular fluid H+ and/or HCO3-
Loss of acid-base balance disorders characterized by a decrease in plasma HCO3-. Ag-increasing acid substitute: refers to metabolic acidosis when plasma concentrations of any fixed acid other than chlorine are increased. Characteristics: increased AG and normal blood chloride.
AG normal acid substitute: refers to HCO3-
When the concentration is low and accompanied by a compensatory increase in Cl- concentration, there is a normal AG or hyperchloremic metabolic acidosis. Characteristics: normal AG, elevated blood chlorideMetabolic alkalosis (alkaloidosis) is caused by a decrease in nonvolatile acids or an increase in alkali in extracellular fluid, and its main characteristics are an increase in plasma HCO3 concentration and a compensatory increase in PAC2.
May be present alone or mixed with respiratory acidosis. The main compensatory mechanisms are respiratory CO2 retention and renal excretion of bicarbonate with H retention. Symptoms of alkali substitutes include numbness and tingling in the fingers, carpal and foot spasms, and arrhythmias.
However, it is often masked by the underlying disease. In patients with hypocalcemia, tetany may occur; In patients with hypokalemia, polyuria, polydipsia, and paralysis may occur; In patients with hypovolaemia, postural vertigo and muscle weakness may occur. In severe cases, confusion, unresponsiveness, and even delirium may occur.
Hope it helps.
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Anonymous users2024-02-06ag stands for anion gap.
Anion gap) = difference between unmeasured anions (UA) and unmeasured cations (UC). This is not easy to calculate, but it can be calculated directly by subtracting the concentration of chloride ions from the concentration of HCO3- that can be measured, and the general value is 12 2mmol L
Can distinguish between different metabolic acidosis.
Analysis of mixed acid-base disorders
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Anonymous users2024-02-05Acetacetic acid, beda-hydroxybutyrate, and ketone bodies.
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Anonymous users2024-02-04a.Patients with ketoacidosis.
b.Patients with advanced chronic renal failure.
c.Patients with lactic acidosis.
d.Patients with salicylate poisoning.
e.Patients with vomiting.
Correct Answer: Ketoacidosis patients; Patients with chronic renal failure in the late excavation and demolition stage; patients with papillae without acidic acidosis; Patients with salicylate poisoning.
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Anonymous users2024-02-03The cause of hyper-ag metabolic acidosis is () aTaking too many chlorine-containing medications.
b.Ketoic acid is poisonous.
c.Carbonic acid tardihydrase inhibitors are used.
d.Diarrhoea. e.Distal renal tubular acidosis.
Correct answer: B
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Anonymous users2024-02-02Answer] :(1) Excessive intake of fixed acids: Overdose of salicylic acid drugs such as aspirin can cause metabolic acidosis. (2 points).
2) Excessive production of fixed acid: lactic acidosis: when tissues are hypoperfused or hypoxic due to various reasons, such as shock, heart failure, hypoxia, severe anemia, etc., insufficient oxygen supply enhances the anaerobic digestion of glucose and imitates aerobic oxidation disorder, resulting in a large increase in lactic acid; Ketoacidosis:
It is more common in diabetes, severe hunger, and alcoholism. Ketoacidosis occurs due to decreased glucose utilization or insufficient glycogen stores, which accelerates lipolysis and produces a large number of ketone bodies. (5 points).
3) Renal excretion of high excretion of fixed acid: in the late stage of acute and chronic renal failure, the body produces phosphate (HPO42-) during metabolic processesSulfate ((SO4, 2-), etc., cannot be fully excreted in the urine, so that the fixed acid in the blood increases, and the AG increases.
3 points).
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Anonymous users2024-02-01The following can cause normal metabolic acidosis of the mask disturbance ().
a.Diabetes.
b.Shock. C. Digestive tract macro Li Nao lost hc03-
d.Severe hunger.
e.Overdose of salicylic acid drugs.
Correct answer: c
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Anonymous users2024-01-31Which of the following is **()aRenal failure and acid excretion disorders.
b.Renal tubular sophora fibrillic acidosis.
c.Diabetic ketoacidosis.
d.Shock: lactic acid, and acidosis.
e.Salicylic acid poisoning.
Correct answer: B
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Anonymous users2024-01-30Anion gap (AG), which refers to the amount of anion in the blood that has not been measured, is usually expressed as (Na+-C1--HCO3-). This is an important indicator of metabolic acidosis and provides important clues to the diagnosis of many potentially fatal conditions. Reference Range:
8 16 mmol l, with an average of 12 mmol l.
Clinical significance: AG is a useful indicator for early detection of metabolic acidosis combined with metabolic alkalosis, chronic respiratory acidosis combined with metabolic acidosis, respiratory alkalosis combined with metabolic acidosis, mixed metabolic acidosis and triple acid-base imbalance. When using AG as an index, serum electrolytes should be accurately measured, and the influence of experimental errors on AG has been ruled out.
Elevated AG indicates the presence of metabolic acidosis, which can be masked by other phenomena in patients with mixed acid-base disorders, and many potentially valuable clues can be found through AG values.
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Anonymous users2024-01-29ag=ua-uc。Refers to the difference between the total number of cations and the total number of anions measured in the serum.
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Anonymous users2024-01-28There are three main causes of AG enlarged metabolic acidosis: Excessive intake of non-chlorinated acid drugs: such as salicylic acid poisoning can increase the anion content of organic acids in the blood, increase AG, deplete HCO3- due to neutralizing organic acids, and decrease [HCO3-].
Increased acid production: hunger, diabetes, etc., due to the large decomposition of body fat, increased ketone production; Hypoxia, shock, cardiorespiratory arrest, etc., make aerobic oxidation disorders, anaerobic digestion increases, lactate production increases. Elevated ketone bodies and lactate content can lead to an increase in the concentration of organic acid anions in the blood, an increase in AG, and a large consumption of HCO3- in plasma to neutralize these acids, resulting in AG-enlarged metabolic acidosis.
Decreased acid excretion: hyper-AG metabolic acidosis due to renal dysfunction occurs in severe renal failure. At this time, in addition to the decrease in tubular epithelial cell secretion H+, the glomerular filtration rate is significantly reduced.
The phosphate, sulfate and other fixed acids produced by the body in the metabolic process cannot be excreted through the kidneys, and the anions in the blood are not measured, the ag increases, and the plasma HCO3- content decreases due to the decrease in renal reabsorption and consumption, resulting in hyper-ag metabolic acidosis.
The causes and mechanisms of AG normal metabolic acidosis are as follows:
1) Direct loss of HCO3- in the digestive tract: the concentration of HCO3- in intestinal fluid is higher than that of plasma [HCO3-], and the loss of intestinal fluid caused by any reason can cause HCO3- loss, so that plasma [HCO3-] decreases.
2) Mild or moderate renal failure, decreased H+ secretion and reabsorption of HCO3- by renal tubular epithelial cells.
3) Renal tubular acidosis, due to the lesion of renal tubular epithelial cells, resulting in a decrease in HCO3- reabsorption by proximal tubular epithelial cells and a decrease in the H+ function of collecting ducts, resulting in a decrease in plasma HCO3- concentration.
4) Use of carbonic anhydrase inhibitors: Carbonic anhydrase inhibitors can inhibit the activity of carbonic anhydrase in renal tubular epithelial cells, so the production of intracellular H2CO3 is reduced, resulting in a decrease in H+ secretion and reabsorption of HCO3- by renal tubular epithelial cells.
5) Excessive intake of chlorine-containing acidogenic drugs: due to the use of too many chlorine-containing salt drugs, such as ammonium chloride, arginine hydrochloride, etc., HCl is easy to decompose HCl in the body, and HCl consumes HCO3- in plasma, resulting in AG metabolic acidosis.
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