Acid-Base Imbalances and Metabolic Acidosis

What are the two main types of metabolic acidosis?

What is the normal range for the anion gap?

Which of the following is NOT a common etiology of anion gap metabolic acidosis (AGMA)?

Which of the following medications can decrease the activity of the electron transport chain, leading to lactic acidosis?

Incidental toxic alcohol ingestion, such as methanol, ethylene glycol, and paint thinner, can lead to metabolic acidosis.

Which of the following is NOT a common cause of non-anion gap metabolic acidosis (NAGMA)?

In cases of chronic kidney disease, the kidneys are unable to excrete hydrogen ions (H+) and reabsorb bicarbonate.

Diarrhea can cause excessive loss of bicarbonate, leading to non-anion gap metabolic acidosis.

What is the major issue that causes complications in metabolic acidosis?

What is a common complication of metabolic acidosis resulting from the body's attempt to buffer the blood?

Elevated hydrogen ion levels can impair myocardial contractility, leading to reduced cardiac output and blood pressure.

Which of the following is NOT a manifestation of metabolic acidosis?

Chronic acidemia can have a negative impact on the musculoskeletal system due to the leaching of calcium from bone in order to buffer the excess H+ ions.

What is the primary characteristic of metabolic alkalosis?

Which of the following is NOT a common cause of metabolic alkalosis?

Loop diuretics can interrupt sodium reabsorption, leading to a decrease in blood volume and a subsequent increase in H+ ion excretion.

What is the primary mechanism for the development of hypervolemia in hyperaldosteronism?

GI losses resulting from conditions like vomiting and nasogastric suctioning can lead to hypokalemia.

Which of the following conditions is characterized by a shift in bicarbonate from the intracellular fluid (ICF) to the extracellular fluid (ECF), resulting in alkalosis?

Hypochloremia can trigger the kidneys to compensate by reabsorbing more chloride at the expense of bicarbonate, further contributing to alkalosis.

Calcium carbonate-based antacids, like Alka-Seltzer and Tums, can lead to metabolic alkalosis.

Hypercalcemia, or high levels of calcium in the blood, can actually inhibit sodium reabsorption, leading to hypovolemia.

What is the primary complication associated with metabolic alkalosis?

Hypokalemia, or low potassium levels, is a common complication of metabolic alkalosis because the body normally relies on potassium to buffer the hydrogen ions when they are absent.

Chemoreceptors, which detect changes in blood pH and oxygen levels, play a role in regulating breathing, and in cases of metabolic alkalosis, chemoreceptors can trigger hypoventilation to help increase pCO2 and acidify the blood.

Hypocalcemia (low free calcium levels) can occur in cases of metabolic alkalosis because albumin now binds to calcium instead of hydrogen ions.

Respiratory acidosis is characterized by an increase in pCO2, leading to a decrease in blood pH.

What is the primary cause of respiratory acidosis?

In metabolic acid-base imbalances, compensation occurs more quickly than in respiratory acid-base imbalances because the body can immediately adjust ventilation.

Which of the following is NOT a common etiology of respiratory acidosis?

When the respiratory centers in the pons and medulla oblongata are damaged or depressed, signals are unable to be sent to the respiratory muscles, leading to respiratory acidosis.

Which of the following neuromuscular diseases can lead to respiratory acidosis?

Airway obstruction can lead to respiratory acidosis because it can prevent proper exhalation of air, causing a buildup of CO2.

Patients with lung diseases like COPD, exacerbated asthma, chest injuries, or pulmonary edema are at an increased risk of developing respiratory acidosis.

Hypoxemia, or low blood oxygen levels, typically precedes acidosis in airway obstruction because oxygen diffuses slower than CO2. This means that CO2 builds up more quickly, leading to acidosis.

Shallow breathing with wheezing is a common sign of respiratory acidosis caused by airway obstruction.

Oxygen administration in COPD patients can sometimes exacerbate respiratory acidosis because it inhibits chemoreceptor control of breathing, leading to further hypoventilation and a buildup of pCO2.

CO2 can easily cross the blood-brain barrier, causing vasodilation at elevated levels, leading to cerebral vasodilation.

Increased intracranial pressure can occur in respiratory acidosis as cerebral vasodilation causes a greater volume of blood to flow to the brain, potentially leading to cognitive deficiencies and arousal problems.

Respiratory alkalosis is a less serious condition compared to other imbalances and is characterized by a decrease in pCO2, leading to increased blood pH.

What are the two primary etiologies of hyperventilation in respiratory alkalosis?

Pain and anxiety can cause hyperventilation by increasing the activity of the respiratory centers.

Aspirin toxicity can increase the metabolic rate of neurons in the respiratory centers, leading to hyperventilation.

Conditions like early sepsis, pregnancy, and fever can all be associated with hyperventilation.

The kidneys compensate for respiratory alkalosis by decreasing H+ secretion and bicarbonate reabsorption.

A major complication of respiratory alkalosis is the opposite of respiratory acidosis, namely cerebral vasoconstriction.

Reduced cerebral blood flow due to vasoconstriction can decrease intracranial pressure and cause syncope, or fainting.

It is common practice to program a ventilator to cause mild hypoventilation in patients with elevated intracranial pressure to help counteract the vasoconstriction caused by respiratory alkalosis.

What is the initial chemical change that distinguishes metabolic acidosis from other acid-base imbalances?

What is the initial chemical change that distinguishes respiratory acidosis from other acid-base imbalances?

The anion gap helps differentiate metabolic acidosis caused by an increase in fixed acids from that caused by hyperchloremia.

Acute respiratory acidosis is characterized by a high pCO2 and a normal HCO3- level. Chronic respiratory acidosis is characterized by a high pCO2 and a high HCO3- level.

The main criteria for identifying metabolic acidosis is a low blood pH.

Acute metabolic acidosis is typically characterized by a normal or slightly decreased pCO2, while chronic metabolic acidosis is typically characterized by a decreased pCO2.

The main criteria for identifying respiratory acidosis is a high pCO2.

What is the primary treatment for diabetic ketoacidosis?

What is the primary treatment for lactic acidosis caused by hypovolemia?

What is the primary treatment for uremic acidosis?

What is the primary treatment for alcohol ingestion that results in metabolic acidosis?

The treatment for NAGMA is sodium bicarbonate.

Which of the following treatments is NOT typically used for metabolic alkalosis?

The primary treatment for drug overdoses leading to respiratory acidosis involves administering naloxone for opioids and flumazenil for benzodiazepines.

Bronchodilators, steroids, and BIPAP (bilevel positive airway pressure) are often used in cases of COPD or asthma to improve airway obstruction and reduce the severity of respiratory acidosis.

The primary treatment for pain and anxiety as a cause of respiratory alkalosis is the administration of pain medications and anti-anxiolytics.

What is a common cause of non-anion gap metabolic acidosis?

Which of the following best describes a consequence of chronic acidemia on the musculoskeletal system?

What primary physiological change characterizes metabolic alkalosis?

Which condition is primarily associated with renal losses leading to metabolic alkalosis?

How do loop diuretics primarily affect fluid balance in the body?

What mechanism leads to hypokalemia in cases of metabolic alkalosis?

Which of the following best defines the role of chemoreceptors in metabolic alkalosis?

What effect do diuretics have on H+ ion secretion in the kidneys?

Which condition is characterized by an inability to excrete organic acids due to damage to the glomeruli and proximal convoluted tubule?

What is the major cause of elevated lactate levels in lactic acidosis?

Which type of metabolic acidosis results from chronic kidney disease?

Which of the following is a false statement regarding medications that can contribute to lactic acidosis?

In cases of diabetic ketoacidosis, what contributes to the increased production of keto acids?

Why might incidental ingestion of methanol lead to metabolic acidosis?

What distinguishes anion gap metabolic acidosis from non-anion gap metabolic acidosis?

What is the normal range for the anion gap in metabolic acidosis?

What condition is characterized by airway obstruction and decreased respiratory rate, leading to high levels of pCO2?

Which of the following is a potential complication of elevated levels of CO2 in the blood?

What compensatory mechanism occurs in the kidneys during respiratory alkalosis?

What triggers hyperventilation leading to respiratory alkalosis?

Which of the following symptoms is commonly associated with respiratory acidosis due to airway obstruction?

What effect does high levels of CO2 have on cerebral blood flow?

Which of the following scenarios may lead to respiratory alkalosis?

What is a significant consequence of respiratory alkalosis on cerebral blood flow?

What is the primary treatment for metabolic acidosis in a patient with diabetic ketoacidosis?

In which condition would you administer acetazolamide as a treatment?

What is a common treatment for respiratory acidosis caused by drug overdoses?

What does hypovolemia require in cases of lactic acidosis?

Which of the following is an indicator of chronic metabolic acidosis?

What effect does sodium do in hypovolemic patients with metabolic alkalosis?

How can respiratory alkalosis be compensated by the kidneys?

What common condition can lead to respiratory alkalosis due to hyperventilation?

What is primarily stimulated during hyperaldosteronism to increase sodium reabsorption?

How does hypochloremia contribute to metabolic alkalosis?

What effect does hypercalcemia have on sodium reabsorption in the kidneys?

Which mechanism helps the kidneys compensate during hypochloremia?

What condition is characterized by a loss of H+ ions and chloride ions due to gastrointestinal (GI) losses?

What is the effect of using calcium carbonate-based antacids on blood volume?

During metabolic alkalosis caused by chloride loss, what happens to bicarbonate concentrations?

What is a consequence of low hydrogen ion levels in the bloodstream during metabolic alkalosis?

Which of the following conditions is characterized by hypoventilation?

Which ion's reabsorption is directly affected by the presence of hypercalcemia?

What mechanism does the body use to compensate for respiratory acidosis?

Which neuromuscular disease is associated with shallow breathing and respiratory acidosis?

What role do chemoreceptors play in metabolic alkalosis?

In which scenario does carbon dioxide (CO2) buildup occur more slowly?

What is a common manifestation of hypokalemia resulting from metabolic alkalosis?

What is the first step in compensating for respiratory acidosis?