Acetaminophen/acidosis/ acromegaly

Question 1

How does acetaminophen differ from salicylates?

Answer 1

Acetaminophen does not cause gastric irritation, affect platelet aggregation, or have anti-inflammatory properties.

Question 2

What are the two primary indications for the use of acetaminophen?

Answer 2

Analgesia and antipyrexia

Question 3

What is the adult oral dose of acetaminophen in the treatment of fever and acute pain?

Answer 3

325-650 mg every 4-6 hours

Question 4

What is the half-life of acetaminophen?

Answer 4

2-3 hours

Question 5

What are some early symptoms associated with acetaminophen-induced liver damage?

Answer 5

Abdominal pain, diarrhea, nausea, and vomiting

Question 6

What drug is administered in the treatment of acetaminophen toxicity?

Answer 6

Acetylcysteine. It is most effective if administered within the first 8 hours of overdose.

Question 7

How effective is intravenous acetaminophen in treating postoperative pain?

Answer 7

Intravenous acetaminophen has been shown to provide approximately 4 hours of analgesia in 37 percent of patients with postoperative pain.

Question 8

What is the definition of respiratory acidosis?

Answer 8

Respiratory acidosis occurs when alveolar ventilation decreases enough that the PaCO2 rises, leading to a pH less than 7.35

Question 9

What are the major cardiac effects of acidosis and at what pH does this occur?

Answer 9

Acidosis decreases myocardial contractility. The effects are usually not clinically evident until the pH is less than 7.2 when the ability of the heart to respond to catecholamines is decreased. It is more evident, however, in patients with impaired left ventricular function, those on beta-blockers, or patients under general anesthesia.

Question 10

What is the most likely cause of respiratory depression in the perioperative period?

Answer 10

Drug-induced depression of ventilation due to opioids or general anesthetics

Question 11

A patient is suffering from an exacerbation of chronic ventilatory failure and exhibits severe acidosis. You are about to intubate the patient and place him on the ventilator. Should the acidosis be corrected urgently or slowly? Why?

Answer 11

Chronic respiratory acidosis should not be corrected too rapidly because the lungs are able to eliminate CO2 much more quickly than the kidneys can eliminate bicarbonate. If the CO2 is eliminated too quickly, the patient will suffer from a metabolic alkalosis that can lead to neuromuscular irritability and CNS excitation that can lead to seizures.

Question 12

What are the primary causes of respiratory acidosis?

Answer 12

The primary causes of respiratory acidosis can be divided into two categories: those due to alveolar hypoventilation and those due to increased CO2 production. Factors that impair CO2 elimination such as pulmonary diseases, neuromuscular disorders, chest wall abnormalities, and obtundation can potentially result in alveolar hypoventilation. Factors such as intense shivering, malignant hyperthermia, prolonged seizure activity, thyroid storm, and extensive burns result in an increase in CO2 production.

Question 13

A patient with metabolic acidosis has a sodium of 148 mEq/L, a chloride of 103 mEq/L, and a bicarbonate level of 19 mEq/L. Is this a normal anion gap acidosis or a high anion gap acidosis?

Answer 13

The formula for the anion gap is: [Na+] - ([Cl-] + [HCO3-]). In this instance, the anion gap is 26 mEq/L. The normal anion gap is 7 to 12 mEq/L, so this is a high anion gap acidosis.

Question 14

What are the two major classifications of metabolic acidosis?

Answer 14

Normal anion gap acidosis and high anion gap acidosis

Question 15

What are the characteristics of normal anion gap acidosis?

Answer 15

Normal anion gap acidosis is due to an increase in chloride concentration. This usually occurs in instances where bicarbonate is lost, so the kidneys retain chloride ions to maintain electrical neutrality.

Question 16

What are the most common causes of a normal anion gap acidosis?

Answer 16

Acidosis with a normal anion gap can be produced by increased gastrointestinal losses of HCO3- from diarrhea, fistulas, or ingestion of CaCl2 or MgCl2. Other factors that can produce a normal anion gap acidosis include hypoaldosteronism, renal tubular acidosis, carbonic anhydrase inhibitors or the administration of large volumes of bicarbonate-free intravenous fluids. Conditions that result in an increased production of nonvolatile acids such as renal failure, ketoacidosis, nonketotic hyperosmolar coma, and rhabdomyolysis or the ingestion of toxins such as salicylates, methanol, paraldehyde, and ethylene glycol can result in an acidosis with an increased anion gap.

Question 17

How does acidosis affect the oxyhemoglobin dissociation curve?

Answer 17

The oxyhemoglobin dissociation curve shifts to the right in acidosis to allow for a greater unloading of oxygen from the hemoglobin in the tissue bed. Other factors that shift the oxyhemoglobin dissociation curve to the right include: increased 2,3 DPG, fever, elevated CO2, and low carbon monoxide levels.

Question 18

What is another name for normal anion gap acidosis?

Answer 18

Hyperchloremic metabolic acidosis

Question 19

How does high anion gap acidosis occur?

Answer 19

A high anion gap acidosis occurs when a fixed acid is introduced into the extracellular space. As the acid dissociates, the hydrogen ion bonds with bicarbonate to form carbonic acid. It is the drop in bicarbonate that produces the anion gap. The causes of a high anion gap acidosis can be remembered with the mnemonic: SLUMPED = Salicylates, Lactate, Uremia, Methanol, Paraldehyde, Ethanol and Ethylene Glycol, and Diabetic Ketoacidosis.

Question 20

What systemic abnormalities may occur with acidosis?

Answer 20

Severe acidosis is associated with decreased cardiac contractility, decreased responsiveness to catecholamines, sensitization to re-entrant tachydysrhythmias, lowered threshold for ventricular fibrillation, hyperkalemia, hyperventilation, insulin resistance, and inhibition of anaerobic glycolysis.

Question 21

When using the Henderson-Hasselbach equation, what number is used to represent the pKa of carbonic acid?

Answer 21

The pKa of carbonic acid is 6.1. This value is used when implementing the Henderson-Hasselbach equation.

Question 22

When using the Henderson-Hasselbach equation, what number is used to represent the solubility coefficient in blood of carbon dioxide (C02)?

Answer 22

The solubility coefficient in blood of C02 is 0.03. This value is used when implementing the Henderson-Hasselbach equation.

Question 23

What agent is a carbonic anhydrase inhibitor used in the treatment of metabolic alkalosis?

Answer 23

Treatment for metabolic alkalosis can include administration of acetazolamide. Acetazolamide is a carbonic anhydrase inhibitor that causes the renal excretion of bicarbonate.

Question 24

How would rapid expansion of the extracellular volume with normal saline affect acid-base balance?

Answer 24

When the extracellular volume is expanded rapidly via the infusion of a fluid that does not contain any bicarbonate (like normal saline), the HCO3- in the plasma decreases as the extracellular HCO3- gets diluted. This results in a hyperchloremic metabolic acidosis.

Question 25

Which value is primarily increased in metabolic alkalosis and decreased in metabolic acidosis?

Answer 25

Metabolic alkalosis and acidosis are described as alterations where primarily HC03- is shifted up or down, respectively.

Question 26

What is acromegaly and what is the most common cause?

Answer 26

Acromegaly is the excessive release of growth hormone. It is most commonly due to an adenoma in the anterior pituitary gland.

Question 27

What are the most common clinical features of acromegaly?

Answer 27

The increased growth hormone levels stimulate the release of insulin-like growth factor I. These two hormones result in an increase in the proliferation of cartilage, bone, protein synthesis, and lipolysis. It also decreases insulin sensitivity and promotes the retention of sodium. As a result of these effects, common manifestations include enlargement of the jaw, hands, and feet as well as hypertension and diabetes mellitus.

Question 28

What airway abnormalities are associated with acromegaly?

Answer 28

Acromegaly results in numerous anatomical changes that can complicate airway management including prolonged mandible, overgrowth of pharyngeal tissue, recurrent laryngeal nerve damage, macroglossia, and decreased subglottic diameter. Hoarseness or stridor are indications that the upper airway is probably involved. Tracheal compression and deviation can occur due to thyroid enlargement. Sleep apnea is often present. The risk of respiratory failure is three times higher in patients with acromegaly.

Question 29

What are the cardiac manifestations of acromegaly?

Answer 29

The chronic hypertension results in ventricular dysfunction, enlarged heart, congestive heart failure, ischemic heart disease, and dysrhythmias.

Question 30

How does acromegaly affect the peripheral nervous system?

Answer 30

Overgrowth of soft tissue results in trapping of peripheral nerves. Carpal tunnel syndrome is a common finding, as is decreased ulnar artery flow due to compression by soft tissue.

Question 31

How does acromegaly affect the integumentary system?

Answer 31

Acromegaly results in thick, oily skin and hyperhidrosis.

Question 32

How does acromegaly affect the respiratory system?

Answer 32

Lung volumes are typically increased and V/Q mismatching may occur.

Question 33

How is the musculoskeletal system affected by acromegaly?

Answer 33

Osteoarthritis and osteoporosis are common. Skeletal muscle weakness is a typical finding and may manifest as an increased sensitivity to muscle relaxants.

Question 34

What are the symptoms of Addison’s disease?

Answer 34

Weakness, anorexia, nausea, vomiting, hyperpigmentation, chronic hypotension, hypovolemia, hyponatremia, and hyperkalemia.

Question 35

What are the two types of adrenal insufficiency?

Answer 35

There are two classifications of adrenal insufficiency: primary and secondary. In primary adrenal insufficiency the adrenal glands cannot produce enough hormones. Secondary adrenal insufficiency is due to suppression or disease of the hypothalamic/pituitary axis. Addison’s disease is the idiopathic autoimmune destruction of the adrenal gland and is a form of primary adrenal insufficiency.

Question 36

How do the effects of primary adrenal insufficiency differ from secondary insufficiency?

Answer 36

Primary adrenal insufficiency results in the inadequate release of glucocorticoid, mineralocorticoid, and androgen hormones. Secondary adrenal insufficiency results in the inadequate release of glucocorticoid only.

Question 37

What are the most common causes of secondary adrenal insufficiency?

Answer 37

Iatrogenic causes are the most common and include administration of synthetic glucocorticoids and pituitary surgery or irradiation.

Question 38

What patients are at risk for adrenal insufficiency?

Answer 38

Any patient on chronic exogenous steroid therapy is at risk for adrenal insufficiency during periods of stress such as surgery.

Question 39

What plasma cortisol level is diagnostic of adrenal insufficiency?

Answer 39

Plasma levels less than 20 mcg/dL indicate adrenal insufficiency

Question 40

Which induction agent would be least appropriate for a patient in acute Addisonian crisis?

Answer 40

Etomidate can suppress the HPA axis and even a single dose should be avoided in patients prone the adrenal insufficiency.

Question 41

How long after discontinuation of long-term steroid use will it take for adrenal function to return to normal?

Answer 41

It can take 6 to 12 months for adrenal function to return to baseline after chronic exogenous corticosteroid use.

Question 42

What is the most potent mineralocorticoid produced by the adrenal gland?

Answer 42

The most potent mineralocorticoid produced by the adrenal gland is aldosterone.

Question 43

Which is the most potent endogenous glucocorticoid and produced by the adrenal cortex?

Answer 43

The most potent endogenous glucocorticoid produced by the adrenal cortex is cortisol.

Question 44

Is the presence of an AICD of special concern in patients undergoing extracorporeal shock wave lithotripsy (ESWL)?

Answer 44

Pacemakers and AICDs are no longer considered contraindications to ESWL. AICD and lithotripter manufacturing companies generally state that AICDs are a contraindication to lithotripsy, but patients with AICDs have been shown to complete the procedure successfully. Older abdominally-implanted AICDs present a greater hazard than transvenous pacemakers. The AICD should be shut off prior to treatment and then reactivated immediately after the procedure.

Question 45

Can unipolar electrocautery be used in a patient with an AICD?

Answer 45

Unipolar cautery may produce electrical interference that may be interpreted as a ventricular dysrhythmia by an AICD. This could potentially trigger a defibrillation pulse. It is best to consult with someone who has experience with the specific device prior to surgery or place a magnet over the device to temporarily disable it.

Question 46

What are the basic components of an automatic implantable cardioverter defibrillator (AICD)?

Answer 46

It contains a pulse generator, a high capacity battery, a capacitor, lead wire, and shock coil in a single unit.

Question 47

How is an AICD implanted?

Answer 47

The generator is typically placed in a pectoral pocket on either side of the chest and the lead and shock coil are placed in the right atrium and ventricle. The lead ad shock coil are inserted transvenously. The procedure is typically performed under sedation with local anesthesia but may be performed under general anesthesia.

Question 48

What interventions can an AICD perform?

Answer 48

They can treat bradydysrhythmias via pacing and sensing cardiac electrical activity, use overdrive pacing to treat tachydysrhythmias, cardiovert, and defibrillate.

Question 49

What nerves are blocked when performing an ankle block?

Answer 49

Deep peroneal, Saphenous, Posterior tibial, Sural, Superficial peroneal

Question 50

When performing an ankle block, how is the deep peroneal nerve anesthetized? What other nerves can be anesthetized at the same time?

Answer 50

With the patient supine, draw a line across the top of the ankle from the superior edge of the medial malleolus to the superior edge of the lateral malleolus. Insert the needle toward the tibia through this line between the tendons of the tibial muscle and the great toe and inject 5-8 ml of local anesthetic. If you redirect the needle towards the inferior edge of the lateral malleolus and inject another 5 mL of anesthetic, you can also block the superficial peroneal nerve.