A 34-year-old white female goes to the funeral of her dear friend and suddenly develops chest pain, sweating and palpitations. She is rushed to an ER and an EKG is taken which is normal. On examination, she is tachycardiac and tachypneic. Her ABG shows pH of 7.48, PaCO2 of 33 mmHg, and HCO3- of 24 meq/L. Which of the following would be the most appropriate treatment of her alkalosis?
A. IV Ringer lactate.
B. IV Ammonium chloride.
C. IV Sodium bicarbonate.
D. IV Hydrochloric acid.
E. Ask the patient to breathe in a small paper bag.
F. Sedation with diazepam.
the answer is E. Ask the patient to breathe in a small paper bag.
Explanation:
This patient is experiencing a panic attack as characterized by her tachypnea, tachycardia, chest pain, sweating and palpitations in the absence of EKG abnormalities. Her ABG shows acute respiratory alkalosis (high pH with low PaCO2 and near normal bicarbonate) secondary to hyperventilation.
The treatment of respiratory alkalosis is essentially the correction of the underlying cause. Respiratory alkalosis usually occurs in response to some stimulus, so treatment is usually unsuccessful unless the stimulus is controlled. In this patient with a panic attack, the underlying cause of alkalosis is the increased respiratory rate. Therefore, the best intervention is to calm the patient and let her breathe in a closed bag (Choice E). This would expose her to a high concentration of carbon dioxide and thus reduce her respiratory drive and decrease her respiratory rate, thereby correcting the underlying cause.
Respiratory alkalosis itself is rarely life threatening; therefore, emergent treatment is usually not indicated unless the pH is greater than 7.5 (Choice A, B, D are thus incorrect).
Sedation with diazepam (Choice F) should be reserved as a next step for this patient if she does not improve with the conservative treatment.
Tuesday, December 21, 2010
Saturday, December 18, 2010
MYOCARDIAL INFARCTION
A 63-year-old white male presents to the ER with sudden onset of severe retrosternal chest pain associated with nausea, vomiting and diaphoresis. His EKG shows ST segment elevation in leads aVL and I. The patient was treated with thrombolytic therapy in the ED. He is known to have insulin requiring diabetes mellitus for the past 3 years as well as hypertension for the past 2 years. His medications include insulin and enalapril. Which of the following set of medications has been shown to reduce mortality after an acute MI?
A. Nitrates, beta blockers, and aspirin
B. ACE inhibitors, nitrates, and beta blockers
C. Magnesium, beta blockers, and aspirin
D. Oxygen, morphine, aspirin, and nitrates
E. Aspirin, beta blockers, and ACE inhibitors
the answer is E. Aspirin, beta blockers, and ACE inhibitors
Explanation:
Of all the above choices, only ACE inhibitors, aspirin, and beta-blockers have been shown to reduce mortality after acute MI.
The proposed mechanism for ACE inhibitors is the reduction of ventricular remodeling and thus reduced incidence of left ventricular dysfunction / aneurysmal dilatation after MI. They are recommended in all patients of acute MI with CHF as well as to those who are hemodynamically stable and have ST segment elevation or left bundle branch block. They are usually started within the first 24 hours of acute MI and are continued indefinitely in those who have CHF, HTN or LV dysfunction.
Aspirin has also been shown to be effective and should be given in all patients, as early as possible in the setting of an acute MI, because it has been shown to reduce mortality by as much as 30%.
3 doses of IV beta-blockers, followed by oral beta-blockers in doses titrated for a heart rate of 50-60, have also been shown to reduce the mortality significantly in acute coronary syndromes.
Morphine is an effective analgesic and is used for pain relief in the setting of an acute MI. Oxygen is useful only when pulse oximetry shows hypoxemia. Its routine use in all patients of acute MI is not cost effective. Nitrates are used only for pain relief in the setting of acute MI and they don’t incur any survival advantage. IV nitrates should be avoided when there is hypotension or evidence of right ventricular infarction. IV magnesium is indicated only when initial testing shows low serum magnesium level. Routine use of IV magnesium in all MI patients does not provide any survival benefit.
A. Nitrates, beta blockers, and aspirin
B. ACE inhibitors, nitrates, and beta blockers
C. Magnesium, beta blockers, and aspirin
D. Oxygen, morphine, aspirin, and nitrates
E. Aspirin, beta blockers, and ACE inhibitors
the answer is E. Aspirin, beta blockers, and ACE inhibitors
Explanation:
Of all the above choices, only ACE inhibitors, aspirin, and beta-blockers have been shown to reduce mortality after acute MI.
The proposed mechanism for ACE inhibitors is the reduction of ventricular remodeling and thus reduced incidence of left ventricular dysfunction / aneurysmal dilatation after MI. They are recommended in all patients of acute MI with CHF as well as to those who are hemodynamically stable and have ST segment elevation or left bundle branch block. They are usually started within the first 24 hours of acute MI and are continued indefinitely in those who have CHF, HTN or LV dysfunction.
Aspirin has also been shown to be effective and should be given in all patients, as early as possible in the setting of an acute MI, because it has been shown to reduce mortality by as much as 30%.
3 doses of IV beta-blockers, followed by oral beta-blockers in doses titrated for a heart rate of 50-60, have also been shown to reduce the mortality significantly in acute coronary syndromes.
Morphine is an effective analgesic and is used for pain relief in the setting of an acute MI. Oxygen is useful only when pulse oximetry shows hypoxemia. Its routine use in all patients of acute MI is not cost effective. Nitrates are used only for pain relief in the setting of acute MI and they don’t incur any survival advantage. IV nitrates should be avoided when there is hypotension or evidence of right ventricular infarction. IV magnesium is indicated only when initial testing shows low serum magnesium level. Routine use of IV magnesium in all MI patients does not provide any survival benefit.
Thursday, December 16, 2010
Acid base imbalance
A 56-year-old male, with chronic renal insufficiency (CRF), comes with the complaints of lethargy and dizziness. His EKG shows tall T waves and increased PR interval. His serum K+ is 6.4 meq/L. A bolus of calcium gluconate is given and the patient is started on hemodialysis. As the patient is suffering from active peptic ulcer disease, you decide to go for citrate hemodialysis, instead of heparin hemodialysis. Which of the following acid base imbalance is likely to occur in this patient because of this type of hemodialysis?
A. Anion gap metabolic acidosis.
B. Non-anion gap metabolic acidosis.
C. Metabolic alkalosis.
D. Respiratory acidosis.
E. Respiratory alkalosis.
correct answer is C
Explanation:
This patient is having dialysis for his resistant hyperkalemia. However, because active peptic ulcer disease is a contraindication for heparin use, this patient is given citrate instead of heparin hemodialysis. Citrate is an alkaline compound and high doses of citrate in a patient with CRF can lead to citrate intoxication and metabolic alkalosis secondary to citrate accumulation. In this patient, as citrate is used for hemodialysis and he already has severe CRF, he runs a high risk of developing metabolic alkalosis secondary to citrate intoxication. Infusion of more than eight units of bank blood (anticoagulated with acid-citrate-dextran) is also associated with citrate intoxication.
Metabolic acidosis is also possible because of underlying renal disease but not due to citrate hemodialysis.
Primary respiratory acid base disorders due to CRF or hemodialysis are not usually seen.
A. Anion gap metabolic acidosis.
B. Non-anion gap metabolic acidosis.
C. Metabolic alkalosis.
D. Respiratory acidosis.
E. Respiratory alkalosis.
correct answer is C
Explanation:
This patient is having dialysis for his resistant hyperkalemia. However, because active peptic ulcer disease is a contraindication for heparin use, this patient is given citrate instead of heparin hemodialysis. Citrate is an alkaline compound and high doses of citrate in a patient with CRF can lead to citrate intoxication and metabolic alkalosis secondary to citrate accumulation. In this patient, as citrate is used for hemodialysis and he already has severe CRF, he runs a high risk of developing metabolic alkalosis secondary to citrate intoxication. Infusion of more than eight units of bank blood (anticoagulated with acid-citrate-dextran) is also associated with citrate intoxication.
Metabolic acidosis is also possible because of underlying renal disease but not due to citrate hemodialysis.
Primary respiratory acid base disorders due to CRF or hemodialysis are not usually seen.
dysphagia
A 65-year-old Caucasian male presents to your office with a several month history of swallowing difficulty. He also noticed the appearance of a mass on the right side of his neck recently that increases in size after he drinks water. His past medical history is significant for hypertension, gastroesophageal reflux disease, and osteoarthritis of his right knee. His current medications include hydrochlorothiazide, ranitidine, and occasional naproxene. You order a barium examination of the esophagus to visualize the abnormality. Which of the following is the most important pathogenetic factor in the development of this patient’s problem?
A. Motor dysfunction
B. Acid reflux
C. Inflammation
D. Abnormal proliferation
E. Metabolic abnormalities
correct answer is A
Explanation:
Pharyngoesophageal (Zenker’s) diverticulum develops immediately above the upper esophageal sphincter by herniating posteriorly between the fibers of cricopharyngeal muscle. Upper esophageal sphincter dysfunction and esophageal dysmotility are believed to be the cause of the problem. Incoordination between upper esophageal sphincter contraction and pharyngeal contraction may result in herniation of the mucosa by pulsion mechanism. The patients with Zenker’s diverticulum are usually older than 50 years of age and present with oropharyngeal dysphagia and neck mass. The neck mass may cause gurgling in the throat and may vary in the size depending on the food and fluid intake. The potential complications of the diverticulum include tracheal compression, ulceration with bleeding, regurgitation, and pulmonary aspiration. A barium examination helps to delineate the diverticulum. The surgical treatment of the disorder includes excision and frequently cricopharyngeal myotomy.
Although gastroesophageal reflux disease (Choice B) is frequently associated with Zenker’s diverticulum, it is not the cause of this condition. External inflammation (Choice C) may cause traction diverticula, usually in the mid-esophageal zone, but it is uncommon. Metabolic abnormalities, like iron deficiency (Choice E), may be associated with upper esophageal webs. Abnormal proliferation (Choice D) is responsible for neoplasia.
A. Motor dysfunction
B. Acid reflux
C. Inflammation
D. Abnormal proliferation
E. Metabolic abnormalities
correct answer is A
Explanation:
Pharyngoesophageal (Zenker’s) diverticulum develops immediately above the upper esophageal sphincter by herniating posteriorly between the fibers of cricopharyngeal muscle. Upper esophageal sphincter dysfunction and esophageal dysmotility are believed to be the cause of the problem. Incoordination between upper esophageal sphincter contraction and pharyngeal contraction may result in herniation of the mucosa by pulsion mechanism. The patients with Zenker’s diverticulum are usually older than 50 years of age and present with oropharyngeal dysphagia and neck mass. The neck mass may cause gurgling in the throat and may vary in the size depending on the food and fluid intake. The potential complications of the diverticulum include tracheal compression, ulceration with bleeding, regurgitation, and pulmonary aspiration. A barium examination helps to delineate the diverticulum. The surgical treatment of the disorder includes excision and frequently cricopharyngeal myotomy.
Although gastroesophageal reflux disease (Choice B) is frequently associated with Zenker’s diverticulum, it is not the cause of this condition. External inflammation (Choice C) may cause traction diverticula, usually in the mid-esophageal zone, but it is uncommon. Metabolic abnormalities, like iron deficiency (Choice E), may be associated with upper esophageal webs. Abnormal proliferation (Choice D) is responsible for neoplasia.
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