Wednesday, October 28, 2009

chest pain case 4

Chest pain Case 4

A 45-year-old man presents with a 3-day history of persistent, severe chest pain. Prior to this, he had flu-Iike symptoms for 2 weeks, including
fever, cough, myalgias, and arthralgias. His pain is worse when he takes a deep breath and is improved when he sits up. On physical
examination, he is febrile, and his pulse is 110/min. His oxygen saturation is normaI, and his breath sounds are equal and clear to
auscultation over all lung fields. There is a scratching and scraping, high-pitched sound on auscultation of the heart over the left third
intercostal space, which is increased when the patient is sitting forward.

Question 1 of 4
Which of the following is the most likely diagnosis?
/ A. Acute pericarditis
/ B. Aortic dissection
/ C. Pneumonia
/ D. Pulmonary embolus
/ E. Tension pneumothorax

Question 2 of 4
Which of the following would help confirm the diagnosis?
/ A. Angiogram showing a clot in one of the coronary arteries
/ B. Chest radiograph showing multiple emphysematous bullae
/ C. CT scan of the chest showing a widened mediastinum
/ D. EIectrocardiogram showing diffuse ST elevation
/ E. Endoscopy revealing esophageal varices

Question 3 of 4
Other than an antecedent viral syndrome, which of the following conditions can predispose a patient to this problem?
/ A. AIcohol abuse
/ B. Liver failure
/ C. Peptic ulcer disease
/ D. Recent total hip replacement
/ E. Renal failure

Question 4 of 4
The patient is treated with a nonsteroidal anti-inflammatory agent. Which of the following was prescribed?
/ A. AIIopurinol
/ B. Gemfibrozil
/ C. Indomethacin
/ D. Labetalol
/ E. Methocarbamol


Chest pain Case 4 answers

The correct answer is A.
This patient has symptoms that are typical of inflammation of the pericardial sac. In addition, the sound that is heard over his heart is a pericardial friction rub. Acute pericarditis is often associated with viral syndromes, connective tissue diseases, renal failure, myocardial infarction, and tumor invasion of the pericardium.
Aortic dissection (choice B) will also present with severe chest pain, but it is tearing in quality, and is not positional, nor pleuritic in nature.
Pneumonia (choice C) may present similarly, but auscultation of the lung fields should reveal abnormal breath sounds, and a pericardial friction rub should not be heard.
Pulmonary embolus (choice D) can present with chest pain that is worse with deep breaths. However, it is not positional in nature, and it is not associated with a pericardial friction rub. Depending on the size of the embolus, the oxygen saturation may be abnormal.
Tension pneumothorax (choice E) is not associated with flu-like symptoms nor a pericardial friction rub. Furthermore, there should be an absence of breath sounds over the affected part of the lung.

The correct answer is D.
Acute pericarditis often presents with diffuse ST elevation on an electrocardiogram.
An angiogram showing a clot in one of the coronary arteries (choice A) would be seen in a patient having an acute myocardial infarction.
A chest radiograph showing multiple emphysematous bullae (choice B) would be seen in a chronic smoker, and would be a possible cause of spontaneous pneumothorax.
CT scan of the chest showing a widened mediastinum (choice C) would be seen in a patient with an acute aortic dissection.
Endoscopy revealing esophageal varices (choice E) is seen in patients with chronic liver disease or portal hypertension.

The correct answer is E.
Patients with renal failure or uremia can often present with a fibrinous or serofibrinous pericarditis.
Alcohol abuse (choice A) and liver failure (choice B) do not necessarily predispose a patient to pericarditis, nor are they associated with pericarditis.
Peptic ulcer disease (choice C) may cause epigastric pain that can be confused with chest pain, and patients may have recurrent bleeding, but this disorder is not associated with pericarditis.
A recent total hip replacement (choice D) predisposes patients to the development of a deep venous thrombosis, which can embolize and cause a pulmonary embolus. This is not associated with pericarditis.

The correct answer is C.
Indomethacin or any of the other nonsteroidal anti-inflammatory agents can be used in the treatment of acute pericarditis.
Allopurinol (choice A) is used for the treatment of gout. It inhibits xanthine oxidase, which decreases the production of uric acid.
Gemfibrozil (choice B) is a lipid lowering agent used in patients with hypercholesterolemia.
Labetalol (choice D) is a beta blocker and is used in hypertensive emergencies.
Methocarbamol (choice E) is a muscle relaxant, which helps to relieve pain associated with muscle spasms.

chest pain case 3

Chest pain Case 3

A 35-year-old man with no significant past medical history presents to clinic with a six week history of worsening chest discomfort and pain.
He describes the pain as a substernal burning sensation that occasionally wakes him up at night and is often worse after he eats. He
sometimes notices a sour taste in his mouth when he wakes up in the morning. He has no dysphagia or odynophagia. The pain is unrelated
to exertion, and he jogs 3 miles every other day without difficulty or chest pain. His vital signs and physical examination are normaI.

Question 1 of 6
Which of the following is the most likely diagnosis?
/ A. Acute viral pericarditis
/ B. Aortic dissection
/ C. Candida esophagitis
/ D. Gastroesophageal reflux disease (GERD)
/ E. Stable angina

Question 2 of 6
Which of the following tests would be most likely to confirm the probable diagnosis?
/ A. 24-hour ambulatory esophageal luminal pH monitoring
/ B. Cardiac angiogram
/ C. Chest radiograph
/ D. Exercise treadmill test
/ E. Serologic blood tests for H. Pylori infection

Question 3 of 6
The patient is treated with cimetidine, which completely relieves his symptoms. Which of the following is the mechanism of action of this
/ A. Beta-1 adrenergic blockade
/ B. Histamine H2 receptor blockade
/ C. Inhibition of cell wall synthesis
/ D. Inhibition of cyclooxygenase
/ E. Smooth muscle relaxation

Question 4 of 6
The physician cautions the patient about cimetidine because of which of the following potential side effects?
/ A. CNS depression
/ B. Hypertensive crisis
/ C. Inhibition of hepatic metabolism
/ D. Masking symptoms of hypoglycemia
/ E. Ototoxicity

Question 5 of 6
The patient's symptoms are initially controlled on cimetidine. After 10 years, he develops refractory symptoms, and the physician places him
on a proton pump inhibitor. Which of the following medications was most likely prescribed?
/ A. Lansoprazole
/ B. Loperamide
/ C. Metoclopramide
/ D. Ondansetron
/ E. Ranitidine

Question 6 of 6
Histologic examination of the affected tissue shows Barrett's esophagus. This is most correctly described as which of the following?
/ A. Adenocarcinoma
/ B. Esophageal stricture
/ C. H.Pylori infection
/ D. Localized outpouching of the esophageal wall
/ E. Metaplasia of the squamous epithelium


Chest pain Case 3 answers

The correct answer is D.
A patient who presents with chest discomfort that is burning in nature, and worsened after eating without symptoms of dysphagia or odynophagia, most likely has gastroesophageal reflux disease (GERD). GERD occurs when there is reflux of gastric contents into the esophagus. This may occur with or without inflammation. It is often caused by inappropriate relaxation of the lower esophageal sphincter. Certain foods such as peppermint, caffeine, and high-fat and spicy foods are often associated with GERD.
Acute viral pericarditis (choice A) would present with more severe and sudden onset of chest pain that is relieved with leaning forward or sitting up. Acute viral pericarditis is often associated with a prodrome and usually presents with a fever. Occasionally, a pericardial friction rub can be heard on exam.
Aortic dissection (choice B) would also present as sudden onset of severe chest pain, which often radiates to the back. Patients can have hypotension, depending on the severity of the dissection. Patients can also have unequal pulses in their extremities if the dissection affects one of the major arteries branching off the aortic arch.
Candida esophagitis (choice C) would present with dysphagia and odynophagia. Patients also have oral thrush, and generally are immunocompromised. These patients usually have a fever.
Stable angina (choice E) should present with typical chest pain that is worsened after exertion. The fact that this patient can jog 3 miles without difficulty goes against stable angina. Furthermore, he is young and does not have any risk factors for cardiac disease such as hypertension, diabetes, or hypercholesterolemia.

The correct answer is A.
Twenty-four hour ambulatory esophageal luminal pH monitoring is one of the most sensitive tests for GERD. In most cases, the disease is diagnosed clinically by history, but pH monitoring would help confirm the diagnosis.
Cardiac angiograms (choice B) are used to evaluate the coronary arteries for signs of blockage, to evaluate heart function, or to evaluate cardiac valve function.
A chest radiograph (choice C) can be used to evaluate the structures in the thorax, but will not help confirm the diagnosis because GERD patients generally have normal chest radiographs.
An exercise treadmill test (choice D) is used to evaluate patients who are believed to have underlying coronary heart disease or to rule out heart disease.
Serologic blood testing for H. pylori infection (choice E) only documents the presence of a current infection or the history of an H. pylori infection. A past or present infection does not confirm a diagnosis, because GERD can occur in the setting with or without H. pylori. Furthermore, the role of H. pylori in GERD is still unclear.

The correct answer is B.
Cimetidine and other histamine H2 receptor blockers such as ranitidine block the action of histamine on H2 receptors, resulting in a decrease in gastric acid production, thus decreasing the symptoms of GERD.
Beta-1 adrenergic blockade (choice A) (e.g., atenolol, metoprolol) is used to lower blood pressure, which is not related to GERD.
Inhibition of cell wall synthesis (choice C) (e.g., amoxicillin) is a mechanism that is used by many antibiotics. GERD can be associated with the presence of H. pylori, but the treatment of H. pylori with antibiotics in GERD patients remains controversial, and its benefit remains questionable.
Inhibition of cyclooxygenase (choice D) (e.g., ibuprofen, naproxen) does not play a role in the treatment of GERD. GERD may or may not be associated with inflammation of the esophagus, but anti-inflammatory agents may actually worsen symptoms.
Smooth muscle relaxation (choice E) (e.g., nitroglycerin) does play a role in the relief of esophageal spasm, but this patient does not complain of dysphagia or odynophagia.

The correct answer is C.
Many drugs can lead to clinically significant drug interactions via inhibition of the hepatic drug-metabolizing enzymes, particularly the cytochrome P450 isozymes. This can lead to unwanted elevations of plasma drug levels. Cimetidine is a classic example of one of these drugs. Other examples include erythromycin, ketoconazole, sulfonamides, quinidine, and disulfiram.
Benzodiazepines and barbiturates are examples of drugs that can cause CNS depression (choice A).
MAO inhibitors prior to the ingestion of tyramine-containing foods can cause a hypertensive crisis (choice B).
Beta blockers can mask the symptoms of hypoglycemia (choice D).
Aminoglycosides can produce ototoxicity (choice E). The risk of ototoxicity may be further increased if the patient is also taking loop diuretics.

The correct answer is A.
Lansoprazole is a proton pump inhibitor and acts directly to inhibit the gastric parietal cell hydrogen-potassium ATPase. It can be used as the initial treatment for GERD, or for refractory cases.
Loperamide (choice B) is an anti-diarrheal agent, which inhibits peristalsis. Using it in this setting may worsen the symptoms of GERD.
Metoclopramide (choice C) stimulates upper gastrointestinal motility. It can be used in refractory cases of GERD, but it is not a proton pump inhibitor.
Ondansetron (choice D) is an antiemetic and acts by selectively antagonizing serotonin 5-HT3 receptors. It is primarily used is severe cases of nausea, such as in patients receiving chemotherapy for cancer treatment.
Ranitidine (choice E) is also an histamine H2 receptor blocker, like cimetidine. Some patients who do not respond to one histamine H2 receptor blocker, may respond to another, but ranitidine blocks the action of histamine on H2 receptors, resulting in a decrease in gastric acid production. It is not a proton pump inhibitor.

The correct answer is E.
Patients who have long-standing GERD are at risk for development of Barrett's esophagus, which is the replacement of the normal esophageal squamous epithelium with columnar epithelium (metaplasia). This is a premalignant lesion that needs to be monitored regularly for the development of adenocarcinoma.
Adenocarcinoma (choice A) is a malignant lesion that can result from cellular metaplasia, but Barrett's esophagus is the premalignant lesion that occurs before the development of adenocarcinoma of the esophagus.
Esophageal strictures (choice B) can occur in patients with long-standing GERD, but the presence of a stricture does not mean that there is cellular dysplasia, or Barrett's esophagus.
H. pylori infection (choice C) can occur in the setting of GERD, but it is not synonymous with Barrett's esophagus.
An esophageal diverticulum is a localized outpouching of the esophageal wall (choice D). This is unrelated to Barrett's esophagus.

chest pain case 2

Chest pain Case 2

A 52-year-old man presents to the emergency department because of severe chest pain. The excruciating pain began abruptly, 30 minutes
previously, and feels to the patient as if something were "ripping." When asked to point to where the pain is worst, the patient points to the
precordium. The man additionally reports that the pain seems to be changing in position slowly.

Question 1 of 6
Which of the following is most likely causing the patient's severe pain?
/ A. Aortic dissection
/ B. Atherosclerotic aortic aneurysm
/ C. Esophageal reflux
/ D. Myocardial infarction
/ E. Peptic ulcer

Question 2 of 6
Extension of this patient's disease process would be most likely to produce which of the following?
/ A. Aortic insufficiency
/ B. Aortic stenosis
/ C. Mitral insufficiency
/ D. Mitral stenosis
/ E. Tricuspid stenosis

Question 3 of 6
If enzyme chemistries were sent, which would be the most likely results?
/ A. Decreased AST, elevated CK, decreased LDH
/ B. EIevated AST, elevated CK, normal to decreased LDH
/ C. EIevated AST, normaI CK, normaI LDH
/ D. NormaI AST, elevated CK, elevated LDH
/ E. NormaI AST, normaI CK, normal to elevated LDH

Question 4 of 6
If surgery is necessary to repair this problem, the surgeon will be required to understand the anatomic relationship of the aorta to the
surrounding structures. Which of the following most accurately describes the descending portion of the thoracic aorta?
/ A. It descends on the right side of the thoracic vertebrae
/ B. It flattens the posterior aspect of the trachea
/ C. It is to the left of the esophagus at the hiatus
/ D. It is to the left of the thoracic duct at the T10 Ievel
/ E. It is to the right of the inferior vena cava

Question 5 of 6
Which of the following would be most likely to be seen on pathological examination of a specimen removed from this patient at surgery?
/ A. Bacterial vegetations
/ B. Cystic medial degeneration
/ C. Multiple small granulomas
/ D. Parasitic organisms
/ E. Polyarteritis nodosa

Question 6 of 6
Which of the following conditions has been associated with this patient's disease?
/ A. Cushing syndrome
/ B. Dandy-Walker syndrome
/ C. Kawasaki syndrome
/ D. Marfan syndrome
/ E. Tourette syndrome


Chest pain Case 2 answers

The correct answer is A. This patient has a classic presentation of aortic dissection. Any time a patient in excruciating chest pain describes the pain as "tearing" or "ripping," you should strongly consider the diagnosis of aortic dissection. The pain may move with time as the dissection progresses. Aortic dissection is a highly lethal condition that may lead to aortic rupture, most often into the pericardial cavity or left pleural space. The two most common sites of origin of the dissection are in the proximal aorta within 5 cm of the aortic valve and in the descending thoracic aorta just distal to the origin of the left subclavian artery. CT scan with contrast is often used to confirm the diagnosis suspected clinically. Therapy is promptly initiated with medications that lower the blood pressure to try to prevent extension of the dissection. Surgery is usually then performed in patients in which the dissection begins in the proximal aorta near the aortic root; medical therapy alone can sometimes be used for those with distal aortic dissection that has not compromised blood flow to limbs or organs.
Atherosclerotic aortic aneurysm (choice B) more commonly involves the abdominal aorta, and, when rupturing, may produce excruciating pain that is usually referred to the lower abdomen and back.
The pain of esophageal reflux (choice C) is rarely excruciating, and usually does not produce a ripping or tearing sensation.
Myocardial infarction (choice D) can produce severe precordial chest pain, but the pain usually does not move with time and does not have a tearing or ripping character.
Peptic ulcer pain (choice E) may be severe and referred to the chest, but patients are more likely to use terms like "burning" than ripping or tearing, and the pain does not slowly change position.

The correct answer is A.
Dissecting aneurysms tend to start near the root of the aorta, and aortic insufficiency is a common complication. This can be very helpful in the initial evaluation of the patient, since up to 2/3 of the patients with proximal aortic dissection demonstrate, on auscultation, the characteristic murmur of aortic insufficiency, which is a pandiastolic decrescendo murmur that is loudest over the sternum and left lower sternal border. Aortic stenosis (choice B) usually does not occur.
Involvement of the mitral (choices C and D) and tricuspid valves (choice E) would be very rare, and probably only seen if the aortic dissection interrupted the orifices of the coronary arteries and induced a secondary myocardial infarction.

The correct answer is E.
Unless aortic dissection secondarily causes a myocardial infarction secondary to occlusion of the coronary arteries, aspartate aminotransferase (AST) and creatine kinase (CK) levels should be normal. Lactic dehydrogenase (LDH) levels may be normal, or elevated if some hemolysis is occurring within the area of dissection.
In general, AST can be elevated (choices B and C) in a variety of cardiac diseases (e.g., myocardial infarction, heart failure, myocarditis, pericarditis), muscle damage (e.g., myositis, muscular dystrophy, trauma), and damage to liver, pancreas, kidney, or brain. AST is decreased (choice A) in pyridoxine (vitamin B6) deficiency and in the terminal stages of liver disease. In general, CK can be elevated (choices A, B, and D) in disease or damage involving heart, muscle, or brain. Decreased CK has no medical significance. Lactic dehydrogenase (LDH) can be elevated (choice D) in myocardial infarction, pulmonary infarct, hemolytic and pernicious anemia, hematologic malignancies, and disease of liver, kidney, or brain. Decreases in LDH (choices A and B) are not medically significant.

The correct answer is D.
The thoracic duct is the main lymphatic duct and it lies on the bodies of the inferior seven thoracic vertebrae. It conveys most of the lymph of the body to the venous system. It passes superiorly from the cisterna chyli (the expanded inferior end of the thoracic duct) through the aortic hiatus in the diaphragm. The thoracic duct ascends in the posterior mediastinum, on the right of the thoracic aorta and to the left of the azygos vein. At the level of T4, T5, or T6, the thoracic duct crosses to the left, posterior to the esophagus and ascends to the superior mediastinum. The thoracic duct empties into the venous system near the union of the left internal jugular and subclavian veins.
As a continuation of the aortic arch, the descending aorta begins on the left side of the inferior border of the body of the T4 vertebra and descends in the posterior mediastinum on the left sides of T5 to T12 (choice A).
The trachea travels in the superior mediastinum and does not have direct contact with the descending thoracic aorta. The trachea is kept patent by a series of C-shaped tracheal cartilages. The posterior aspect is flat where it is applied to the esophagus, not the aorta (choice B).
At the level of the esophageal hiatus (choice C), the esophagus lies anterior to the descending thoracic aorta.
The inferior vena cava (choice E) is located to the right of the abdominal aorta, not the thoracic aorta. The IVC returns blood from the lower limbs, most of the abdominal wall, and the abdominopelvic viscera. This vessel begins anterior to L5 vertebra by union of the common iliac veins. It then ascends on the right psoas major muscle to the right of the median plane and aorta. It passes through the vena caval foramen in the diaphragm at the level of T8 to enter the right atrium.

The correct answer is B.
Cystic medial degeneration is a disruption and fragmentation of the elastic tissue in aortic media, with formation of areas devoid of elastin. These changes weaken the aortic wall, predispose for dissection, and are seen in the majority of cases of aortic dissection.
Bacterial vegetations (choice A) are a feature of endocarditis.
Multiple small granulomas (choice C) can be seen in temporal arteritis and Takayasu arteritis.
Parasitic organisms (choice D) do not usually affect the aorta; the organisms of trichinosis and Chagas disease can affect the heart.
Polyarteritis nodosa (choice E) is a focal inflammation that usually involves smaller blood vessels than the aorta.

The correct answer is D.
Marfan syndrome is an autosomal dominant connective tissue disease characterized by skeletal changes (e.g., tall stature, long limbs, long fingers, lax joints), a tendency to develop dislocations of the lens of the eye, and a tendency to develop aortic dissection secondary to prominent cystic medial degeneration in the aortic media. A similar condition, Ehlers-Danlos syndrome, also predisposes for dissecting aneurysm. Other predisposing factors include congenital cardiovascular abnormalities (e.g., coarctation of the aorta, patent ductus arteriosus, bicuspid aortic valve) that increase the turbulence of blood flow in the aorta, atherosclerosis, and trauma (including iatrogenic trauma during arterial catheterization and cardiovascular surgical procedures). The other conditions listed in the choices are unrelated to aortic dissection.
Cushing syndrome (choice A) is a characteristic pattern of physical changes (truncal obesity, moon face, buffalo hump), biochemical/hormonal changes (hypertension, altered carbohydrate and protein metabolism, amenorrhea), and sometimes psychiatric disturbances that are seen in patients with increased levels of adrenocortical hormones.
Dandy-Walker syndrome (choice B) is a congenital abnormality of the cerebellum and fourth ventricle.
Kawasaki syndrome (choice C) is a febrile childhood disease that predisposes for the formation of tiny aneurysms of the coronary arteries.
Tourette syndrome (choice E) is a motor and vocal tic disorder.

chest pain case 1

>Chest pain Case 1

A 45-year-old man presents to the emergency department complaining of chest pain, which began twenty minutes before while he was filling
up his car with gasoline. He describes the pain as substernaI, intense, dulI, and squeezing. It does not change with respiration. He also
complains that he is nauseated. He has never experienced anything like this before. His temperature is 37.5 C (99.5 F), blood pressure is
124/76 mm Hg, pulse is 80/min, respiratory rate is 22/min, and oxygen saturation is 95% on room air. On physical examination, he is
diaphoretic. His lungs are clear, his heart rate is regular, and he has a normaI S1 and S2 without murmur, rub, or gallop. The examiner
estimates that his jugular venous pressure is elevated to the angle of the jaw. His abdomen is nontender, with normal bowel sounds. An
electrocardiogram is performed, which reveals sinus rhythm, normal axis, normal intervals, and ST elevation in leads lI, III, and aVF. A chest x-
ray film reveals no apparent cardiac or pulmonary abnormalities.

Question 1 of 7
Which of the following is the most likely diagnosis?
A. Acute myocardial infarction
B. Aortic dissection
C. Gastroesophageal reflux
D. Pericarditis
E. Pulmonary embolus

Question 2 of 7
What is the pathophysiologic process most likely to be responsible for this patient's presentation?
A. Atherosclerotic plaque rupture resulting in thrombus formation
B. Buildup of atherosclerotic stenosis to produce high-grade obstruction of the artery
C. Dissection of the vessel
D. Embolization of blood clot, air, or foreign material
E. Myocardial hypertrophy resulting in vessel narrowing

Question 3 of 7
Which of the following vessels is most likely to be diseased in this patient?
A. Coronary sinus
B. Left anterior descending coronary artery
C. Left circumflex coronary artery
D. Left main coronary artery
E. Right coronary artery

Question 4 of 7
This patient is given aspirin in the emergency department. Decreased production of which of the following mediators is responsible for the
beneficial effects of aspirin in this disorder?
B. PIatelet glycoprotein lIB/IIIA
C. Prostacyclin
D. Thromboxane A2
E. Ubiquinone (coenzyme Q)

Question 5 of 7
EIevation of which of the following serum proteins is the most specific biochemical marker for this patient's condition?
A. AIanine aminotransferase
B. Creatine phosphokinase
C. Lactate dehydrogenase
D. Transferrin
E. Troponin

Question 6 of 7
Three days after hospital admission, the patient suddenly develops shortness of breath and becomes hypotensive. His heart rate is 100/min,
with a normaI PR and QRS intervaI. His blood pressure is 75/50 mm Hg. His respiratory rate is 38/min and his oxygen saturation on 2 Iiters
via nasal cannula drops to 60%. A chest x-ray reveals bilateral fluffy infiltrates in the lung fields. Which of the following complications of his
condition has most likely occurred?
A. Dilation of the left ventricle
B. Dressler syndrome
C. Rupture of the left ventricular free wall
D. Rupture of the posteromedial papillary muscle
E. Ventricular tachycardia

Question 7 of 7
The patient is taken emergently to the operating room. During surgery, a sample of affected myocardial tissue is sent to the pathology
Iaboratory for examination. Which of the following would be the likely pathologic finding(s)?
A. Acellular fibrosis
B. Monocyte infiltration, absent nuclei and striations
C. Myocyte disarray
D. Myocyte edema, hemorrhage, and dense neutrophil infiltration
E. Wavy myofibers with eosinophilic contraction bands


Chest pain Case 1 answers

The correct answer is A
. The differential diagnosis of chest pain is broad and includes all the answers on this list, all of which can present, as in this patient, with a relatively normal examination of the heart and lungs. Acute myocardial infarction is the only one of these findings that is associated with ST segment elevation in an anatomical distribution (in this case, the "inferior" leads). His elevated jugular venous pressure is also a clue to abnormal cardiac function; however, this might be present in severe constrictive pericarditis or pulmonary embolism as well.
Aortic dissection (choice B) often presents with chest pain or pain radiating to the back. It is not, however, typically associated with ST segment changes on the EKG, unless the dissection extends proximally into the ostia of the coronary arteries, obstructing flow, and resulting in secondary acute myocardial infarction, in which case a patient could present like this. However, this presentation would be an uncommon presentation of a relatively uncommon disease. The risk for aortic dissection is increased with long-standing essential hypertension, other peripheral vascular disease, hyperlipidemia, and advanced age, as well as connective tissue disorders such as Marfan syndrome or Ehlers-Danlos syndrome.
Patients with gastroesophageal reflux (choice C) may complain of intense substernal chest pain that is difficult to distinguish from the pain of myocardial infarction. However, the ST elevations on the EKG suggest transmural ischemia of the myocardium and do not occur with isolated gastroesophageal reflux. Do not let relatively normal vital signs and gastrointestinal symptoms such as nausea fool you!
Pericarditis (choice D), an inflammatory disease of the pericardium, presents with chest pain and is often associated with ST elevation on the EKG, as well as PR interval depression. However, the ST elevation usually involves multiple leads of the EKG, and is not in a strictly anatomic distribution. Pericarditis is often associated with a friction rub.
Pulmonary thromboembolism (choice E) can also present with chest pain. A patient who has had a large PE, however, typically will not have normal vital signs, and is likely to have tachycardia, tachypnea, and possibly hypoxemia. Hemodynamically significant pulmonary embolism can present with elevated JVP due to right heart strain. The patient might have ST depression in the inferior leads, but will not have ST elevation. The pain associated with pulmonary embolus is generally pleuritic in nature, that is, lateralizing, and changing with inspiration. Risk factors for pulmonary embolism include hypercoagulable states, immobilization, and vascular injury (Virchow's triad).

The correct answer is A. Acute coronary syndromes are thought to be the result of rupture of a pre-existing atherosclerotic plaque, often one that is not producing high-grade stenosis. When the endothelial surface covering the lipid core of an unstable plaque ruptures, a platelet plug forms and the clotting cascade is activated, rapidly propagating thrombus formation and suddenly occluding the vessel. This results in transmural ischemia, which becomes infarction, should the clot fail to recanalize quickly.
Atherosclerotic stenosis (choice B) is an important pathologic component of coronary artery disease. However, high-grade coronary stenoses most frequently cause stable angina, that is, chest pain and myocardial ischemia induced when an increase in myocardial oxygen demand exceeds the fixed supply that can be obtained through a severely stenotic vessel. As vessels progressively narrow over time, they produce ischemia, but not sudden infarction. Often distal to a narrowed vessel, collaterals will form from less diseased vessels, compensating for the reduced flow.
Coronary artery dissection (choice C) is a rare phenomenon that can produce transmural ischemia and infarction, but most commonly occurs in the setting of instrumentation of the vessel.
Embolization (choice D) is a relatively rare phenomenon in the coronary circulation under normal circumstances. Foreign material can only enter the left side of the heart via right-to-left intracardiac shunt, pulmonary vein interruption, or surgical opening of the left heart. Thrombus that forms in the left atrium (usually the result of low-flow states such as mitral stenosis or atrial fibrillation) can also embolize; patients with atrial fibrillation are anticoagulated to reduce the risk of cerebral embolization of left atrial clot.
Myocardial hypertrophy (choice E) can restrict subendocardial oxygen supply by creating high capillary pressure relative to arteriolar pressure. This does not occur in large coronary vessels, but can produce subendocardial ischemia in disease states that are associated with hypertrophic myocardium, such as aortic stenosis, long-standing essential hypertension, and idiopathic hypertrophic subaortic stenosis (IHSS).

The correct answer is E. Acute myocardial infarction is usually due to obstruction of one coronary vessel. The right coronary artery exits the right sinus of Valsalva of the aorta and gives off branches to the right ventricle, the SA nodal artery (in 70% of patients), the AV nodal artery, and, in the 85% of patients whose circulations are said to be "right-dominant," the posterior descending artery, which supplies the inferior wall of the RV and the LV as well as the posterior 1/3 of the interventricular septum. This patient has EKG signs of an inferior myocardial infarction, with ST elevation in the inferior leads, II, III, and aVF. He also has a physical sign of right ventricular dysfunction (elevated jugular venous pressure).
The coronary sinus (choice A) is the principal vein draining the left ventricle and runs alongside the circumflex artery in the posterior AV groove. It is not a common site for atherosclerotic disease or for obstruction.
The left anterior descending artery (choice B) supplies the anterior and anteroseptal portions of the left ventricle. Obstruction would produce ST elevation in the anterior (V2-V6) and occasionally the lateral (I, aVF) leads of the EKG, with possible "reciprocal" ST depression in the inferior leads.
The left circumflex artery (choice C) supplies the lateral wall of the left ventricle. 85% of patients have a "right-dominant" coronary anatomy. That is, the right coronary artery gives off the posterior descending artery (PDA). In the "left-dominant" remaining 15%, the PDA comes off the circumflex. Isolated inferior EKG lead changes are, therefore, most likely to be due to RCA obstruction; circumflex obstruction typically produces EKG lead changes in the lateral (I, aVL, V5, V6) leads.
The left main coronary artery (choice D) exits the aorta at the left sinus of Valsalva and divides into the left anterior descending and left circumflex arteries. Obstruction of the left main makes the entire left ventricle ischemic, often resulting in cardiogenic shock. This would produce ST segment elevation in leads I, aVL, and V2-V6.

The correct answer is D. Aspirin irreversibly inhibits the enzyme cyclooxygenase, which produces all the prostaglandin mediators from arachidonic acid. Cyclooxygenase in platelets produces thromboxane A2, which is a potent promoter of platelet aggregation and vasoconstriction. By blocking this, aspirin irreversibly inhibits platelet function, preventing aggregation at the site of plaque rupture. Platelets, having no nuclei, are unable to synthesize more cyclooxygenase, and therefore thromboxane production is inhibited for the life of the platelet, approximately 10 days.
Cyclic AMP (choice A) is an intracellular small molecule responsible for multiple signal transduction pathways. In cardiac myocytes, it activates protein kinases responsible for the phosphorylation of calcium channels, promoting entry of calcium into the cell. cAMP is broken down by phosphodiesterase, the inhibition of which is responsible for the beneficial effects of inotropic phosphodiesterase inhibitors such as milrinone.
Platelet surface glycoprotein IIb/IIIA (choice B) binds fibrinogen and von Willebrand factor, promoting aggregation and clot formation. It is inhibited by drugs like eptifibatide and tirofiban, which are used in acute coronary syndromes to further inhibit platelet aggregation and thrombus formation.
Prostacyclin (choice C) is produced by cyclooxygenase in endothelial cells, where it promotes vasodilation and inhibits platelet aggregation. Prostacyclin should therefore be a beneficial mediator. Aspirin inhibits prostacyclin formation, however, endothelial cells can produce more cyclooxygenase and are able to continue to synthesize adequate amounts of prostacyclin.
Ubiquinone (choice E), or coenzyme Q, is a naturally occurring coenzyme that plays a vital role in the mitochondrial electron transport chain. Studies have shown an association between decreased levels of coenzyme Q and heart disease, so inhibition of ubiquinone production would not likely be beneficial.

The correct answer is E. Troponins (in isoforms troponin C, troponin I, and troponin T) are required for actin-myosin cross linking in cardiac muscle. Small elevations in serum troponin levels are currently the most sensitive clinical serum markers for myocardial injury, elevating within 3-12 hours of infarction. Levels remain elevated for 5-14 days.
Alanine aminotransferase (choice A) occurs in both cardiac muscle and in the liver, and has been used in the past as a marker of cardiac injury. However, currently, its more common clinical use is as a marker of hepatocyte injury. Its time course of elevation in MI is intermediate between CPK and LDH (see below).
Creatine phosphokinase (choice B) has been the mainstay of diagnosis of myocardial injury for many years. CPK has several isoforms, of which the MB isoform is specific for cardiac muscle. The fraction of the total CPK that is the MB isoform has been used to differentiate myocardial injury from other injury processes elevating CPK. CPK is also elevated with skeletal muscle and with brain injury, but neither of these tissues contains significant amounts of MB isoform. In MI, CPK levels usually rise within 8 to 24 hours and return to normal after 48 to 72 hours.
Lactate dehydrogenase (choice C) is, like alanine aminotransferase, an enzyme that is released both with cardiac injury and with hepatocellular injury. It can also be elevated in hemolysis and with some neoplasms. In MI, it generally rises within 12 hours and peaks after 24-48 hours, remaining elevated for 10-14 days. These properties made LDH, prior to the introduction of troponin assays, the test used to detect MI occurring more than a day previously.
Transferrin (choice D) is a plasma protein responsible for the uptake of iron after absorption in the small intestine, and is responsible for iron-binding capacity in the blood. It is measured (usually as "total iron-binding capacity") in the differential diagnosis of the anemias.

The correct answer is D. This patient is suddenly in cardiogenic shock with severe pulmonary edema. This could be the result of arrhythmia, cardiac tamponade, or left ventricular valvular dysfunction. He had an inferior MI, which is most likely due to thrombosis of the right coronary artery. The posteromedial papillary muscle is supplied by the RCA alone in most patients and is prone to rupture in inferoposterior MI. Rupture leads to acute and severe mitral valve dysfunction, resulting in pulmonary edema and poor forward ejection.
Dilation of the left ventricle (choice A) typically occurs after extensive damage occurs, which would have appeared on this patient's acute EKG as ST elevation in the anterior leads. Dilation can result in mitral regurgitation, but typically of an insidious onset.
Dressler syndrome (choice B) is a late complication of MI that may occur weeks to months later, characterized by symptoms of pericarditis including pleuritic chest pain, fever, friction rub, and elevated white blood cell count. Patients can also develop early postinfarction pericarditis in the days to weeks following MI with friction rub and pericardial effusion. This is seldom associated with cardiac tamponade.
Rupture of the LV free wall (choice C) is a complication more likely to occur with more extensive damage to the LV than is produced in an inferior MI such as this patient had. However, LV free wall rupture would produce cardiac tamponade, which could produce this clinical picture.
Ventricular tachycardia (VT) (choice E) is a complication of MI (though risk is highest early in the course of infarction) and could also produce this clinical picture. However, it is excluded by the EKG, which reveals an atrial-ventricular conducted rhythm (VT displays no P waves) and a narrow-complex QRS (VT typically has a QRS much greater than 0.12 s).

The correct answer is B. Three days after infarction, coagulation necrosis is complete, with complete loss of cellular structure (hence the high risk of mechanical complications such as rupture) and infiltration of monocytes to phagocytize debris.
Acellular fibrosis (choice A) replaces necrosis after many weeks when debris is removed and fibroblasts have invaded the dead tissue and replaced it with collagen.
Myocyte disarray (choice C) is associated with hypertrophic subaortic stenosis (IHSS), rather than myocardial infarction.
Myocyte edema, with hemorrhage and neutrophil infiltration (choice D) occurs within 4-12 hours after infarction.
Wavy myofibers and contraction bands (choice E) are the first light microscopic pathologic changes to occur after MI, and appear within 1-3 hours after infarction.