Ischemic Heart Disease and Atherosclerosis

Question 1

How often should you screen for hypertension?

Answer 1

Although there is no absolutely correct answer, all individuals should be screened roughly

every 2 years, starting at the age of 3 years.

Question 2

Define hypertension

Answer 2

Persistent blood pressure greater than 140/90 mm Hg.

Individuals with a systolic blood pressure of 120 to 139 mm Hg or a diastolic pressure of 80 to 89 mm Hg should be considered as prehypertensive.

Remember that 145/60 mm Hg is hypertension, as is 115/95 mm Hg (isolated systolic and diastolic hypertension, respectively).

In grading the severity of hypertension, use the worst number, whether it is diastolic or systolic. Table 4-1 lists the 2003 Joint National Committee (JNC-7) classification. Please note that this classification system was not addressed in the updated 2013 JNC-8 classification.

Question 3

What is the “two measurement” rule in the diagnosis of hypertension?

Answer 3

Blood pressure should be measured two times on each of two separate office visits before the diagnosis and pharmacologic treatment of hypertension.

However, if asked, institute conservative measures and address associated comorbidities (e.g., obesity, diabetes) after the first abnormal measurement.

There are a few important exceptions to the “start conservative and remeasure” strategy, however, and more aggressive approaches are gaining favor.

Patients with marked blood pressure elevation (generally >200/120 mm Hg) and acute end-organ damage (e.g., encephalopathy, MI, unstable angina, pulmonary edema, stroke) require hospitalization and parenteral drug therapy. Patients with markedly elevated blood pressure but without end- organ damage usually do not require hospitalization but should be given immediate combination oral antihypertensive therapy. In pregnant or recent postpartum women, preeclampsia may be the cause of hypertension. Waiting to treat in this setting can have devastating consequences for the mother and fetus.

Question 4

What does lowering of blood pressure accomplish?

Answer 4

Hypertension is the leading modifiable risk factor for strokes.

Lowering of blood pressure decreases the incidence of heart disease, MI, atherosclerosis, stroke, renal failure, and aortic aneurysms.

Question 5

What are the conservative (i.e., nonpharmacologic) treatments for hypertension?

Answer 5

Dietary changes (i.e., low salt, low fat, low calorie),

reduced smoking and alcohol intake,

weight loss, and

exercise

may each have a positive effect on blood pressure and, in some cases, return the patient to the normotensive range.

Question 6

List the first-line medications for treatment of hypertension.

Answer 6

JNC-8 recommends treatment with an angiotensin-converting enzyme inhibitor (ACEI), angiotensin receptor blocker (ARB), and calcium channel blocker (CCB) or diuretic.

There are a few groups for whom treatment is more specific.

In the general black population, including those with diabetes, initial antihypertensive treatment should include a thiazide-type diuretic or CCB.

In the population aged 18 years or older with chronic kidney disease (CKD) and hypertension,
initial (or add-on) antihypertensive treatment should include an ACEI or ARB to improve kidney outcomes.

This applies to all CKD patients with hypertension regardless of race or diabetes status.

In some cases, medications from multiple classes may be needed to reach blood pressure goals.

Beta-blockers and alpha-blockers are NOT recommended for initial management.

Note: In diabetes, ACEIs reduce progression to nephropathy and neuropathy. All patients with stable CHF or diabetes should take an ACEI (if they can tolerate it) even in the absence of hypertension.

Question 7

What about women of reproductive age and pregnant women with hypertension?

Answer 7

Labetalol, hydralazine, and alpha-methyldopa are safe.

If preeclampsia is present, remember that magnesium sulfate lowers blood pressure and is the first-line agent of choice.

Question 8

Define hypertensive urgency.

Answer 8

Hypertensive urgency is defined as blood pressure greater than 200/120 mm Hg without symptoms.

Patients with hypertensive urgency should be started on oral antihypertensives as an outpatient.

Question 9

hypertensive urgency, How is it different from hypertensive emergency?

Answer 9

Hypertensive emergency is defined as blood pressure greater than 200/120 mm Hg with symptoms or evidence of end-organ damage.

Examples include acute left ventricular failure, chest pain or angina, MI, encephalopathy (watch for headaches, confusion, retinal hemorrhages, papilledema, mental status changes, vomiting, blurry vision, dizziness, and/or seizures), or acute renal failure (from necrotizing arteriolitis).

Hypertensive emergency requires immediate treatment with intravenous antihypertensives such as nitroprusside, labetalol, and nicardipine.

Patients with hypertensive urgency should be started on oral antihypertensives as an outpatient.

Question 10

What causes hypertension?

Answer 10

Roughly 90% to 95% of cases are idiopathic, multifactorial, or essential hypertension.

About 5% to 10% of cases are due to secondary (known) causes.

Question 11

What are the common causes of secondary hypertension in younger men and women?

Answer 11

In younger men, a common cause of secondary hypertension is excessive alcohol intake (get the patient to quit!).

In younger women, common and classic causes are birth control pills (stop them!) and

renal artery stenosis (RAS) from fibromuscular dysplasia (which may cause a bruit and should be treated with balloon angioplasty).

Question 12

List less common causes of secondary hypertension.

Answer 12

Pheochromocytoma. Look for wild swings in blood pressure with diaphoresis and confusion. As a screening test, order 24-hour urine collection to assess catecholamine products (metanephrines, vanillylmandelic acid, homovanillic acid). RAS. Unlike young patients with fibromuscular dysplasia, elderly patients typically have RAS caused by atherosclerosis. A renal artery bruit is classically present (although not sensitive); an MRI scan or conventional angiography aids in making a definitive diagnosis. Giving ACEIs to patients with RAS may precipitate acute renal failure (sometimes the first diagnostic clue to its presence). Polycystic kidney disease. Look for a flank mass, a positive family history (autosomal-dominant pattern of inheritance), and elevations in creatinine and blood urea nitrogen. Cushing syndrome. Look for stigmata of Cushing syndrome on examination. Order a 24-urine collection to assess free cortisol or a dexamethasone suppression test. Conn syndrome (primary hyperaldosteronism). The cause is an aldosterone-secreting adrenal neoplasm. Look for high aldosterone levels, low renin levels, hypernatremia, hypokalemia, metabolic alkalosis, and/or an adrenal mass on a CT scan. The screening test of choice is the ratio of plasma aldosterone to plasma rennin activity; a ratio of greater than 30 is indicative of primary hyperaldosteronism. Coarctation of the aorta. Look for hypertension in the upper extremities only, with unequal pulses, radiofemoral delay, and rib notching on a chest radiograph; this condition is associated with Turner syndrome. MRI or angiography can aid in making a definitive diagnosis. Renal failure from any cause. In children, watch for poststreptococcal glomerulonephritis or hemolytic uremic syndrome.

Question 13

Pheochromocytoma.

Answer 13

Look for wild swings in blood pressure with diaphoresis and confusion. As a screening test, order 24-hour urine collection to assess catecholamine products (metanephrines, vanillylmandelic acid, homovanillic acid).

Question 14

RAS.

Answer 14

Unlike young patients with fibromuscular dysplasia, elderly patients typically have RAS caused by atherosclerosis. A renal artery bruit is classically present (although not sensitive); an MRI scan or conventional angiography aids in making a definitive diagnosis. Giving ACEIs to patients with RAS may precipitate acute renal failure (sometimes the first diagnostic clue to its presence).

Question 15

Polycystic kidney disease.

Answer 15

Look for a flank mass, a positive family history (autosomal-dominant pattern of inheritance), and elevations in creatinine and blood urea nitrogen.

Question 16

Cushing syndrome.

Answer 16

Look for stigmata of Cushing syndrome on examination.

Order a 24-urine collection to assess free cortisol or a dexamethasone suppression test.

Question 17

Conn syndrome (primary hyperaldosteronism).

Answer 17

The cause is an aldosterone-secreting adrenal neoplasm.

Look for high aldosterone levels, low renin levels, hypernatremia, hypokalemia, metabolic alkalosis, and/or an adrenal mass on a CT scan.

The screening test of choice is the ratio of plasma aldosterone to plasma rennin activity;
a ratio of greater than 30 is indicative of primary hyperaldosteronism.

Question 18

Coarctation of the aorta.

Answer 18

Look for hypertension in the upper extremities only, with unequal pulses, radiofemoral delay, and rib notching on a chest radiograph;

this condition is associated with Turner syndrome. MRI or angiography can aid in making a definitive diagnosis.

Question 19

Renal failure from any cause.

Answer 19

In children, watch for poststreptococcal glomerulonephritis or hemolytic uremic syndrome.

Question 20

What tests should be ordered for every patient with a diagnosis of hypertension? Why?

Answer 20

1. ECG: to determine whether the heart has been affected (e.g., left ventricular hypertrophy).
2. Chemistry 7 panel (i.e., basic metabolic panel): clues to possible secondary cause of hypertension (e.g., electrolyte disturbances in Conn syndrome) and evaluation for diabetes and renal dysfunction.
3. Urinalysis: clues to possible secondary cause of hypertension (e.g., red blood cell casts in poststreptococcal glomerulonephritis) and for kidney damage (proteinuria).
4. Hemoglobin and hematocrit: to evaluate for anemia or polycythemia.
5. Lipid panel: to evaluate for dyslipidemia as an additional risk factor for coronary artery disease.

Question 21

When is cholesterol screening performed?

Answer 21

Although no protocol is universally accepted,

measurement of total cholesterol and high-density lipoprotein (HDL) cholesterol every 5 years once a person turns 20 years of age is considered reasonable by most authorities.

Start sooner and screen more frequently for obese patients and patients with a family history of hypercholesterolemia.

Question 22

Why is cholesterol so important?

Answer 22

Cholesterol is one of the main known modifiable risk factors for atherosclerosis.

Atherosclerosis is involved in about half of all deaths in the United States and one third of deaths between the ages of 35 and 65 years.

Atherosclerosis is the most important cause of permanent disability and accounts for more hospital days than any other illness.

Question 23

What physical findings will the Step 3 test use as clues to hypercholesterolemia?

Answer 23

Xanthelasma, tendon xanthomas (cholesterol deposits in the skin, classically over tendons in the lower extremities), corneal arcus in younger patients, milky-appearing serum, and obesity are possible markers for familial hypercholesterolemia. Family members should be tested if a case of familial hypercholesterolemia is found. Pancreatitis in the absence of obvious risk factors may be a marker for familial hypertriglyceridemia.

Question 24

What are the current recommendations for management of cholesterol levels?

Answer 24

The following information is from the 2013 American College of Cardiology/American Heart Association (ACC/AHA) Guidelines on the Treatment of Blood Cholesterol to Reduce Atheroscleroitc Cardiovascular Risk in Adults.

This new guideline differs from the previous recommendations in that it moves away from specific low-density lipoprotein (LDL) targets.

Anyone with LDL ≥190 mg/dL:
Reduce LDL by >50%
treat with High-intensity statin

Diabetics aged 40-75 yr with LDL >70 mg/dL: Reduce LDLby 30-50%
treat with Moderate-intensity statin

Anyone with current or past CVD (angina, MI, PAD) and LDL >70 mg/dL Reduce by >50% High-intensity statin

Anyone with current or past CVD (angina, MI, PAD) and LDL >70 mg/dL
Reduce LDL by >50%
Tx w/ High-intensity statin

Anyone with ≥7.5% chance of developing atherosclerotic CVD in the next 10 yr, using a specific calculator∗
Reduce LDL by 30-50%
Tx with Moderate-intensity statin

Question 25

What is meant by high-intensity and moderate-intensity statins?

Answer 25

High-dose statin means a statin at a sufficient dose to reduce LDL by at least 50%.
This includes atorvastatin 40 to 80 mg and rosuvastatin 20 to 40 mg.

Moderate-dose statin means a statin at a sufficient dose to reduce LDL by 30% to 50%.
This includes atorvastatin 10 to 20 mg, simvastatin 20 to 40 mg, rosuvastatin 5 to 10 mg, pravastatin 40 to 80 mg, and lovastatin 40 mg.

Question 26

What about nonstatin cholesterol-lowering drugs such as ezetimibe and the fibrates?

Answer 26

These medications are not included in the current ACC/AHA guidelines because there is insufficient evidence that they reduce atherosclerotic coronary vascular disease (ASCVD) events.

Question 27

List the major risk factors for coronary heart disease (CHD).

Answer 27

Although elevated levels of LDL and total cholesterol are risk factors for CHD, do not count them as risk factors when deciding whether or not to treat high cholesterol.

The following factors should be counted:

• Family HISTORY of premature heart attack (defined as definite MI or sudden death in a first-degree male relative aged <55 years or a first-degree female relative aged <65 years)
• AGE (men aged ≥45 years; women aged ≥55 years or with premature menopause and no estrogen replacement therapy)
• Cigarette SMOKING
• HYPERTENSION (≥140/90 mm Hg or prescription for antihypertensive medications)
• Diabetes Mellitus
• LOW HDL (<40 mg/dL)

Mnemonic HAS HDL

Note: A HDL level greater than or equal to 60 mg/dL is considered protective and negates one risk factor.

Question 28

What causes hypercholesterolemia?

Answer 28

Genetic factors certainly play a role (e.g., familial hyperlipidemia), but most cases are thought to be multifactorial.

A Western diet and an inactive lifestyle certainly contribute.

Secondary causes of increased cholesterol include uncontrolled diabetes, hypothyroidism, uremia, nephrotic syndrome, obstructive liver disease, excessive alcohol intake (which increases triglycerides), and medications (e.g., birth control pills, glucocorticoids, thiazides, beta-blockers).

Question 29

In a patient with chest pain, what elements of the history and physical examination steer you away from a diagnosis of MI?

Answer 29

Wrong age: in the absence of known heart disease, strong family history, or multiple risk factors for coronary artery disease, a patient younger than 40 years is extremely unlikely to have an MI.

Lack of risk factors: a 60-year-old marathon runner who eats well and has a high HDL level and no cardiac risk factors (other than age) is unlikely to have a heart attack.

Physical characteristics of pain: if the pain is reproducible by palpation, it is from the chest wall, not the heart.
The pain associated with an MI is usually not sharp or well localized.
The pain should not be related to certain foods or eating.

Having said all of this, many physicians still want to make sure that a heart attack has not occurred with at least an ECG and possibly one or more sets of cardiac enzyme levels.
For the Step 3 exam, however, these clues should steer you toward an alternative diagnosis.

Question 30

What clues suggest the common noncardiac causes of chest pain?. Esophageal problems (achalasia, nutcracker esophagus, or esophageal spasm):

Answer 30

this is often a difficult differential diagnosis. The question will probably give negative results for a workup for MI or mention the lack of atherosclerosis risk factors. Look for abnormalities on a barium swallow (achalasia) or esophageal manometry. Treat achalasia with pneumatic dilation or botulism toxin administration, and treat nutcracker esophagus or esophageal spasm with CCBs. If medical treatments are ineffective, surgical myotomy may be needed.

Question 31

What clues suggest the common noncardiac causes of chest pain? Gastroesophageal reflux/peptic ulcer disease:

Answer 31

look for a relation to certain foods (spicy foods, chocolate), smoking, caffeine, or lying down. Pain is relieved by antacids or acid-reducing medications. Patients with peptic ulcer disease often test positive for Helicobacter pylori.

Question 32

What clues suggest the common noncardiac causes of chest pain?. Chest wall pain (costochondritis, bruised or broken ribs):.

Answer 32

pain is well localized and reproducible on chest wall palpation

Question 33

What clues suggest the common noncardiac causes of chest pain?
Pericarditis:

Answer 33

look for a viral infection prodrome for the upper respiratory tract. The ECG shows diffuse ST-segment elevation, the erythrocyte sedimentation rate is elevated, and a low-grade fever is present. Classically, the pain is relieved by sitting forward. The most common cause is infection with Coxsackie virus. Other causes include tuberculosis, uremia, malignancy, and lupus erythematous or other autoimmune diseases

Question 34

What clues suggest the common noncardiac causes of chest pain?
Pneumonia

Answer 34

Chest pain is due to pleuritis. Patients also have a cough, fever, and/or sputum production. Ask about possible sick contacts

Question 35

What clues suggest the common noncardiac causes of chest pain?
Aortic dissection

Answer 35

Associated with a severe tearing or ripping pain that may radiate to the back. Look for hypertension or evidence of Marfan syndrome (tall, thin patient with hyperextensible joints). Blunt chest trauma can cause aortic laceration and pseudoaneurysm, which are different conditions that are often managed similarly.

Question 36

What historical points should steer you toward a diagnosis of MI?

Answer 36

Patients often have a history of angina or previous chest pain, murmurs, arrhythmias, risk factors for coronary artery disease, hypertension, or diabetes. They also may be taking digoxin, furosemide, cholesterol medications, antihypertensive agents, or other cardiac medications.

Question 37

What findings on ECG should make you suspect an MI?

Answer 37

After a heart attack you should see flipped or flattened T waves, ST-segment elevation (depression means ischemia; elevation means injury), and/or Q waves in a segmental distribution (e.g., leads II, III, and aVF for an inferior MI)

Question 38

Describe the classic pattern of chest pain in an MI.

Answer 38

The pain is classically described as a crushing or pressure sensation; it is a poorly localized substernal pain that may radiate to the shoulder, arm, or jaw. The pain is usually not reproducible on palpation, and in patients with a heart attack often does not resolve with nitroglycerin (as it often does in angina). The pain usually lasts for at least half an hour.

Question 39

Describe the classic physical examination findings in patients with MI.

Answer 39

Patients are often diaphoretic, anxious, tachycardic, tachypneic, and pale; they may have nausea and vomiting. For large heart attacks that cause heart failure, look for bilateral pulmonary rales in the absence of other pneumonia-like symptoms, distended neck veins, S3 or S4 heart sounds, new murmurs, hypotension, and/or shock.

Question 40

Describe the treatment for an ST-elevation MI (STEMI).

Answer 40

Treatment involves admission to the intensive or cardiac care unit. Several basic principles should be kept in mind:

1. Early reperfusion is crucial. Percutaneous coronary intervention (PCI) is the preferred method (i.e., balloon angioplasty/stent). Bringing the patient to the catheterization laboratory should be the priority for all patients with STEMI. Fibrinolytic therapy with t-PA is only indicated in patients who cannot receive PCI within 2 hours of medical contact. Fibrinolytics can only be given within 12 hours of symptom onset. There is a long list of contraindications to t-PA given its risk for severe hemorrhage.
2. Administer aspirin.
3. ECG monitoring is essential. If ventricular tachycardia occurs, use amiodarone (or cardioversion if the patient is hemodynamically unstable).
4. Give oxygen to maintain an oxygen saturation of greater than 90%.
5. Administer nitroglycerin for symptomatic relief if the patient’s blood pressure can tolerate this vasodilatory medication; avoid nitroglycerin for inferior MIs because a decrease in the patient’s preload can lead to hypotension in the case of a right ventricular infarction.
6. Control pain with morphine, which may improve pulmonary edema, if present.
7. Administer unfractionated or low–molecular-weight heparin.
8. Administer clopidogrel.
9. Beta-blockers, which patients without contraindications should take for life, reduce the MI mortality rate and the incidence of a second heart attack.
10. An ACEI or ARB should be started within 24 hours.
11. Administer an HMG-CoA reductase inhibitor (statin).

Question 41

Describe the treatment for an ST-elevation MI (STEMI). Very brief

Answer 41

admission to the intensive or cardiac care unit.

1. Early reperfusion
2. Aspirin.
3. ECG monitoring
4. oxygen po2> 90%.
5. Administer nitroglycerin
   avoid nitroglycerin for inferior MIs - right ventricular infarction.
6. Control pain - Morphine
7. Heparin.
8. Clopidogrel.
9. Beta-blockers
10. ACEI or ARB w/in 24hr
11. Statin

MONA BASH
Morphine, Oxygen, Nitroglycerin, Aspirin
B-Blocker, ACE-I, Statin, Heparin

+clopidogrel
+EKG
+reperfussion

Question 42

When is heparin indicated in the setting of chest pain and MI?

Answer 42

Heparin should be started if acute coronary syndrome is diagnosed (unstable angina, non-STEMI [NSTEMI], or STEMI), if the patient has a cardiac thrombus, or if severe CHF is seen on echocardiography. The Step 3 exam will not ask about other indications, which are not as clear cut. Do not give heparin to patients with contraindications to its use (e.g., active bleeding).

Question 43

How can you recognize stable angina?

Answer 43

The chest pain of stable angina begins with exertion or stress and remits with rest or on calming down.

The key to a diagnosis of stable angina is that it is stable, not increasing in duration of pain, not occurring with less exertion, and not becoming more frequent.

The pain is described as a pressure or squeezing pain in the substernal area and may radiate to the shoulders, neck, and/or jaw. It often is accompanied by shortness of breath, diaphoresis, and/or nausea.

The pain is usually relieved by nitroglycerin.

An ECG performed during an acute attack often shows ST-segment depression, but in the absence of pain, the ECG is often normal.

The pain should last for less than 20 minutes or be relieved after sublingual nitroglycerin administration; otherwise, there may be progression to unstable angina or MI.

Question 44

Define unstable angina. How is it diagnosed and treated?

Answer 44

In strict terms, unstable angina is defined as a change from previously stable angina.

If a patient used to experience angina once a week and now experiences it once a day, the patient technically has unstable angina.

Patients with unstable angina usually exhibit normal or only minimally elevated cardiac enzymes, ECG changes (ST depression), and prolonged chest pain that does not respond to nitroglycerin initially (like a heart attack).
The pain often begins at rest.

Treatment is similar to that for MI.
The patient is admitted to the coronary or intensive care unit.
Initial treatment begins with oxygen, aspirin, and nitroglycerin administration. The patient should be given a beta-blocker, clopidogrel, and heparin (unfractionated or the low–molecular-weight form).

A glycoprotein IIb/IIIa receptor inhibitor should be administered to patients with continuing ischemia or with other high-risk features. (abciximab, eptifibatide, and tirofiban)

An ACEI or ARB should be given as well.

Consider emergent percutaneous tranluminal coronary angiography (PTCA) if the pain does not resolve. Almost all patients have a history of stable angina and coronary artery disease risk factors.

Question 45

Describe variant (Prinzmetal) angina.

Answer 45

This rare type of angina is characterized
by pain at rest (unrelated to exertion)
and ST-segment elevation;

cardiac enzymes are Normal.

The cause is coronary artery spasm.

Prinzmetal angina usually responds to
nitroglycerin and is treated over the long term with
CCBs, which reduce arterial spasms.

Question 46

Define silent MI. How common is it?

Answer 46

Patients with a silent MI do not develop chest pain.

Their symptoms include CHF, shock, or confusion and delirium (especially elderly patients).

MIs are silent in up to 25% of cases (especially in diabetics with neuropathy).

Question 47

Injury to what organ (other than the heart) causes elevated levels of creatine kinase (CK)?

Answer 47

Muscle.

Watch for trauma,
rhabdomyolysis,
HMG-CoA reductase inhibitors (which can cause muscle damage), and
burns.

CK-MB is a subtype of CK that is more specific to the myocardium.

Question 48

What is the relationship between aspirin and MI?

Answer 48

It has been proved that low-dose aspirin is of benefit in reducing the risk of MI in patients who have had a previous MI and patients with stable or unstable angina who have not had an MI.
The 2012 American College of Chest Physicians (ACCP) clinical practice guidelines on antithrombotic and thrombolytic therapy recommend that all patients with chronic stable angina or other clinical or laboratory evidence of coronary artery disease receive

aspirin indefinitely.

There is strong medical literature support for the net benefit of aspirin for primary prevention of a first MI in individuals at moderate to high risk.

Aspirin is recommended in ALL Diabetic patients with CardioVascular Disease and for

primary prevention in diabetic patients with one or more risk factors (e.g., age >40 years, cigarette smoking, hypertension, hyperlipidemia, obesity, albuminuria, or family history of cardiovascular disease).

The risks of aspirin prophylaxis may outweigh the benefits in patients with a history of liver disease, kidney disease, peptic ulcer disease or gastrointestinal bleeding, poorly controlled hypertension, or a bleeding disorder.

Question 49

True or false: Patients should be given aspirin as soon as possible in the emergency department for a suspected MI or unstable angina.

Answer 49

True, but beware the patient with chest pain who ends up having an aortic dissection (aspirin should be avoided in such patients).

Question 50

How is smoking related to heart disease?

Answer 50

Smoking is the best risk factor to eliminate for prevention of deaths related to heart disease; it is responsible for 30% to 45% of such deaths in the United States. This risk is decreased by 50% within 1 year of quitting, and by 15 years after quitting, the risk is the same as for someone who has never smoked.

Question 51

What is the most common cause of death during vascular surgery?

Answer 51

MI, regardless of the procedure performed. Peripheral vascular and aortic diseases are generalized markers for atherosclerosis, and almost all patients have significant coronary artery disease. Always evaluate patients for modifiable and treatable atherosclerosis risk factors (i.e., hyperlipidemia, hypertension, smoking, diabetes).

Question 52

Describe the classic symptoms of chronic mesenteric ischemia.

Answer 52

The classic patient has a long history of postprandial abdominal pain (also known as intestinal angina; eating exercises the intestines), which causes fear of food and extensive weight loss. This diagnosis is difficult because, like all atherosclerotic disease, it occurs in patients older than 40 years who have other conditions that may cause the same problem (e.g., peptic ulcer disease, pancreatic cancer, stomach cancer). Look for a history of extensive atherosclerosis (known coronary artery disease, peripheral vascular disease, stroke, or multiple risk factors), abdominal bruit, Hemoccult-positive stool, and lack of jaundice (jaundice suggests pancreatic cancer). Most patients undergo a CT scan of the abdomen; negative results raise the suspicion of ischemia. The diagnosis can be made on the basis of selective angiography of the superior mesenteric artery. MRI angiography and CT angiography are emerging tools, but angiography is still the preferred modality. Patients are treated with surgical revascularization because of the risks of bowel infarction and malnutrition.

Question 53

What are the symptoms of an acute bowel infarction?

Answer 53

Classically, a patient with a history of atrial fibrillation, atherosclerosis, or multiple atherosclerosis risk factors has symptoms of abdominal pain and bloody diarrhea. Patients classically have pain out of proportion to the examination, but may have peritoneal signs (e.g., rebound tenderness, guarding). Watch for the thumbprinting sign (thickened bowel walls that resemble thumbprints) on abdominal radiographs. Patients may also have tachycardia, hypotension, and/or shock.