PCM Fall Exam
Notes on Asthma, COPD, Cystic Fibrosis, Community-Acquired Pneumonia,
Pulmonary Embolism, Mitral Stenosis
Asthma
Essentials of Diagnosis:
 Episodic or chronic symptoms of airflow obstruction: breathlessness, cough,
wheezing, and chest tightness.
 Symptoms frequently worse at night or in the early morning.
 Prolonged expiration and diffuse wheezes on physical examination.
 Limitation of airflow on pulmonary function testing or positive
bronchoprovocation challenge.
 Complete or partial reversibility of airflow obstruction, either spontaneously or
following bronchodilator therapy.
General Considerations:
 Common disease affecting 5% of population.
 Men and women equally affected.
 470,000 hospital admissions and 5,000 deaths in USA attributable to asthma.
 Hospitalization and death rates highest among blacks aged 15 – 24 years.
 Prevalence, hospitalizations, and fatal asthma have all increased in USA over the
past 20 years.
Definitions and Pathogenesis:
 Asthma is a chronic inflammatory disorder of the airways.
 Airway inflammation underlies disease chronicity and contributes to airway
hyperresponsiveness, airflow limitation, and to respiratory symptoms.
 Genetic predispostion recognized, related to atopy.
 Both specific and nonspecific precipitants exist.
Clinical Findings:
 Episodic wheezing, difficulty breathing, chest tightness, cough.
 Frequency of symptoms is highly variable.
 Symptoms may occur spontaneously or be precipitated or exacerbated by many
different triggers.
 Asthma symptoms are frequently worse at night.
 Nasal mucosal swelling, increased nasal secretions, and nasal polyps are often
seen in patients with allergic asthma.
 Eczema, atopic dermatitis, or other manifestations of allergic skin disorders may
also be present.
 Hunched shoulders and use of accessory muscles of respiration suggest increased
work of breathing.
 Chest examination may be normal between exacerbations in patients with mild
asthma.
 Wheezing during normal breathing or prolonged forced expiration correlates well
with the presence of airflow obstruction.
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During severe asthma wheezing may disappear, and the only diagnostic clue on
auscultation may be globally reduced breath sounds with prolonged expiration.
 The evaluation for asthma should included spirometry (FEV1, FVC, FEV1/FVC)
before and after the administration of a short-acting bronchodilator.
Complications:
 Exhaustion, dehydration, airway infection, cor pulmonale, tussive syncope.
 Rare pneumothorax.
 Hypercapnic and hypoxic respiratory failure in severe disease.
Differential Diagnosis:
 Upper airway disorders: vocal cord paralysis, vocal cord dysfunction syndrome,
foreign body aspiration, laryngotracheal masses, tracheal narrowing,
tracheomalacia, airway edema.
 Lower airway disorders: COPD, bronchiectasis, allergic brochopulmonary
mycosis, cystic fibrosis, eosinophilic pneumonia, bronchiolitis obliterans.
 Systemic vasculitides: Churg-Strauss syndrome, others with pulmonary
component.
 Psychiatric: conversion disorders, Munchausen syndrome, malingering.
Classification:
 Mild intermittent: Symptoms ≤ 2 times a week with normal function between
exacerbations. Nighttime symptoms ≤ 2 times a month.
 Mild persistent: Symptoms > 2 times per week but < 1 time a day. Nighttime
symptoms > 2 times a month.
 Moderate persistent: Daily symptoms and/or daily use of inhaled short-acting β2agonist. Exacerbations affect activity. Nighttime symptoms > 1 time a week.
 Severe persistent: Continual symptoms. Limited physical activity. Frequent
exacerbations and nighttime symptoms.
Treatment:
 Corticosteroids: most potent and consistently effective anti-inflammatory agents
currently available. Inhaled agents used for long-term control and systemic
agents used for prompt control of short-term exacerbations.
 Long-acting bronchodilators
 Short-acting bronchodilators: β2-agonists and others.
Approach to Treatment:
 Principal goals: correction of hypoxemia, reversal of airflow obstruction,
reduction of the likelihood of recurrence of obstruction.
 Periodic assessments and ongoing monitoring of asthma are essential to determine
if the goals of therapy are being met.
COPD
Essentials of Diagnosis:
 History of cigarette smoking.
 Chronic cough and sputum production (in chronic bronchitis) and dyspnea (in
emphysema).
 Rhonchi, decreased intensity of breath sounds, and prolonged expiration on
physical examination.
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 Airflow limitation on pulmonary function testing.
General Considerations:
 COPD is a disease state characterized by the presence of airflow obstruction due
to chronic bronchitis or emphysema; the airflow obstruction is generally
progressive, may be accompanied by airway hyperreactivity, and may be partially
reversible.
 Most patients with COPD have features of both emphysema and chronic
bronchitis.
 Chronic bronchitis: characterized by excessive secretion of bronchial mucus and
is manifested by productive cough for 3 months or more in at least 2 consecutive
years in the absence of any other disease that might account for this symptom.
 Emphysema: abnormal, permanent enlargement of air spaces distal to the terminal
bronchiole, with destruction of their walls and without obvious fibrosis.
 Cigarette smoking is clearly the most important cause of COPD.
Clinical Findings:
 Patients with COPD characteristically present in the fifth or sixth decade of life
complaining of excessive cough, sputum production, and shortness of breath.
 Symptoms have often been present for 10 years or more.
 Dyspnea is often noted initially only on heavy exertion, but this exacerbates as the
condition progresses.
 Clinical findings may be completely absent early in the course of COPD.
 “Pink puffers” = emphysema predominant.
 “Blue bloaters” = bronchitis predominant.
Differential Diagnosis:
 Clinical, imaging, and laboratory findings should enable the clinician to
distinguish COPD from other obstructive pulmonary disorders.
 These include: bronchial asthma, bronchiectasis, cystic fibrosis,
bronchopulmonary mycosis, central airflow obstruction.
Complications:
 Stable COPD: acute bronchitis, pneumonia, pulmonary thromboembolism,
concomitant left ventricular failure.
 Advanced COPD: pulmonary hypertension, cor pulmonale, chronic respiratory
failure.
 Spontaneous pneumothorax and hemoptysis are also possible.
Prevention:
 Elimination of chronic exposure to tobacco smoke.
 Smoking cessation.
Treatment:
 Smoking cessation.
 Oxygen therapy.
 Bronchodilators.
 Antibiotics for treating acute exacerbations.
 Lung transplantation.
Prognosis:
 Poor.
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Median survival time of patients with severe COPD is about 4 years.
Degree of pulmonary dysfunction at the time the patient is first seen is the most
important predictor of survival.
Cystic Fibrosis
Essentials of Diagnosis:
 Chronic or recurrent cough, sputum production, dyspnea, and wheezing.
 Recurrent infections or chronic colonization of the airways with nontypeable
Haemophilus influenzae, mucoid and nonmucoid Pseudomonas aeruginosa,
Staphylococcus aureus, or Burkholderia cepacia.
 Pancreatic insufficiency, recurrent pancreatitis, distal intestinal obstruction
syndrome, chronic hepatic disease, nutritional deficiencies, or male urogenital
abnormalities.
 Bronchiectasis and scarring on chest radiographs.
 Airflow obstruction on spirometry.
 Sweat chloride concentration above 60 meq/L on two occasions or mutations in
genes known to cause cystic fibrosis.
General Considerations:
 Most common cause of severe chronic lung disease in young adults.
 Most common fatal hereditary disorder of Caucasians in the USA.
 Autosomal recessive disorder affecting about one in 3200 Caucasians; one in 25 is
a carrier.
 Caused by abnormalities in CFTR protein that results in altered chloride transport
and water flux across the apical surface of epithelial cells.
 Mutation referred to as ΔF508 accounts for 60% of CF cases.
Clinical Findings:
 CF should be suspected in a young adult presenting with a history or chronic lung
disease (especially bronchiectasis), pancreatitis, or infertility.
 Cough, sputum production, decrease exercise tolerance, and recurrent hemoptysis
are typical complaints.
 Patients also often complain of facial (sinus) pain or pressure and purulent nasal
discharge.
 Steatorrhea, diarrhea, and abdominal pain are also common.
 Digital clubbing, increase anteroposterior chest diameter, hyperresonance to
percussion, and apical crackles are noted on physical examination.
 Sinus tenderness, purulent nasal secretions, and nasal polyps may also be seen.
 Chloride sweat test used for diagnosis.
Treatment:
 Early recognition and comprehensive multidisciplinary therapy improve symptom
control and the chances or survival and amelioration of symptoms.
 Tx includes: clearance and reduction of lower airway secretions, reversal of
bronchoconstriction, treatment of respiratory tract infections and airway bacterial
burden, pancreatic enzyme replacement, nutritional and psychosocial support.
 Lung transplantation for advanced cystic fibrosis.
Prognosis:
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Median survival age is now 31 years.
Death occurs from pulmonary complications or as a result of terminal chronic
respiratory failure and cor pulmonale.
Community-Acquired Pneumonia
Essentials of Diagnosis:
 Symptoms and signs of an acute lung infection: fever or hypothermia, cough with
or without sputum, dyspnea, chest discomfort, sweats or rigors.
 Bronchial breath sound or rales are frequent auscultatory findings.
 Parenchymal infiltrate on chest radiographs.
 Occurs outside of the hospital or less than 48 hours after admission in a patient
who is not hospitalized or residing in a long-term facility for more than 14 days
before the onset of symptoms.
General Considerations:
 Approximately 2 – 3 million cases diagnosed each year in the USA.
 Most deadly infectious disease and sixth leading cause of death in USA.
 Mortality and morbidity risk factors include: advanced age, alcoholism, comorbid
medical conditions, altered mental status, respiratory rate ≥ 30 breaths/min,
hypotension, and BUN > 30 mg/dL.
Definitions and Pathogenesis:
 Pulmonary defense mechanisms (cough reflex, mucociliary clearance system,
immune responses) normally prevent the development of lower respiratory tract
infections following aspiration of oropharyngeal secretions containing bacteria or
inhalation of infected aerosols.
 Community-acquired pneumonia occurs when there is a defect in one or more of
the normal host defense mechanisms or when the infectious pathogen overwhelms
the host.
 Streptococcus pneumoniae is the most common bacterial pathogen (2/3 of
bacterial isolates).
 Other common bacterial pathogens include Haemophilus influenzae, Mycoplasma
pneumoniae, Chlamydia pneumoniae, Staphylococcus aureus, Neisseria
meningitidis, Moraxella catarrhalis, Klebsiella pneumoniae, other gram-negative
rods, and legionella species.
 Viral causes of community-acquired pneumonia include influenza virus,
respiratory syncytial virus, adenovirus, and parainfluenza virus.
Clinical Findings:
 Acute or subacute onset of fever, cough with or without sputum production, and
dyspnea.
 Other common symptoms include rigors, sweats, chills, chest discomfort,
pleurisy, fatigue, myalgias, anorexia, headache, and abdominal pain.
 Common physical findings include fever or hypothermia, tachypnea, tachycardia,
and mild arterial oxygen desaturation.
 Chest examination is often remarkable for altered breath sounds and rales.
 Dullness to percussion may be present if a parapneumonic pleural effusion is
present.
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Differential diagnosis includes upper respiratory tract infections, reactive airway
diseases, congestive heart failure, bronchiolitis obliterans organizing pneumonia,
lung cancer, pulmonary vasculitis, pulmonary thromboembolic disease, and
atelectasis.
 Sputum gram stains are often used to help identify causative organisms.
 Chest radiography may confirm the diagnosis and detect associate lung diseases.
Treatment:
 Antimicrobial therapy should be indicated promptly after the diagnosis of
pneumonia is established and appropriate specimens are obtained.
 Decisions regarding hospitalization should be based on prognostic criteria.
 Local resistance pattern data should guide empirical antibiotic therapy.
Prevention:
 Polyvalent pneumococcal vaccine has the potential to prevent or lessen the
severity of the majority of pneumococcal infections in immunocompetent
patients.
 Influenza vaccine is also an important prevention technique.
Pulmonary Embolism
Essentials of Diagnosis:
 Predisposition to venous thrombosis, usually of the lower extremities.
 Usually one of the following: dyspnea, chest pain, hemoptysis, syncope.
 Tachypnea and a widened alveolar-arterial PO2 difference.
 Characteristic defects on ventilation-perfusion lung scan, spiral CT scan of the
chest, or pulmonary angiogram.
General Considerations:
 Common, serious, and potentially fatal complication of thrombus formation
within the deep venous circulation.
 Estimated to cause 50,000 deaths each year in the USA and is the third leading
cause of death among hospitalized patients.
 Management demands a vigilant systematic approach to diagnosis and an
understanding of risk factors so that appropriate preventative therapy can be
given.
 Many substances can embolize to the pulmonary circulation, and deep venous
thrombi of the calf muscle circulation are the most common.
 Pulmonary embolism and deep venous thrombosis are two manifestations of the
same disease.
 Risk factors include: venous stasis, injury to the vessel wall, and
hypercoaguability.
Clinical Findings:
 Clinical diagnosis is notoriously difficult for two reasons: (1) the clinical findings
depends on both the size of the embolus and the patient’s preexisting
cardiopulmonary status; (2) common symptoms and signs of pulmonary emboli
are not specific to this disorder.
 The most sensitive findings are dyspnea, pain on inspiration, and tachypnea.
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Other common findings are cough, leg pain, hemoptysis, crackles, tachycardia,
and abnormal heart sounds.
 ECG abnormalities are found in 70% of PE patients.
 D-dimer testing is extremely sensitive, such that the absence of D-dimer using
ELISA provides strong evidence against PE.
 Chest radiograph and perfusion scan are used together to evaluate PE.
 Spiral CT, MRI, and venous thrombosis studies can also be used.
 Pulmonary angiography remains the reference standard for the diagnosis of PE.
Prevention:
 Prophylactic intervention is extremely important, but remains underutilized.
 Mechanical devices such as compression stockings and pneumatic compression
devices are utilized.
 Heparin therapy is also utilized in the hospital setting.
Treatment:
 Anticoagulation with heparin is a form of secondary prevention.
 Thrombolytic therapy for patients with established PE.
Mitral Stenosis
Essentials of Diagnosis:
 Dyspnea, orthopnea, and paroxysmal nocturnal dyspnea.
 Symptoms often precipitated by onset of atrial fibrillation or pregnancy.
 Prominent mitral first sound, opening snap (usually), and apical diastolic
crescendo rumble.
 ECG shows left atrial abnormality and, commonly, atrial fibrillation. EchoDoppler confirms diagnosis and quantifies severity.
General Considerations:
 Nearly all patients with mitral stenosis have underlying rheumatic heart disease,
though a history of rheumatic fever is often absent.
Clinical Findings:
 Characteristic finding of mitral stenosis is a localized middiastolic murmur low in
pitch whose duration varies with the severity of the stenosis and the heart rate.
 The valve opens in early diastole with an opening snap; the sound is sharp and
widely distributed over the chest.
 Echocardiography is the most valuable technique for assessing mitral stenosis.
Treatment and Prognosis:
 Mitral stenosis may be present for a lifetime with few or no symptoms, or it may
become severe in a few years.
 In most cases, there is a long asymptomatic phase, followed by subtle limitation
of activity.
 Atrial fibrillation often precipitates more severe symptoms, which usually
improve with control of the ventricular rate or restoration of sinus rhythm.
 Once atrial fibrillation occurs, the patient should receive warfarin anticoagulation
therapy even if sinus rhythm is restored.
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Indications for relieving the stenosis include the following: (1) uncontrollable
pulmonary edema; (2) limiting dyspnea and intermittent pulmonary edema; (3)
evidence of pulmonary hypertension with right ventricular hypertrophy or
hemoptysis; (4) limitation of activity despite ventricular rate control and medical
therapy; (5) recurrent systemic emboli despite anticoagulation with moderate or
severe stenosis.
Surgery is the definite therapeutic intervention.
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Arteriosclerotic heart disease AKA
Coronary Heart Disease
Genetics: Tendency is inheritable
Incidence/Prevalence in USA: Common. Causes 35% of deaths in men age 35-50. Death rate age 55-64 1:100.
Predominant age: Men 50-60, women 60-70, for peak clinical manifestations
Predominant sex: Male > Female
SIGNS AND SYMPTOMS:
• Variable. May remain clinically asymptomatic even in advanced disease states, eg, silent ischemia.
• Clinical manifestations
◊ Substernal chest pain
◊ Exertional dyspnea
◊ Orthopnea
◊ Paroxysmal nocturnal dyspnea
◊ Cardiac arrhythmias
◊ Systolic murmur
◊ Cardiomegaly
◊ Pedal edema
CAUSES:
• Atherosclerosis
• Narrowing of coronary arteries
• Embolism compromising coronary arteries at orifices
• Subintimal atheromas in large and medium vessels
RISK FACTORS:
• Elevated low density lipoprotein (LDL)
• Decreased high density lipoprotein (HDL)
• Elevated triglycerides
• Smoking
• Family history of premature arteriosclerosis
• Obesity
• Hypertension
• Stress
• Sedentary life style
• Increasing age
• Male sex
• Diabetes mellitus
LABORATORY:
• Elevated triglycerides
• Elevated total cholesterol
• Elevated low density lipoproteins
• Decreased high density lipoproteins
• Elevated cholesterol/HDL ratio
IMAGING:
• Angiography - narrowed coronary arteries
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• Echocardiography - wall motion abnormalities
• Pharmacologic stress tests (dobutamine, dipyridamole, adenosine) - positive
• Stress thallium test - positive
TREATMENT
APPROPRIATE HEALTH CARE:
• Outpatient for management of risk factors
• Inpatient for acute ischemic syndromes
GENERAL MEASURES:
• Prevention of further progression of the disease
◊ Smoking cessation
◊ Treatment of hypercholesterolemia (diet, drugs)
◊ Increase high density lipoprotein (diet, exercise)
◊ Control of blood pressure
◊ Diabetes mellitus treated early and adequately
◊ Exercise
◊ Prophylactic aspirin
◊ Stress reduction
◊ Diet changes
◊ Weight loss
◊ Estrogen replacement therapy in postmenopausal women is currently controversial
• Treatment of complications
◊ Covered elsewhere under the individual topics (e.g., angina pectoris, myocardial infarction, heart failure,
stroke, peripheral arterial occlusion, etc.)
MEDICATIONS
DRUG(S) OF CHOICE:
• Aspirin, 160-325 mg/day, unless contraindicated
• Cholesterol-lowering agents
◊ Cholestyramine or colestipol, (bile acid sequestrants) 12-32 gm orally BID-QID
◊ Niacin 2-6 gm daily in divided doses (highly efficacious, but side effects restrict use)
◊ Gemfibrozil 600 mg bid
◊ Probucol 500 mg bid
◊ Colesevelam 3.75-4.375 g/day
◊ Ezetimibe 10 mg/day
◊ HMG-CoA reductase inhibitors (dose varies with product): atorvastatin (Lipitor), fluvastatin (Lescol),
lovastatin (Mevacor), pravastatin (Pravachol), simvastatin (Zocor)
PATIENT MONITORING:
Monitor cholesterol, triglyceride levels, other preventive programs (weight loss, smoking cessation)
POSSIBLE COMPLICATIONS:
• Myocardial infarction
• Ventricular fibrillation
• Congestive heart failure
• Angina pectoris
• Sudden cardiac death
EXPECTED COURSE/PROGNOSIS:
Guardedly favorable. Many risk factors can be modified.
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Aortic regurgitation
DESCRIPTION:
Retrograde flow from the aorta into the left ventricle through incompetent aortic cusps. Symptoms include
dyspnea, shortness of breath, palpitations, orthopnea. Usual course - acute; chronic.
SYNONYMS:
• aortic valve insufficiency
Murmur: Systolic. Aortic area, radiating to the neck, gets louder then quiter ie. Diamond shaped,
medium pitch, harsh quality
Associated signs: Decreased A2, Ejection click, S4, Narrow pulse pressure, slow rising and
delzyed pulse.
CAUSES:
• bacterial endocarditis, aortic dissection, ankylosing spondylitis, aortic stenosis, rheumatic fever, giant cell
arteritis, syphilis, Marfan syndrome, osteogenesis imperfection, Reiter's syndrome, rheumatoid arthritis,
cystic medial necrosis, sinus of Valsalva aneurysm, hypertension, arteriosclerosis, myxomatous
degeneration of valve, dissection of aorta, bicuspid aortic valve
TREATMENT:
• aortic valve replacement
Aortic valvular stenosis
An acquired or congenital obstruction to systolic left ventricular outflow across the aortic valve
Incidence/Prevalence in USA:
• Except for mitral regurgitation due to myocardial disease, valvular aortic stenosis is the most common
fatal cardiac valve lesion
• Bicuspid aortic valve has a frequency of 400 per 100,000 live births
Predominant age:
• Age < 30 years - predominantly congenital
• Age 30 to 70 years - most commonly congenital or rheumatic
• Age > 70 years - most commonly degenerative calcification of the aortic valve
Predominant sex:
• Congenital bicuspid valves: Male > Female (4:1)
• Congenital unicuspid valves: Male > Female (3:1)
SIGNS AND SYMPTOMS:
• Angina pectoris (most frequent symptom, occurring in 50-70% of patients with severe aortic stenosis)
• Near syncope
• Syncope (often exertional, occurs in 15-30% of patients with severe aortic stenosis)
• Exertional dyspnea
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Palpitations
• Fatigue
• Neurologic events (transient ischemic attack or cerebrovascular accident) due to embolization
• Systolic crescendo-decrescendo murmur, usually best heard at the second right sternal border (may have
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associated thrill) and may radiate into the carotid arteries
• Ejection (early systolic) click
• Prolonged ejection time
• Delayed, small carotid upstroke
• Delayed/decreased intensity of A2
• Paradoxical splitting of S2
• Left ventricular heave
• A high pitched diastolic blow may be present at the left sternal border (associated aortic regurgitation)
CAUSES:
• Congenital etiologies
◊ Unicuspid valve
◊ Bicuspid valve (not inherently stenotic, but becomes so as a result of 'wear and tear' thickening and
calcification; a calcified bicuspid valve is the most common cause of isolated aortic stenosis in adults)
◊ 3 cusped valve with fusion of commissures
◊ Hypoplastic annulus
• Acquired etiologies
◊ Rheumatic (or, rarely, other inflammatory disease)
◊ Degenerative calcific aortic stenosis in the elderly
DIFFERENTIAL DIAGNOSIS:
• Mitral regurgitation, either primary or secondary to underlying coronary artery disease or dilated
cardiomyopathy. Mitral regurgitation, however, is usually an apical, high frequency, pansystolic murmur,
often radiating to the axilla.
• Hypertrophic obstructive cardiomyopathy. This murmur is also a systolic crescendo-decrescendo murmur,
but is best heard at the left sternal border and may radiate into the axilla. However, this murmur
characteristically is intensified by moving from squatting to standing position and/or Valsalva maneuver,
and lessened by changing from standing to squatting.
• Aortic supravalvular stenosis
• Discrete subaortic stenosis
• 50% incidence of concomitant coronary artery disease
SPECIAL TESTS:
ECG: Left ventricular hypertrophy, often with associated ST segment depression, conduction defects, left
atrial enlargement, ventricular arrhythmias
IMAGING:
• Chest x-ray
◊ May be normal in compensated, isolated valvular aortic stenosis
◊ Cardiac hypertrophy early, later cardiomegaly
◊ Post stenotic dilatation of the ascending aorta
◊ Calcification of aortic valve cusps (may require fluoroscopy to visualize)
DIAGNOSTIC PROCEDURES:
• Echocardiography:
◊ Aortic valve morphology, thickening, calcifications
◊ Decreased aortic valve excursion
◊ Planimetry of aortic valve area
◊ Left ventricular hypertrophy
◊ Left ventricular ejection fraction
◊ Chamber dimensions
◊ Presence or absence of wall motion abnormalities suggestive of coronary artery disease
• With Doppler echocardiography:
◊ Transvalvular gradient
◊ Valve area
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◊ Diastolic function
◊ Associated aortic regurgitation
• Cardiac catheterization:
◊ Transvalvular gradient
◊ Valve area
◊ Left ventricle ejection fraction
◊ Concomitant coronary artery disease
TREATMENT
APPROPRIATE HEALTH CARE:
Outpatient except for surgical intervention
GENERAL MEASURES:
• Aortic stenosis is a progressive disease. The asymptomatic patient with non-critical aortic stenosis can be
closely followed with appropriate evaluation.
• All patients with valvular aortic stenosis should receive endocarditis prophylaxis, prior to dental work or
invasive procedures regardless of age, etiology or severity of the stenosis (as recommended by the
American Heart Association in Circulation, 1997; 96: 358-366)
• Patients with a rheumatic etiology should receive (in addition to endocarditis prophylaxis prior to dental
work or invasive procedures) rheumatic fever prophylaxis, especially if less than 35 years of age, or
continue to be in close contact with young children
SURGICAL MEASURES:
• Prompt aortic valve replacement is clearly indicated in patients with symptomatic severe aortic stenosis
• Balloon angioplasty of stenotic aortic valves may be of benefit in the pediatric patient with congenital
disease. Also feasible (although one must expect suboptimal results) in the elderly, debilitated patient who
may not tolerate valve replacement.
ACTIVITY:
In known or suspected severe aortic stenosis, vigorous physical activity is contraindicated
PATIENT EDUCATION:
• Educate the patient about the symptoms of symptomatic aortic stenosis and to report these promptly
should they occur
• If moderate or severe aortic stenosis is known or suspected, instruct the patient to avoid vigorous physical
activity
• Instruct the patient when prophylactic antibiotics are needed for medical or dental procedures
FOLLOWUP
PATIENT MONITORING:
• Asymptomatic patients without critical aortic stenosis should be followed with a history and physical
examination every 3-6 months
• An echocardiogram should be performed every 6-12 months to assess progression
• Advise the patient to immediately report any symptoms referable to the aortic stenosis
PREVENTION/AVOIDANCE:
• Bacterial endocarditis prophylaxis
• Rheumatic fever prophylaxis, where indicated
• Avoidance of vigorous physical activity
POSSIBLE COMPLICATIONS:
• Progressive stenosis
• Sudden death
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• Congestive heart failure
• Angina
• Syncope
• Hemolytic anemia
• Infective endocarditis
EXPECTED COURSE/PROGNOSIS:
• Mean life expectancy without intervention in patients with aortic stenosis is 5 years after the onset of
exertional chest discomfort, 3 years after the onset of syncope, 2 years after the development of heart
failure
• Sudden death occurs in 15 to 20% of patients with symptomatic aortic stenosis
ASSOCIATED CONDITIONS:
• Coronary artery disease is present in 50% of patients with aortic stenosis
• Aortic regurgitation (particularly seen in calcified bicuspid valves and rheumatic disease)
• Mitral valve disease (primarily in rheumatic heart disease)
Aortic valvular stenosis
DESCRIPTION:
An acquired or congenital obstruction to systolic left ventricular outflow across the aortic valve
Incidence/Prevalence in USA:
• Except for mitral regurgitation due to myocardial disease, valvular aortic stenosis is the most common
fatal cardiac valve lesion
• Bicuspid aortic valve has a frequency of 400 per 100,000 live births
Predominant age:
• Age < 30 years - predominantly congenital
• Age 30 to 70 years - most commonly congenital or rheumatic
• Age > 70 years - most commonly degenerative calcification of the aortic valve
Predominant sex:
• Congenital bicuspid valves: Male > Female (4:1)
• Congenital unicuspid valves: Male > Female (3:1)
SIGNS AND SYMPTOMS:
• Angina pectoris (most frequent symptom, occurring in 50-70% of patients with severe aortic stenosis)
• Near syncope
• Syncope (often exertional, occurs in 15-30% of patients with severe aortic stenosis)
• Exertional dyspnea
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Palpitations
• Fatigue
• Neurologic events (transient ischemic attack or cerebrovascular accident) due to embolization
• Systolic crescendo-decrescendo murmur, usually best heard at the second right sternal border (may have
associated thrill) and may radiate into the carotid arteries
• Ejection (early systolic) click
• Prolonged ejection time
• Delayed, small carotid upstroke
• Delayed/decreased intensity of A2
• Paradoxical splitting of S2
• Left ventricular heave
• A high pitched diastolic blow may be present at the left sternal border (associated aortic regurgitation)
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CAUSES:
• Congenital etiologies
◊ Unicuspid valve
◊ Bicuspid valve (not inherently stenotic, but becomes so as a result of 'wear and tear' thickening and
calcification; a calcified bicuspid valve is the most common cause of isolated aortic stenosis in adults)
◊ 3 cusped valve with fusion of commissures
◊ Hypoplastic annulus
• Acquired etiologies
◊ Rheumatic (or, rarely, other inflammatory disease)
◊ Degenerative calcific aortic stenosis in the elderly
RISK FACTORS:
Prior rheumatic fever
DIFFERENTIAL DIAGNOSIS:
• Mitral regurgitation, either primary or secondary to underlying coronary artery disease or dilated
cardiomyopathy. Mitral regurgitation, however, is usually an apical, high frequency, pansystolic murmur,
often radiating to the axilla.
• Hypertrophic obstructive cardiomyopathy. This murmur is also a systolic crescendo-decrescendo murmur,
but is best heard at the left sternal border and may radiate into the axilla. However, this murmur
characteristically is intensified by moving from squatting to standing position and/or Valsalva maneuver,
and lessened by changing from standing to squatting.
• Aortic supravalvular stenosis
• Discrete subaortic stenosis
PATHOLOGICAL FINDINGS:
• Left ventricular hypertrophy
• Myocardial interstitial fibrosis
• Aortic valvular calcification in older patients
• 50% incidence of concomitant coronary artery disease
SPECIAL TESTS:
ECG: Left ventricular hypertrophy, often with associated ST segment depression, conduction defects, left
atrial enlargement, ventricular arrhythmias
IMAGING:
• Chest x-ray
◊ May be normal in compensated, isolated valvular aortic stenosis
◊ Cardiac hypertrophy early, later cardiomegaly
◊ Post stenotic dilatation of the ascending aorta
◊ Calcification of aortic valve cusps (may require fluoroscopy to visualize)
DIAGNOSTIC PROCEDURES:
• Echocardiography:
◊ Aortic valve morphology, thickening, calcifications
◊ Decreased aortic valve excursion
◊ Planimetry of aortic valve area
◊ Left ventricular hypertrophy
◊ Left ventricular ejection fraction
◊ Chamber dimensions
◊ Presence or absence of wall motion abnormalities suggestive of coronary artery disease
• With Doppler echocardiography:
◊ Transvalvular gradient
◊ Valve area
◊ Diastolic function
◊ Associated aortic regurgitation
Page 15 of 35
• Cardiac catheterization:
◊ Transvalvular gradient
◊ Valve area
◊ Left ventricle ejection fraction
◊ Concomitant coronary artery disease
TREATMENT
GENERAL MEASURES:
• Aortic stenosis is a progressive disease. The asymptomatic patient with non-critical aortic stenosis can be
closely followed with appropriate evaluation.
• All patients with valvular aortic stenosis should receive endocarditis prophylaxis, prior to dental work or
invasive procedures regardless of age, etiology or severity of the stenosis (as recommended by the
American Heart Association in Circulation, 1997; 96: 358-366)
• Patients with a rheumatic etiology should receive (in addition to endocarditis prophylaxis prior to dental
work or invasive procedures) rheumatic fever prophylaxis, especially if less than 35 years of age, or
continue to be in close contact with young children
SURGICAL MEASURES:
• Prompt aortic valve replacement is clearly indicated in patients with symptomatic severe aortic stenosis
• Consider aortic valve replacement in asymptomatic patients with critical aortic stenosis (aortic valve area
< 1.0 cm2 or gradient > 50 mm Hg [> 6.6 kPa]) particularly if there is left ventricular dysfunction,
increasing cardiomegaly, and clinical symptoms
• Surgical valve replacement consists of the removal of the stenotic, native valve and placement of a
prosthetic mechanical or tissue valve
• Balloon angioplasty of stenotic aortic valves may be of benefit in the pediatric patient with congenital
disease. Also feasible (although one must expect suboptimal results) in the elderly, debilitated patient who
may not tolerate valve replacement.
ACTIVITY:
In known or suspected severe aortic stenosis, vigorous physical activity is contraindicated
DIET:
No restrictions except sodium restriction in presence of congestive heart failure
PATIENT EDUCATION:
• Educate the patient about the symptoms of symptomatic aortic stenosis and to report these promptly
should they occur
• If moderate or severe aortic stenosis is known or suspected, instruct the patient to avoid vigorous physical
activity
• Instruct the patient when prophylactic antibiotics are needed for medical or dental procedures
MEDICATIONS
DRUG(S) OF CHOICE:
• None for treatment. Prophylactic antibiotics when needed.
• The use of vasodilators, nitrates, calcium channel blockers, beta blockers as well as diuretics are
potentially hazardous in aortic stenosis and should be used cautiously, if at all
FOLLOWUP
PATIENT MONITORING:
• Asymptomatic patients without critical aortic stenosis should be followed with a history and physical
examination every 3-6 months
• An echocardiogram should be performed every 6-12 months to assess progression
• Advise the patient to immediately report any symptoms referable to the aortic stenosis
Page 16 of 35
PREVENTION/AVOIDANCE:
• Bacterial endocarditis prophylaxis
• Rheumatic fever prophylaxis, where indicated
• Avoidance of vigorous physical activity
POSSIBLE COMPLICATIONS:
• Progressive stenosis
• Sudden death
• Congestive heart failure
• Angina
• Syncope
• Hemolytic anemia
• Infective endocarditis
EXPECTED COURSE/PROGNOSIS:
• Mean life expectancy without intervention in patients with aortic stenosis is 5 years after the onset of
exertional chest discomfort, 3 years after the onset of syncope, 2 years after the development of heart
failure
• Sudden death occurs in 15 to 20% of patients with symptomatic aortic stenosis
MISCELLANEOUS
ASSOCIATED CONDITIONS:
• Coronary artery disease is present in 50% of patients with aortic stenosis
• Aortic regurgitation (particularly seen in calcified bicuspid valves and rheumatic disease)
• Mitral valve disease (primarily in rheumatic heart disease)
AGE RELATED FACTORS:
Pediatric: N/A
Geriatric: Increased incidence of degenerative calcific aortic stenosis
Others: N/A
PREGNANCY:
Severe critical aortic stenosis tolerates poorly the hemodynamic changes in pregnancy, labor and delivery.
Pregnancy should be avoided with critical aortic stenosis.
SYNONYMS: N/A
ICD-9-CM:
424.90 Endocarditis, valve unspecified, unspecified cause
SEE ALSO:
OTHER NOTES:
As the left ventricle is relatively noncompliant in aortic stenosis, atrial contraction is an important
component of diastolic filling. The loss of this component with the onset of atrial fibrillation can cause
acute clinical and hemodynamic deterioration.
Page 17 of 35
Mitral regurgitation due to papillary muscle
dysfunction
DESCRIPTION:
Retrograde blood flow from the left ventricle in the left atrium through an incompetent mitral valve.
Characteristics - fatigue, orthopnea, systolic murmur, left ventricular hypertrophy, S3 gallop. Usual course:
chronic; progressive; acute (after myocardial infarction).
Systems(s) affected:
Cardiovascular
CAUSES:
• coronary artery disease
• infiltrative diseases
• cardiac tumors
TREATMENT:
• dental endocarditis prophylaxis
• surgical endocarditis prophylaxis
• nitrates
• calcium channel blockers
• diuretics
• digitalis
• inotropic agents
• afterload reducing agents
• mitral valve replacement
Mitral regurgitation due to rheumatic fever
DESCRIPTION:
Retrograde blood flow from the left ventricle into the left atrium through an incompetent mitral valve.
Characteristics - history of rheumatic fever, fatigue, dyspnea, holosystolic murmur, left ventricular
hypertrophy. Usual course - chronic; progressive disability.
Systems(s) affected:
Cardiovascular
CAUSES:
• autoimmune cross reaction between streptococcal antigens and heart tissue
TREATMENT:
• medical endocarditis prophylaxis
• dental endocarditis prophylaxis
• surgical endocarditis prophylaxis
• afterload reducing agents
• nitrates
• calcium channel blockers
• digitalis
• diuretics
• mitral valve replacement
Page 18 of 35
Angina Pectoris
General Considerations
 Precordial chest pain, usually precipitated by stress or exertion, relieved rapidly
by rest or nitrates.
 Electrocardiographic or scintigraphic evidence of ischemia during pain or stress
testing.
 Angiographic demonstration of significant obstruction of major coronary vessels
 Usually due to atherosclerotic heart disease
o Congenital abnormalities
o Emboli
o Arteritis
o Dissection
o Severe myocardial hypertrophy
o Severe aortic stenosis or regurgitation
o Increased metabolic demands (i.e. hyperthyroidism, marked anemia,
paroxysmal tachycardias with rapid ventricular rates)


History
o Diagnosis depends principally upon the hx
o Circumstances that precipitate and relieve angina
o Characteristics of the discomfort
 Sensation of tightness, squeezing, burning, pressing, chocking,
aching, bursting, “gas”, indigestion or an ill-characterized
discomfort
o Location and radiation
 Behind or slightly to the left of the sternum
 Radiates to left shoulder and upper arm, lower jaw, back of neck,
high in left back
 Location can vary widely in pts
o Durations of attacks
 Short duration and subsides completely w/o residual discomfort
 Attacks more than 30 minutes are unusual and suggest the
development of unstable angina, MI, or an alternative dx
o Effect of nitroglycerin
 Dx of angina is strongly supported if sublingual nitroglycerine
invariable shortens an attack and if prophylactic nitrates permit
greater exertion or prevent angina entirely
o Risk factors – see coronary artery disease
Signs
o Examination during an attack
 Significant elevation in systolic and diastolic BP, although
hypotension may occur
 Gallop rhythm
 Apical systolic murmur
 Arrhythmias
Page 19 of 35
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Differential Diagnosis
o Anterior chest wall syndrome – reproducible by local pressure
o Intercostals neuritis (due to herpes zoster, DM, etc)
o Cervical or thoracic spine disease involving the dorsal roots
o Peptic ulcer
o Chronic cholecystitis
o Esophageal spasm
o Functional GI disease
o Reflux esophagitis
o Degenerative & inflammatory lesions of left shoulder
o Thoracic outlet syndromes
o Spontaneous pneumorthorax
o Pneumonia
o Pulmonary embolization
o Thoracic aorta dissection
Evaluation of pts w/ angina pectoris
o Laboratory
 Serum lipid levels
 Anemia
 Diabetes
o ECG
 Normal in 25%
 Old MI, nonspecific ST-T changes
o Exercise Electrocardiography
Scintigraphic Assessment of Ischemia
o Myocardial perfusion scintigraphy
o Radionuclide angiography
o Positron emission tomography
Echocardiography
Never Imagine Modalities
o CT
o MRI
Ambulatory ECG monitoring
Coronary Angiography
Treatment
 Acute Attack
o Sublingual nitroglycerin – acts in 1-2 minutes
o Nitroglycerin buccal spray
o May be repeated in 3-5 minute intervals
o Pain not responding to 3 doses or lasting more than 20 minutes may
represent evolving infarction and pts should seek immediate medical
attention
 Prevention of further attacks
o Avoiding of aggravating factors
o Nitroglycerin
Page 20 of 35
o Long-acting nitrates
 Isosorbide dintirate
 Isosorbide mononitrate
 Oral sustained-release nitroglycerin preparations
 Nitroglycerin ointment
 Nitroglycerin patches
o Beta-blockers
o Calcium channel blocking agents
o Platelet inhibiting agents
o Risk reduction
o Revasculariztion
Prognosis
 In pts with stable sx’s and normal ejection fraction, mortality is 1-2% per year
 Outlook in individual pts is unpredictable, nearly half of deaths are sudden
 Accelerating sx’s have a poorer outlook
 Poor exercise tolerance and extensive ischemia have more severe disease and a
poorer prognosis
Acute Myocardial Infarction
General Considerations
 Sudden but not instantaneous development of prolonged (>30 minutes) anterior
chest discomfort (sometimes felt as “gas” or pressure) that may produce
arrhythmias, hypotension, shock, or cardiac failure
 Rarely painless, masquerading as acute congestive heart failure, syncope, stroke,
or shock
 ECG: ST segment elevation or depression, evolving Q waves, symmetric
inversion of T waves
 Elevation of cardiac enzymes (CK-MB, troponin, T, or troponin I)
 Appearance of segmental wall motion abnormality by imagine techniques
Clinical Findings
 Symptoms
o Premonitory pain – alteration in the pattern of angina, unusual
“indigestion” or pressure or squeezing felt in the chest
o Pain of infarction – more common at rest and in early morning
 Nitroglycerin has little effect; even opiates may not relieve the pain
o Associated Symptoms - cold sweat, weakness, apprehensiveness, restless
– seeking position of comfort, light-headed, syncope, dyspnea, orthopnea,
cough, wheezing, n&v, abdominal bloating
o Painless infarction – in minority of cases, pain is absent or minor and is
overshadowed by the immediate complications
Page 21 of 35
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



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o Sudden death & arrhythmias – approximately 20% of pts with AMI will
die before reaching the hospital; usually in the first hour and chiefly due to
ventricular fibrillation
Signs
o General – anxiousness, sweating profusely, HR maybe high or low, BP
maybe be high (esp. in HTN) or low due to shock, respiratory distress
usually indicates heart failure, fever may appear after 12 hours and persist
for several days
o Chest – basilar rales, more extensive rales or diffuse wheezing suggests
pulmonary edema
o Heart – may be unimpressive or very abnormal, JVD, atrial gallops,
ventricular gallops, pericardial friction rubs
o Extremities – edema is usually not present, cyanosis and cold temperature
indicate low output. Peripheral pulses should be noted
Laboratory findings
o Cardiac sensitive markers of myocardial damage
 CK-MB
 Troponin I & T
Electrocardiography – normal tracing is rare
o Peaked T waves
o ST segment elevation or depression
o T wave inversion
o New Q waves
Chest x-ray
o Signs of CHF often lag behind the clinical findings
o Signs of aortic dissection should be sought as a possible alternative dx
Echocardiography – normal wall motion makes an infarction unlikely
Scintigraphic studies
Treatment
 Aspirin (clopidogrel in case of allergy)
 Thrombolytic therapy- greatest benefit in first 3 hours
 Acute coronary angiography and stenting
 CCU monitoring
 Low dose oxygen therapy
 Analgesia, morphine, meperidine
 Beta-blockers
 Nitrates
 ACE inhibitors
 Antiarrhythmic prophylaxis
 Calcium channel blockers
 Anticoagulation
Page 22 of 35
Congestive Heart Failure
General Considerations
 Left ventricular failure: exertional dyspnea, cough, fatigue, orthopnea,
paroxysmal nocturnal dyspnea, cardiac enlargement, rales, gallop rhythm,
pulmonary venous congestion
 Right ventricular failure: elevated venous pressure, hepatomegaly, dependent
edema, usually due to left ventricular failure
 Assessment of left ventricular function is a crucial part of dx and tx
Clinical Findings
 Symptoms
o SOB - exertional dysnea, orthopnea, paroxysmal nocturnal dyspnea, rest
dyspnea
o Chronic non-productive cough, worse in the recumbent position
o Nocturia
o Fatigue and exercise intolerance
o RUQ pain, passive congestion of liver
o Loss of appetite and nausea due to edema of the gut or impaired GI
perfusion and peripheral edema
o Pulmonary edema
o Acute exacerbations
 Alternations in therapy (or pt noncompliance)
 Excessive salt & fluid intake
 Arrhythmias
 Excessive activity
 Pulmonary emboli
 Infection
 Propagation of the underlying disease
 Signs
o May appear comfortable at rest
o Dyspneic during conversation
o Vital signs may be normal – tachycardia, hypotension, reduced pulse
pressure may be present
o Cold extremities
o Diaphoresis
o JVD
o Rales / crackles
o Hyperthyroidism or hypothyroidism
o Ascites
o Peripheral pitting edema
o Sustained left ventricular impulse – dilation & hypertrophy
 Laboratory findings
o Anemia
o Renal insufficiency
o Electrolytes – hyponatremia
Page 23 of 35


o Hemochromatosis
ECG & Chest x-ray
o Underlying or second arrythmia
o Size & shape of heart
o Pleural effusions, bilateral or right-sided
Cardiac catheterization
o Valvular disease
o CAD
Pharmacologic Treatment
 Correction of reversible causes – valvular lesions, myocardial ischemia,
arrhythmias (persistant tachycardias), alcohol or durg induced myocardial
depression, intracardial shunts, high-output states, calcium channel blockers,
antiarrhythmic drugs, NSAIDs, hemochromatosis, sarcoidosis, amyloidosis
 Diet and activity – salt restricted, restriction of activity.
o Stable pts – regular exercise regimen
 Diuretic therapy
 ACE inhibitors, Angiotensin II receptor, spironolactone
 Beta-blockers
 Digitalis glycosides
 Vasodilators
o Nitrates
o Hydalazine
o Alpha-adrenergic blockers
 Positive inotropic agents
 Calcium channel blockers
 Anticoagulation
 Antiarrhythmic therapy
Nonpharmacologic treatment
 Case management and exercise training
 Coronary revascularization
 Cardiac transplantation
Prognosis
 Poor, annual mortality rates ranging from 5% in stable pts to 30-50% in pts with
advanced, progressive sx’s
 Poorer prognosis – severe left ventricular dysfunction, prominent symptoms,
limitation of exercise capacity, secondary renal insufficiency, hyponatremia,
elevated plasma catecholamine levels
Page 24 of 35
Peptic Ulcer Disease
General Considerations
 Hx of nonspecific epigastric pain present in 80-90% of pts with variable
relationship to meals
 Ulcer sx’s characterized by rhythmicity and periodicity
 Ten to 20% of pts present with ulcer complications w/o antecedent sx’s
 Of NSAID-induced ulcers, 30-50% are asymptomatic
 Upper endoscopy with antral bx for H. pylori is diagnostic procedure of choice in
most pts
 Gastric ulcer bx or documentation of complete healing necessary to exclude
gastric malignancy
 Slightly more common in men that women
 Can occur in any age group, more commonly occur between 30-55 (duodenal) 5075 (gastric)
Etiology
 NSAIDs, H. Pylori, Zollinger-Ellison
Clinical Findings
 Symptoms & Signs
o Epigastric pain – gnawing, dull, aching or hunger-like
o Relief with food or antacids and recurrence 2-4 hours later
o 2/3 of duodenal and 1/3 gastric ulcers cause nocturnal pain that awakens
pts
o Nausea & anorexia may occur
o Significant vomiting and weight loss are unusual w/ uncomplicated ulcer
disease and suggest gastric outlet obstruction or gastric malignancy
o Mild. Localized epigastric tenderness to deep palpation may be present
o Fecal occult blood testing is positive in 1/3 of pts
o “Coffee grounds” emesis, hematemesis, melena, or hematochezia
 Laboratory findings
o Anemia
o Leukocytosis
o Serum amylase
 Endoscopy
o Procedure of choice for dx
o Bx for H. pylori
o 3-5% of gastric ulcers prove to be malignant
 Imaging
o Barium upper GI series for uncomplicated pts with dyspepsia
o Reevaluation with endoscope after 8-12 weeks of therapy
Page 25 of 35
Differential Dx
 Acute pancreatitis, acute cholecystitis, choledocholithiasis, esophageal rupture,
gastric volvulus, ruptured aortic aneurysm
Treatment
 PPI, H2 receptor antagonists, sucralfate, bismuth, misoprostol
 Antibiotics for H. pylori
 Balanced meals at regular intervals
 Moderate EtOH intake is not harmful
 Smoking retards healing and is discouraged
Appendicitis
General Considerations
 Early: periumbilical pain; later, RLQ pain and tenderness
 Anorexia, N&V, obstripation
 Low-grade fever and leukocytosis
 Most common abdominal surgical emergency
 Most commonly between ages of 10-30
 If untreated, gangrene and perforation develop w/in 36h
Clinical Findings
 Symptoms and signs
o Vague colicky periumbilical or epigastric pain
o Pain shift to RLQ, manifested as a steady ache that is worsened by
walking or coughing
o Nausea and one or two episodes of vomiting
o Protracted vomiting or vomiting before the pain suggests another dx
o A sense of constipation is typical
o Local tenderness and guarding
o Psoas sign and obturator sign
 Laboratory – moderate leukocytosis (10,000-20,000 WBC)
 Imaging – none necessary with typical appendicitis
o Ultrasound has dx accuracy of over 85% - good for younger women
o Abdominal CT
Differential Diagnosis
 Appendicitis should be considered in the DD of all pts with abdominal pain
 Gastroenteritis (typically with NVD)
 Gynecological disorders
o Salpingitis
o Tubo-ovarian abscess
o Tubal pregnancy
o Ureteral colic
Page 26 of 35
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Pyelonephritis
Diverticulitis
Perforated colonic cancer
Crohn’s ileitis
Perforated peptic ulcer
Cholecystitis
Mesenteric adenitis
Meckel’s diverticulitis
Treatment
 SURGERY! YEAH!!
 Systemic antibiotics
Prognosis – mortality is extremely low even with perforated appendicits, mortality is only
0.02% though it reaches 15% in the elderly
Irritable Bowel Syndrome
General Considerations
 Chronic functional disorder characterized by abdominal pain, alternations in
bowel habits
 Limited evaluation to exclude organic causes of symptoms
 Symptoms usually begin in late teens to early 20s
 Chronic lower abdominal sx’s and bowel complaints that may be continuous or
intermittent
 Discomfort or pain
o Relieved with defecation
o Onset associated with a change in frequency of stool
o Onset associated with a change in form of stool
 Abnormal stool frequency, form, passage, feeling of incomplete evaculation,
passage of mucus, bloating or a feeling of abdominal distention
 Other complaints: dyspepsia, heartburn, chest pain, fatigue, urologic dysfunction,
gynecologic symptoms, anxiety, depression

Pathogenesis
o Abnormal motility
o Heightened visceral nociception
o Psychosocial abnormalities
Clinical Findings
 Signs & Symptoms
o Late teens to early 20s, sx’s present for at least 3 months
o Abdominal distention
o Abdominal pain relieved by defecation
o More frequent stools with onset of abdominal pain
Page 27 of 35
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o Looser stools with onset of pain
o Intermittent, crampy lower abdominal pain
o Relieved by defectaion, worsened by stress, and worse for 1-2h after each
meal
o Problems with constipation, diarrhea, alternating constipation & diarrhea
o Physical exam is usually normal – possible abdominal tenderness in lower
abd.
o New onset of sx’s in a pt over 50 warrants further examination
Laboratory findings and special examinations
o CBC, serum albumin, SED rate, stool occult blood
o Thyroid function tests
o Stool O&P
o 24-h stool collection – daily stool in excess of 300g/d is atypical for this
dx
o in pts under 40, flexible sigmoidoscopy should be performed
o pts over 40 who have not had a previous evaluation, barium enema or
colonoscopy should be considered
Differential Diagnosis
o Colonic neoplasia
o Inflammatory bowel disease
o Causes of Chronic constipation
o Causes of Chronic diarrhea
o Endometriosis
o Lactase deficiency
o Depression & anxiety
Treatment
o Reassurance
o Diet
 Food diary
 Lactose intolerance
 Sorbital intolerance
 Trial of high fiber
o Antispasmodic agents
o Antidiarrheal agents
o Anticonstipation agents
o Psychotropic agents
 Depression
 Anxiety
Prognosis
o Majority learn to cope with their sx’s and lead productive lives
Page 28 of 35
PCM SP Final
Notes on Inflammatory Bowel Disease (Crohn's and UC), Colon Polyps, Viral
Hepatitis, Acute Pancreatitis, Ectopic Pregnancy
Inflammatory Bowel Disease (Crohn's and UC)
- IBD includes ulcerative colitis & Crohn’s disease, and although these appear to be
distinct entities, same pharmacologic agents are used to treat both (see below)
Crohn’s Disease – a chronic, recurrent disease characterized by patchy transmural
inflammation involving any segment of the GI tract from the mouth to the anus
Hallmarks
 Insidious onset
 Intermittent bouts of low-grade fever, diarrhea, RLQ pain
 RLQ mass & tenderness
 Perianal disease with abscess, fistulas
 Xray evidence of ulceration, structuring, or fistulas of SI
History: focus on history of fever, constitutional signs, abdominal pain, # of liquid bowel
movements per day, prior surgical resections
PE: focus on patient’s temperature, weight, nutritional status, presence of abdominal
tenderness/mass, rectal examination, extraintestinal manifestations
Common Clinical Constellations





Chronic inflammatory disease – most common presentation, low grade
fever, malaise, weight loss, loss of energy; there may be intermittent,
nonbloody diarrhea; cramping or steady RLQ or periumbilical pain; PE
reveals focal tenderness (usually RLQ); a palpable, tender mass that
represents thickened or matted loops of inflamed intestine, RLQ
Intestinal obstruction – narrow of small bowel as a result of inflammation,
spasm, or fibrotic stenosis; postprandial bloating, cramping pains, loud
borborygmi (def: A rumbling noise produced by the movement of gas
through the intestines)
Fistulization with or w/o infection – subset of patients develop sinus tracts
penetrating through the bowel and forming fistulas to a number of
locations; fistulas to the mesentery usually asymptomatic but can manifest
as fever, chills, tender abd mass, leukocytosis; fistulas from the colon to SI
or stomach can result in bacterial overgrowth with diarrhea, weight loss,
malnutrition; fistulas to bladder/vagina produce recurrent infections
Perianal disease – anal fissures, perianal abscesses, fistulas
Extraintestinal manifestations – erythema nodosum, pyoderma
gangrenosum (def: presence of boggy, purplish ulcers with undermined
borders, appearing mostly on the legs), episcleritis (def: inflammation of
the sclera of the eye), thromboembolic events, arthritis, oral lesions,
increased risk of gallstones
Page 29 of 35
Lab Findings/Labs to Order
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
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
Poor correlation between lab studies and clinical picture
CBC and serum albumin should be obtained – look for anemia,
leukocytosis, hypoalbuminemia
Erythrocyte sedimentation rate, C-Reactive protein – elevated during
active inflammation
Stool samples – examine for routine pathogens, ova, parasites, and C
difficile toxin
Diagnostic Studies




Initial diagnosis of Crohn’s based upon clinical picture with supporting
radiographic findings
Upper GI series with small bowel follow-through – look for ulceration,
strictures, fistulas
Barium enema or colonoscopy – evaluate colon; typical endoscopic
findings include ulcers, strictures, segmental involvement (areas of normal
appearing mucoso next to inflamed mucosa, see Robbins)
Useful serologic tests – antineutrophil cytoplasmic antibodies with
perinuclear staining (pANCA) found in 60-70% of pts with Crohn’s, 510% with UC…. Antibodies to yeast S cerevisiae (ASCA) found in about
the same %
Differential




Irritable bowel syndrome – normal x-rays, abd pain and diarrhea
Acute appendicitis – acute fever, RLQ pain
Intestinal lymphoma – fever, pain, weight loss, xrays may mimic Crohn’s
disease
Undiagnosed AIDS – fever, diarrhea
Treatment



Well balanced diet; advise pt according to presentation (i.e. fiber
supplementation if mainly colonic involvement; no raw fruits/veg,
popcorn, nuts if obstructive symptoms; iron/B12 supplements may be
needed)
Symptomatic treatment of diarrhea – cholestyramine 2-4 g or colestipol 5
g, 2 or 3 times daily before meals
5-aminosalicyclic acid agents – sulfasalazine, oral mesalamine agents, etc;
unclear mechanism of anti-inflam affects
corticosteroids
mercaptopurine/azathioprine – use for refractory Crohn’s/UC



Intestinal lymphoma – fever, pain, weight loss, xrays may mimic Crohn’s
disease
Page 30 of 35
Ulcerative Colitis – chronic, recurrent disease characterized by diffuse mucosal
inflammation involving only the colon, typically involves rectum extending proximally
Hallmarks
 Bloody diarrhea
 Lower abdominal cramps and fecal urgency
 Anemia, low serum albumin
 Negative stool cultures
 Sigmoidoscopy is the key to diagnosis
History: ask about stool frequency, presence and amount of rectal bleeding, cramps, abd
pain, fecal urgency, and tenesmus (def: A painfully urgent but ineffectual attempt to
urinate or defecate)
PE: focus on patient’s volume status (orthostatic BP, pulse), nutritional status; on abd
exam look for tenderness & evidence of peritoneal inflammation; red blood may be
present on rectal exam
3 Stages of Disease



Mild to moderate – gradual onset of infrequent diarrhea (>5 movements
per day) with intermittent rectal bleeding and mucus; stools may be
formed too loose in consistency; fecal urgency and tenesmus; LLQ cramps
relived by defecation; no significant abd tenderness; pts with moderate
disease have increased symptoms (i.e. abd tenderness, more severe
diarrhea, etc)
Severe – more than six to ten bloody movements per day, severe anemia,
hypovolemia, impaired nutrition with hypoalbuminemia; abd pain and
tenderness present; look for rapidly worsening symptoms with signs of
toxicity (known as Fulminant colitis)
Extracolonic manifestations – same as Crohn’s
Lab Findings/Labs to Order


Get hematocrit, Erythrocyte sedimentation rate, serum albumin
Stool sample – to rule out infectious colitis
Diagnostic Studies


Sigmoidoscopy – gold standard for establishing diagnosis of UC; mucosal
appearance characterized by edema, friability, mucous, erosions
Plain abd xrays – look for significant colonic dilation
Differential




Idiopathic ulcerative colitis – initial presentation indistinguishable from
other causes of colitis
Infectious colitis – get stool results to rule out
CMV colitis – immunocompromised pts
Ischemic colitis – may involve rectosigmoid in elderly pts with
cardiovascular disease
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Treatment



2 main goals are to terminate the acute, symptomatic attack and to prevent
recurrence of attacks
same options as with Crohn’s disease, treatments depends on severity of
UC
surgical therapy – for patients with severe disease who fail to improve
after 7-10 days corticosteroid therapy, or with fulminant disease or toxic
megacolon
Colon Polyps – discrete mass lesions that protrude into the lumen of the colon, may be
nonfamilial adenomatous polyps or familial adenomatous polyposis
Hallmarks
 most pts are completely asymptomatic
 chronic occult blood loss may lead to iron deficiency
 large polyps may ulcerate, resulting in intermittent hematochezia
Tests



fecal occult blood testing – detect <40% of adenomas larger than 1 cm
barium enema exam
flexible sigmoidoscopy or colonoscopy
Treatment


colonoscopic polypectomy
postpolypetomy surveillance – 3 years after initial colonoscopy and
polypectomy if high risk, 5 years if lower risk (high risk includes polyps
greater than 1 cm, villous features, high grade dysplasia, or multiple
polyps)
Viral Hepatitis – can be caused by many viruses, clinical manifestations of which may
be quite similar
Hallmarks
 prodrome of anorexia, nausea, vomiting, malaise, symptoms of upper
respiratory infection or flu-like syndrome, aversion to smoking
 fever, enlarged and tender liver, jaundice
 normal to low white cell count; abnormal liver tests, especially markedly
elevated aminotransferases early in course
 liver biopsy shows characteristic hepatocellular necrosis and mononuclear
infiltrate but is rarely indicated
Phases

prodromal phase – onset may be abrupt or insidious, with general malaise,
myalgia, arthralgia, easy fatigability, upper resp symptoms (nasal
discharge, pharyngitis) and anorexia; distaste for smoking, paralleling
anorexia, may occur early; nausea and vomiting are frequent, diarrhea or
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constipation may occur; skin rashes, arthritis, or serum sickness may be
seen in acute HBV; fever is generally present; chills or chilliness; abd pain
is usually mild and constant in the RUQ or epigastrium and is aggravated
by jarring or exertion
 icteric phase – clinical jaundice occurs 5-10 days, most pts will not
develop clinical icterus; with onset of jaundice, often prodromal symptoms
will worsen, followed by progressive clinical improvement
 convalescent phase – there is an increasing sense of well-being, return of
appetite, and disappearance of jaundice, abd pain, tenderness, and
fatigability
PE: look for hepatomegaly (over 50%), liver tenderness, splenomegaly (15% of cases),
soft, enlarged lymph nodes – especially epitrochlear or cervical areas
Lab Findings/Labs to Order






WBC count normal to low
Large, atypical lymphocytes
Mild proteinuria, bilirubinuria which often precedes the appearance of
jaundice
Alcoholic stools
Elevated AST or ALT values
Marked prolongation of PT time in severe hepatitis
Differential



Other viral diseases – such as infectious mononucleosis, CMV, HSV
Drug-induced liver disease
Shock liver (ischemic hepatitis)
Treatment




Bed rest PRN during the acute initial phase of disease when symptoms are
most severe
Return to normal activity during the convalescent period should be gradual
If nausea and vomiting are pronounced or if oral intake is substantially
decreased, IV glucose is indicated
Hospitalization if acute hepatic failure is suspected – signs of
encephalopathy or severe coagulopathy
Acute Pancreatitis – thought to result from “escape” of activated
pancreatic enzyme from acinar cells into surrounding tissues, most cases
related to biliary tract disease (a passed gallstone usually < 5 mm in dm) or
heavy alcohol intake
Hallmarks


Abrupt onset of deep epigastric pain, often with radiation to back
Nausea, vomiting, sweating, weakness
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 Abd tenderness and distention, fever
 Leukocytosis, elevated serum amylase, elevated serum lipase
 History of previous episodes, often related to alcohol intake
History: epigastric abd pain generally abrupt in onset, steady, boring, severe and often
made worse by walking and lying supine and better by sitting and leaning forward; pain
usually radiates into the back but may radiate to the right or left; ask about alcohol
history, weakness, sweating, and anxiety in severe attacks (as described below), nausea
and vomiting, history of milder similar episodes or biliary colic in past
PE: abd is tender mainly in upper abd, most often w/o guarding, rigidity, or rebound; abd
may be distended; bowel sounds may be absent; fever, tachycardia, hypotension, pallor,
cool clammy skin; mild jaundice; occasionally, an upper abd mass due to inflamed
pancreas; acute renal failure may occur early in the course of acute pancreatitis
Lab Findings/Labs to Order









Leukocytosis
Proteinuria, glycosuria
Granular casts
Elevated serum bilirubin
Blood urea nitrogen and serum alkaline phosphatase may be elevated
Abnormal coagulation tests
Decrease in serum calcium
Serum ALT of more than 80 units/L suggest biliary pancreatitis
Serum amylase and lipase are elevated
Diagnostic Studies



Abd xray – may show gallstones, a “sentinel loop” (a segment of air-filled
SI most commonly in the LUQ)
CT scan – to demonstrate an enlarged pancreas when dx is uncertain
Dynamic IV contrast-enhanced CT
Differential
 Acute perforated duodenal ulcer
 Acute cholecystitis
 Acute intestinal obstruction
 Leaking aortic aneurysm
 Ectopic pregnancy
(serum amylase may be elevated, but serum lipase normal in these conditions)
Treatment



In most pts will subside spontaneously within several days
Pancreatic rest program – withhold food and liquids by mouth, bed rest,
and in pts with moderately severe pain or ileus and abd distention or
vomiting, nasogastric suction may be indicated
Pain management – meperidine
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



Clear liquids with gradual advancement to low fat diet
IV fluids as needed
Maintain electrolytes
Severe pancreatitis requires ICU with close follow-up
Ectopic Pregnancy – any pregnancy arising from implantation of the ovum outside the
cavity of the uterus is ectopic
Hallmarks
 Amenorrhea or irregular bleeding and spotting followed by,
 Pelvic pain
 Pelvic mass formation
* may be acute or chronic
acute: 40% - severe LQ pain, sudden in onset, intermittent, and does not radiate;
backache is present during attacks; shock occurs in about 10%, often after pelvic exam,
ask for menstruation history (at least 2/3 will be abnormal)
chronic: 60% - blood leaks from tubal ampulla over a period of days, considerable blood
may accumulate in peritoneum; vaginal spotting; pelvic mass can be palpated; abd
distention and mild paralytic ileus often present
Lab Findings/Labs to Order


Blood studies – may show anemia and slight leukocytosis
Serum pregnancy tests – will show values lower than would be expected
for a normal pregnancy
Diagnostic Studies




Ultrasonography will display gestational sac located in uterus
Empty uterine cavity – strong suspicion of extrauterine pregnancy
HCG level of 6500 mU/mL with an empty uterine cavity by transabd
ultrasound virtually diagnostic of ectopic pregnancy
Laparoscopy surgical procedure of choice both to confirm and treat
Differential



Acute appendicitis
Acute pelvic inflammatory disease
Ruptured corpus luteum cyst or ovarian follicle
Treatment





Follow very closely with hcg titers every 48 hours until diagnosis is made
Hospitalization when surgical therapy is planned or when patient is
unstable
Surgical treatment is definitive
In a stable patient, methotrexate given systemically as a single or multiple
doses is acceptable for early ectopic pregnancy
Iron therapy for anemia may be necessary
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