4.

Internal Medicine

Sushama Rich, MD

Cardiovascular System
Approach to the Cardiac Patient
Most common presenting symptoms: Chest Pain Chest pain of cardiac origin is commonly these types: Pericardial Anginal Myocardial infarction Aortic dissection Pericardial pain Sharp pain that radiates to the trapezius and is aggravated by breathing. Relieved by leaning forward and remaining still. Causes Pericarditis Diagnosis On auscultation shows pericardial friction rub ECG shows ST segment elevation Anginal pain Substernal chest pain that is squeezing in nature radiates to the jaw, left arm, or left shoulder. It is aggravated or brought on by exercise. Relieved by rest or nitroglycerin Chest pain usually never lasts more than 20 minutes Diagnosis Usually clinical ECG shows ST segment changes Myocardial Infarction Same as anginal pain Duration usually greater than 20 minutes Not relieved by rest Diagnosis ECG: ST segment changes Blood tests show CPK-MB, Troponin Aortic dissection Sudden onset, tearing type of pain that radiates to the back mid scapular

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Cardiac Dyspnea Cardiac dyspnea is labored breathing that is caused by edema in the bronchial walls and stiffening of the lungs due to alveolar edema. Dyspnea is due to a reduction in cardiac output Dyspnea is aggravated by exercise and relieved sometimes by rest Causes of cardiac dyspnea Congestive heart failure Coronary artery disease Types of cardiac dyspnea Orthopnea: dyspnea that occurs in the recumbent position due to increased paroxysmal nocturnal dyspnea Paroxysmal nocturnal dyspnea: dyspnea that wakes a patient up in the middle of the night Palpitations Palpitations are the perception of ones own heart beat. Most common cardiac cause is arrhythmias.

Diagnostic and cardiovascular procedures

Chest X-ray Shows Heart size Heart shape Great vessels Electrocardiogram Can diagnose old or current heart attacks Disturbances of heart rhythm Detects thickening of the wall Holter Monitoring Uses a portable recording device worn by the patient under the clothing for 24 hours. This procedure is used for: Documents arrhythmias Classifies arrhythmias Diagnoses silent ischemia Assess results of antiarrhythmic drugs Exercise Stress Test Used to: Diagnose CAD Evaluate known CAD Contra-indications A M.I.-within the last 48 hours Severe aortic stenosis Congestive heart failure Echocardiography Echocardiography reveals the anatomy of the heart. This technique is use for: Valvular disease Congenital heart disease Function of the heart muscle Flow of blood- this can be seen by color Doppler (blue and red)

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Coronary Angiography Coronary angiography is the best test for CAD Vessels as small as 1mm can be visualized Any occlusion of the artery is seen as narrowing, beading or occlusion of the vessel Myocardial perfusion Myocardial perfusion imaging uses radioactive thallium. Indications Initial evaluation of patients Prognosis after an acute M.I. To detect extent of scarring after an acute M.I. MUGA Scan Equilibrium Radionuclide Angiography After receiving a small injection of a radioisotope, the patient lies on a table and multiple images are recorded by scintillation camera. Uses Evaluates cardiac function Measures ejection fraction Show the contraction of different regions of the heart

Coronary Artery Diseases

Two types of coronary artery disease: Atherosclerotic coronary artery disease (ASCAD) Non atherosclerotocic coronary artery disease (NASCAD)

Atherosclerotic Coronary Artery Disease (ASCAD)

Definition
The basic lesion is atherosclerosis of the coronary arteries. The pathological hallmark of this disease is atherosclerotic plaque. Plaque is made up of hypertrophied intimal smooth muscle cells, lipids, and a fibrous cap. Risk factors for the development of ASCAD Increases with age Gender: more common in men Serum cholesterol: high levels of LDL. This is the single most important risk factor, low levels of HDL Smoking Hypertension Diabetes mellitus Family history Oral contraceptives

Pathogenesis of ASCAD
As the typical plaque develops, it begins to occlude the coronary arteries; this leads to a reduction of blood flow to the myocardium. In order for ischemic symptoms to develop at least 70% of the coronary artery has to be occluded by the plaque. A variety of factors influence the clinical course of CAD, like the length of the lesion, vasomotor tone, rupture of the plaque, erosion of the plaque and ultimately thrombus formation.

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Clinical Features of ASCAD

The most common feature of ischemia to the myocardium is angina pectoris Ischemia could proceed without any symptoms to an M.I. Ischemia may cause sudden death Angina could present in three forms. Stable angina Chest pain or pressure produced by exertion Radiates to the jaw or arm Brought on by exercise Relieved by rest Associated with exertional dyspnea Does not last more than 20 minutes If pain lasts more than 20-30 minutes and is not relieved by nitro, suspect M.I. Unstable angina Chest pain same as above It is progressive in nature: The episodes are more frequent and last longer but never more than 20 minutes It is of increasing severity, duration, or frequency Printzmetals angina The hallmark of this disease is S-T segment elevation on ECG S-T segment elevation indicates transmural infarction of the myocardium It is classically caused by coronary vasospasm that occurs near an atherosclerotic plaque It more commonly affects women; it occurs more often at night, not associated with exertion There is no increase serum markers for an M.I.

Diagnosis of Angina
Clinical symptoms are key Resting ECG: is usually normal between episodes Sometimes one may see new horizontal or down sloping S-T segment New T wave inversion S-T segment elevations indicates variant angina Exercise stress test: The appearance of horizontal or down sloping of S-T segment depression of more than 1 mm indicates ischemia Exercise stress test associated with thallium stress test is much more valuable Coronary angiography is done for confirming a suspicion, diagnosis, risk stratification, assessment of CABG or angioplasty

Treatment of Angina
Nitrates B-adrenergic blockers: limit myocardial oxygen demand Calcium antagonists: prevent coronary spasm, hence ideal for variant angina PCTA: percutaneous transluminal angioplasty Rotational atherectomy Coronary artery bypass surgery: indicated for multi-vessel disease Beta blockers should not be used in variant angina because blockade of the alpha receptors cause alpha receptor mediated vasoconstriction

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Myocardial infarction
Occurs when there is 100% occlusion of the coronary artery. Pathogenesis Acute M.I is almost always associated with a thrombus superimposed upon a significant plaque It takes at least 20 minutes of ischemia to cause an irreversible injury Most often occurs in the morning when there is decreased adrenergic activity Myocardial necrosis begins in the sub-endocardium and spreads to the epicardium Most common artery to be blocked is the left anterior descending

Table 1. Classification of Myocardial Infarction

Characteristic Prevalence Complete coronary obstruction Elevated ST-T segment Depressed ST-T segment Postinfarction angina Early reinfarction Infarct size Acute complications Therapy Thrombolysis Beta Blockers Clinical Features
Chest pain for more than 30 minutes Associated symptoms: dyspnea, diaphoresis, nausea, vomiting, palpitations, and light-headedness. Symptoms simulate: GI-upset

Q-Wave MI 47% 80-90% 80% 20% 15-25% 5-8% Moderate to large Common Indicated Indicated

Non-Q Wave MI 53% 15-25% 25% 75% 30-40% 15-25% Usually small Uncommon Not indicated Not indicated

Physical Exam
Signs of ischemia: S4, new MR murmur Signs of heart failure: increased JVP, crackles in lung fields, S3

Diagnostic Studies
ECG: diagnostic in 85% of cases ST segment elevation, Q waves, T wave inversion Serum markers: CPK MB is increased within six to ten hours post MI, troponin I increases within 6-10 hours post MI, LDH1 increases within 48-72 hours Echocardiogram: New wall motion abnormality

Treatment
Treatment of pain: Nitroglycerine, morphine sulfate Thrombolysis Indications for thrombolytic therapy are the following: Chest pain ECG: ST segment elevation Less than 12 hours from onset No contra indication

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 Absolute contra-indications for thrombolytic therapy: Active internal bleeding Suspected aortic dissection Recent head trauma Blood pressure greater than 200/120 Pregnancy CVA Trauma or surgery within two weeks Relative contra-indications: Active peptic ulcer disease Known bleeding diathesis Menstruation Prolonged CPR Drugs used for thrombolytic therapy: Alteplase (TPA): Fifteen mg IV-bolus, .75 mg per kilogram over 30 minutes, 5 mg per kilogram over 60 minutes Streptokinase (SK): 1.5 Mu IV over 30-60 minutes Reteplase (RPA): 10 u IV repeat in 30 minutes Drugs used for arrhythmias Prophylactic Lidocaine Procainamide for acute recalcitrant arrhythmias Treatment of conduction disturbances Atropine Treatment of heart failure Diuretics for mild congestive heart failure Digitaliscontroversial Treatment of mitral regurgitation and acute ventricular septal defect Arteriolar vasodilator therapy Intra-aortic balloon pumping Adjunct therapy Beta-blockers reduce early mortality by reducing ventricular arrhythmias ACE inhibitors reduce the extent of remodeling and incidents of late mortality Anti-coagulants: heparin Aspirin Diltiazem: for non Q wave infarcts Angioplasty

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Complications of MI
Ventricular arrhythmias Acute conduction abnormalities Ventricular aneurysm Pump failure Mitral regurgitation Ventricular septal defect Cardiac rupture Left ventricular aneurysm Dresslers syndrome occurs in 2-10 weeks post MI. Presents as fever, malaise, pericarditis and pleuritis Pericarditis

Prognosis
Depends on the number of vessels affected. Extent of left ventricular damage

Non-atherosclerotic Coronary Artery Disease

Causes
Coronary embolism occurs in infective endocarditis, atrial fibrillation Collagen vascular disease affects medium-sized arteries. Ex: SLE RA, Wegeners granulomatosis Radiation therapy Cardiac transplantation

Heart Failure
Heart failure is the inability of the heart to pump blood to meet the oxygen requirement of the body tissues. Heart failure is a syndrome of many diseases that interfere with cardiac function. There are two types of heart failure, low output and high output. Low-output failure occurs due to reduction in the cardiac output. High-output failure occurs due to an increase in cardiac output. Etiology Ischemic heart disease Hypertensive heart disease Cardiomyopathies Valvular heart disease Pericardial disease High output failure: AI, MR, VSD, AV fistulas, severe anemia, sepsis, thyrotoxicosis, beri beri Pathophysiology Systolic dysfunction: Could be of two types, decrease in contractility or increased after load Decreased contractility occurs due to MI valvular heart disease, hypertension, cardiomyopathies Increased after load occurs due to hypertension, aortic stenosis or dilated cardiomyopathy and valvular regurgitation Diastolic dysfunction: Hypertrophic cardiomyopathy may occur in hypertension and amyloidosis Descriptive Terminology High-output failure occurs due to increased cardiac output. Example, chronic severe anemia causes volume overload Left-sided failure occurs when the left ventricle is failing. Example, MI Right-sided failure: Most common cause is left ventricular failure. It may also occur due to COPDs in which case it is called corpulmonale

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Clinical Features Dyspnea Orthopnea that leads to nocturnal cough Paroxysmal nocturnal dyspnea Nocturia Edema Anorexia Right upper quadrant pain Fatigue

Physical Signs
Acute heart failure Hypo or hypertension, tachycardia, diaphoresis, cyanosis, cold and pale extremities Left-sided failure Pulmonary rales, cardiac murmurs, tachypnea Right-sided failure Increased JVP, pleural effusions, congestive hepatomegaly, ascites, jaundice, peripheral edema

Diagnosis
Chest X-ray shows pulmonary edema, bilateral pleural effusions Echocardiogram: Decreased ejection fraction and increased chamber size indicate systolic dysfunction, hypertrophy and or abnormal inflow across the mitral valve indicates diastolic dysfunction Pulmonary artery catheterization: Increased PCWP, decreased CO and increased SVR indicates low-output failure

Classification
Class 1: Symptomatic only with greater than ordinary activity Class 2: Symptomatic with ordinary activity Class 3: Symptomatic with minimal activity Class 4: Symptomatic at rest

Treatment
Diet: reduction in sodium Diuretics: Loop or thiazide diuretics ACE inhibitors Digoxin Beta-blockers Spironolactone Anti-coagulants

Cardiomyopathies
Cardiomyopathies is myocardial dysfunction that is not due to ischemic valvular hypertensive or congenital heart disease. Types of cardiomyopathy: Dilated cardiomyopathy Restrictive cardiomyopathy Hypertrophic cardiomyopathy

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Dilated cardiomyopathy: Occurs due to ventricular dilation with decrease in contractile function of the left, right or both ventricles in the absence of pressure overload, volume overload or CAD. It almost always results in congestive heart failure.

Etiologies
Ischemia Valvular disease: Chronic AI or MR, hypertension Toxic: most common cause is alcohol induced Drug therapy: Example, Doxirubicin therapy Infectious: Example, viral HIV Idiopathic Endocrine disorders: Example, thyrotoxicosis, hypothyroidism, acromegaly Metabolic disorders: Example, hypophosphotemia, hypocalcemia, thyamine deficiency Hemoglobinopathies: Example, sickle cell anemia, thalassemia Collagen vascular disease: Example, SLE, and scleroderma

Clinical Features
Include both left and right-sided heart failure Chest pain

Physical Signs
Signs of left-sided heart failure

Diagnosis
History Stress test Cardiac catheterization Lab studies Echocardiography is the most important test that reveals dilated, poorly contracting left and right ventricles

Treatment
Standard heart failure therapy Immuno suppressants Cardiac transplantation

Hypertrophic Cardiomyopathy
Hypertrophic cardiomyopathy is a disorder in which there is hypertrophied septum, mitral valve prolapse, and left ventricular outflow obstruction.

Etiology
Inherited autosomal dominant Some sporadic cases are known to occur Specific abnormalities of cardiac myosin occurs

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Pathophysiology
Hypertrophied septum encroaches upon the left ventricular outflow Obstruction of the anterior leaflet of the mitral valve Systolic anterior motion of the anterior leaflet of the mitral valve Which then leads to papillary muscle displacement Diastolic dysfunction, the left ventricle is so stiff that it does not fill properly during diastole Decreased coronary perfusion occurs Leads to syncope

Clinical Features
Dyspnea Angina Syncope Arrhythmias Palpitations Congestive heart failure

Physical Examination
Murmur: mid- to late-holosystolic murmur The murmur is reduced in intensity with the valsalva murmur, and increased in intensity from squatting Carotid upstroke has a spike and a dome character to it

Diagnosis
ECG; left ventricular hypertrophy CXR; cardiomegaly Echocardiogram is the gold standard for diagnosis: shows septal hypertrophy, mitral regurgitation, outflow tract obstruction

Treatment
Medical Therapy Beta blockers Calcium channel blockers Digitalis: only in the end stage of the disease Surgical treatment Myomectomy; surgical reduction of the septum Mitral valve replacement Pacemaker implantation

Restrictive Cardiomyopathy
Definition: Impaired ventricular filling due to decreased compliance caused by increased stiffness of the wall

Etiology
Infiltrative diseases; examples are amyloidosis, hemochromatosis, carcinoid syndrome, sarcoidosis, idiopathic eosinophilia Metastatic diseases Radiation therapy Idiopathic Scleroderma

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Pathology
Increased diastolic stiffness Systolic function is usually normal in the early stages Left ventricular pressure is above normal Systolic function is compromised in the late stages Decreased ventricular cavity size Decreased cardiac output

Clinical Features
Right-sided failure is greater than left-sided failure Peripheral edema Dyspnea Refractory to treatment with diuretics Thromboembolic events

Physical Examination
Increased JVP Cardiac S3 and S4 Congestive hepatomegaly Ascites Jaundice Peripheral Edema

Diagnostic Studies
Chest X-ray shows normal chamber size, enlarged atria, pulmonary congestion ECG Echo shows symmetrical wall thickening, increased diastolic end pressure, decreased atrial filling

Treatment
Treat underlying disease Symptomatic therapy with diuretics

Valvular Disease Aortic Stenosis

Etiology
Congenital (e.g. bicuspid valve): In young and middle-aged adults, bicuspid aortic valve with progressive scarring and calcification is the most common cause Rheumatic Disease Degeneration and calcification of a tricuspid valve Aortic stenosis is more common in men

Disease Process
The outflow obstruction leads to left ventricular hypertrophy

Symptoms
Symptoms are not usually present until the obstruction is advanced

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 Cardiac symptoms Angina Pectoris Syncope Dyspnea

Physical Findings
Ejection murmur is typically harsh and is often loud. The duration of the murmur is proportional to the severity of the obstruction The carotid pulse is characteristically reduced in amplitude and prolonged in duration

Diagnosis
Echocardiography and the Doppler confirms the diagnosis The Doppler flow velocity can determine the severity

Treatment
Surgery for patients with cardiac symptoms and severe aortic stenosis Avoid vigorous activities Cardiac catheterization for patients with severe aortic stenosis

Chronic Aortic Regurgitation

Etiology
Bicuspid Aortic valve Aortic root dilatation Endocarditis Associated with some connective tissue disorders. (e.g. Marfans Syndrome)

Disease Process
Aortic regurgitation results in a volume overload of the LV with ventricular dilatation. The stroke volume is increased as the LV ejects both the forward output and the blood that regurgitated into the ventricle during diastole

Symptoms
Palpitations/pounding in the chest or head Dyspnea due to elevated pulmonary venous pressure Angina pectoris due to decreased diastolic coronary perfusion

Physical Findings
Wide pulse pressure Systolic ejection murmur Third heart sound Diagnosis Endocardiography can determine the cause of aortic regurgitation in many patients

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Treatment
Surgery for patients with LV systolic dysfunction and onset of symptoms Oral vasodilator therapy for asymptomatic patients with significant aortic regurgitation and normal systolic function. By decreasing systemic resistance regugitant volume is reduced

Acute Aortic Regurgitation

Etiology
Infective endocarditis Prosthetic aortic valve dysfunction Proximal dissection of the aorta

Disease Process
Severe acute condition places a volume overload on a left ventricle that has not had the time to dilate in a compensatory manner. The increased ventricular diastolic pressure leads to left atrial pressure and pulmonary congestion

Physical Findings
Sinus tachycardia is often present Diastolic murmur may be less prominent and shorter in duration Third heart sound gallop can be heard

Diagnosis
Endocardiography and Doppler assess the status of Aortic regurgitation, its cause, and the underlying ventricular function

Treatment
Vasodilator therapy IV nitroprusside for severe heart failure Surgical therapy is the definitive treatment

Mitral Stenosis
Etiology
Rheumatic Fever Occurs twice as frequently in female patients as male

Disease Process
Progressive thickening of the valve leaflets and fusion of the commisures. Calcification contributes to the valve immobility and stenosis The chora tendinae also may thicken and fuse The valve scarring progresses slowly before symptoms arise. Elevated left atrial pressure leads to pulmonary artery hypertension that can provoke RV failure and functional tricuspid regurgitation

Symptoms
Exertional dyspnea, orthopnea and paroxysmal nocturnal dyspnea due to pulmonary venous congestion Fatigue and weakness when the cardiac output decreases Symptom onset is most common in the third or the fourth decade of life These patients, who may get atrial fibrillation, a common complication, may not tolerate increased heart rate Embolism from enlarged left atrium can cause stroke, especially when atrial fibrillation is present

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Physical Findings
Left atrium is enlarged because mitral stenosis increases the left atrial pressure Loud first heart sound As the severity of mitral stenosis increases, the interval between the 2nd heart sound and opening snap decreases

Diagnosis
Echocardiography can detect mitral valve thickening, provide information about valve mobility and the degree of calcification.

Treatment
-blockers Control atrial fibrillation Anticoagulants to decrease the risk of thromboembolism Percutaneous mitral valve balloon valvuloplasty Valve replacement

Mitral Regurgitation
Etiology
Mitral valve prolapse Ischemic heart disease can cause papillary muscle ischemia Left ventricular (LV) dilation Mitral Annulus calcification Rheumatic heart disease Acute mitral regurgitation can result from the rupture of chorda tendinae or papillary muscle

Disease Process
Chronic mitral regurgitation produces a volume overload Left atrium is moderately enlarged and there is elevation of left atrial pressure, which can lead to pulmonary congestion and dyspnea

Physical Findings
Holocystic murmur is characteristic, which begins immediately after a soft 1st heart sound. It is high-pitched

Diagnosis
Echocardiography can assess mitral valve structure, cardiac chamber size, and left ventricle function Doppler assesses the severity of the mitral regurgitation

Treatment
Vasodilater therapy to decrease the afterload (e.g. ACE inhibitors) Valve replacement

Mitral Valve Prolapse (MVP)

Etiology
MVP is common and can cause mitral regurgitation ranging from trivial to severe Can be isolated, or associated with connective tissue diseases (e.g. Marfans) More common in women MVP can be inherited (autosomal dominant) MVP is benign in most patients

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Disease Process
Mitral valve in these patients is usually large, floppy, and redundant with elongated chorda tendinae Middle-aged or older men may be more likely to develop severe regurgitation or complications

Complications
Ineffective endocarditis Cardiac arrhythmia Thromboembolism

Symptoms
Most MVP patients are asymptomatic, but the following symptoms can be present: Atypical chest pain Palpitations Fatigue Anxiety Postural phenomena Neuropsychiatric symptoms

Diagnosis
Echocardiography is used to confirm the diagnosis

Treatment
Antibiotic endocarditis prophylaxis in all MVP patients with structural valve changes and/or murmur of regurgitation -blockers

Pericardial Diseases
Pericarditis and pericardial effusion Pericardial tamponade Constrictive pericarditis Pericarditis is an inflammation of the pericardium. Pericardial effusion is an accumulation of fluid within the pericardial cavity.

Etiologies
Infectious Viral: Coxsackie B virus, echovirus, adenovirus, EBV, VZV, HIV Bacterial: (From endocarditis, pneumonia or cardiac surgery), S. Pneumoniae, S. Aureus, and TB Non-infectious Idiopathic Uremia Acute MI Post MI: Dresslers syndrome Post pericardiotomy Neoplastic: Lung, breast, renal cell Trauma: Chest trauma Pericardial effusion without pericarditis, CHF, cirrhosis

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Clinical Features
Chest pain: Burning, stabbing increased by breathing, reduced by leaning forward, radiates to the trapezius Fever

Physical Exam
Pericardial friction rub is the gold standard for clinical diagnosis Pericardial effusion will cause distant heart sounds, dullness over the left posterior lung field (Ewarts sign due to compressive atelectasis)

Diagnostic Studies
ST segment elevation throughout the ECG, depression of the PR segment is diagnostic and unique to pericarditis Echocardiography will show pericardial effusion. Echo-free space between the two layers of the pericardium Chest X-ray: Water bottle appearance of the heart

Treatment
NSAIDS Steroids for refractory idiopathic disease Treat underlying cause

Cardiac Tamponade
Cardiac tamponade is a life-threatening condition due to a rapid development of pericardial effusion that is compressing the heart.

Pathophysiology
The heart cannot fill adequately Increased intra-pericardial pressure Diastolic pressure is elevated Pulsus paradoxus: Inspiration causes a decrease in intra-pericardial and right atrial pressures which leads to an increase in venous return, which leads to increased RV size which leads to septal shift to the left which leads to decrease in left ventricular stroke volume and output

Clinical Features
Dyspnea on exertion Fatigue Orthopnea

Physical Exam
Pulsus paradoxus: When the systolic blood pressure falls more than 10 mm of mercury during inspiration. This implies that stroke volume is falling during inspiration due to compression Neck vein distension

Diagnosis
Echocardiogram shows effusion

Treatment
Emergency pericardiocentesis

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Constrictive Pericarditis
Constrictive pericarditis is caused by diffuse thickening of the pericardium due to inflammatory process

Etiology
Post viral Radiation Uremia TB Idiopathic Post surgical

Clinical Features
Dyspnea Orthopnea Ascites Edema Jaundice Typical symptoms are right-sided heart failure

Diagnosis
ECG shows atrial arrhythmias Echocardiography is not as valuable MRI is capable of measuring pericardial thickness

Treatment
Surgical removal of the pericardium

Aortic Diseases
Aneurysms of the aorta Aortic dissection

Aneurysms of the Aorta

An aneurysm of the aorta is permanent dilation of an artery due to weakness of the wall.

Etiology of Aortic Aneurysms

Aneurysms of the ascending aorta is caused by syphilis, Marfans syndrome, and cystic medial necrosis Aneurysms of the abdominal aorta are caused by atherosclerosis. This type increases with age, smoking, and hypertension and has increased incidence in men. The most common site is at the bifurcation of the aorta Aneurysms of the femoral artery occur due to mycotic infections. It most often occurs in IV drug users

Pathophysiology
Atherosclerosis is the hallmark of aneurysms

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Clinical Features
Small aneurysms are asymptomatic. Large aneurysms cause back pain and pulsating sensations Blue toe syndrome: sudden occurrence of a very painful blue toe most commonly caused by emboli Aortic aneurysms can rupture causing massive bleeding, syncope, hypotension and diarrhea with Tenessmus Musculoskeletal pain

Diagnosis
Most of them are found incidentally on physical exam Ultrasound is the gold standard CT scan is used to localize ruptures Aortograms are rarely used

Treatment
Aneurysms less than 4 cm are usually watched Aneurysms greater than 5 cm or threat of ruptureconsider surgery

Aortic Dissection
Aortic dissection occurs when the tunica intima tears and blood dissects along the media.

Etiology
Aneurysm of the ascending aorta is most commonly caused by hypertensive aneurysm Dissection of the descending aorta occurs due to rupture of an atherosclerotic plaque Blunt trauma can cause either an ascending or a descending aneurysm

Clinical Features
Crushing chest pain that radiates to the back and felt between the scapula Symptoms of aortic insufficiency may occur

Diagnosis
Murmur of aortic insufficiency Chest X-ray will show widened media stinum CT scan confirms diagnosis

Treatment
Stabilize hypotension Lower systolic blood pressuresurgery

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Common Laboratory Values

RBC Count (106/L) [Sl: 1012/L] 4.73-5.49 4.1-4.87 42.9-49.1 37.9-43.9 Hemoglobin (g/dl) [Sl: g/L] 14.40-16.60 12.2-14.7 Hematocrit (%) MCH (pg) [Sl: pg] 27-31 27-31 MCHC (g/dl) [Sl: g/L]3 33-37 33-37 MCV (m3) [Sl: fL] 76-100 76-100 RDW

WBC Count (cells/mm3) [Sl: 109/L] Adult male 4,500-11,000 Adult Female 4,000-11,000

Age

11.5-14.5 11.5-14.5

Age

Platelet Count (103/L)

Lymphocytes Total (%WBC) Adult Male 238,000 34% Adult Female 270,000 34% Increased in Leukemias after Any viral splenectomy, acute infection, hemorrhage, AIDS, MMR, leukemia, Acute and chronic polycythemia vera lymphocytic leukemias

Neutrophils, Band (%WBC) 3.0% 3.0%

Basophils (%WBC) 0.5% 0/5% Chronic myeloid leukemia

Neutrophils, Eosinophils Segmented (%WBC) (%WBC) 56% 2.7% 56% 2.7% Severe exercise, NAACP labor, Neoplasms, newborns, allergies, bacterial Addisons infections, disease, collagen leukemias, non- vascular disease, infective tissue parasites damage Stress, burns, trauma, chemotherapy

Monocytes (%WBC) 4% 4% Bacterial infection, sub acute bacterial endocarditis , chronic infections, leukemia

Decreased in

Disseminated intra-vascular coagulation, TTP, ITP, eclampsia and pre-eclampsia

Pancytopenia, aplastic anemia, neutropenia, severe infections, severe osteomyelitis

Steroids, stress, Acute Cushings rheumatic syndrome fever, lobar pneumonia, steroid therapy, stress, thyrotoxicosis

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