Pathology & Disease Flashcards
What is cor pulmonale?
Cor pulmonale is hypertrophy or failure of the right ventricle resulting from disorders of the lungs, pulmonary vessels, chest wall, or respiratory control center. Living for an extended period at a high altitude may occasionally cause this condition.
Symptoms: Symptoms include chronic productive cough, exertional dyspnea, wheezing, fatigue, weakness, drowsiness, and alterations in level of consciousness. On physical examination, dependent edema is present, and the neck veins are distended. The pulse is weak, and hypotension may occur due to reduced cardiac output. Tachycardia, a gallop rhythm, tricuspid insufficiency, or a right ventricular heave may be present. Sometimes an early right ventricular murmur or a systolic pulmonary ejection sound may be heard. The liver is enlarged and tender, and hepatojugular reflux is present. Pulmonary artery pressure measurements (if assessed in the cardiac catheterization lab or the intensive care unit) show increased right ventricular and pulmonary artery pressures related to increased pulmonary vascular resistance. Angiography or echocardiography documents right ventricular enlargement.
What is no bacterial thrombotic endocarditis (NBTE)?
Non bacterial thrombotic endocarditis (NBTE) is the presence on the heart valves of vegetables but by sterile collections of platelets in fribrin. NTBE is characteristically found in severe cases of systemic lupus erthematosus, tuberculosis, or malignancy. The vegetations of NBTE readily embolism, cause infarctions in other organs.
What is pericarditis?
Pericarditis is Inflammation of the pericardium, marked by chest pain, fever, and an audible friction rub.
Incidence: The precise incidence of pericarditis is unknown. Among patients presenting in ERs with chest pain, approx. 5% have pericarditis rather than coronary artery disease, pulmonary embolism, esophageal gastric or biliary disease or other more common causes. Approx. 1 patient per 1000 admitted to hospital is diagnosed with pericarditis. Infectious causes of pericarditis are more common in patients with HIV/AIDS than in other patient populations.
Causes: Many diseases and conditions can inflame the pericardium, including infections (bacterial, tubercular, viral, fungal); collagen-vascular diseases (such as rheumatic fever, rheumatoid arthritis, or systemic lupus erythematosus); drugs (hydralazine, procainamide, isoniazid, minoxidil); myocardial infarction; cancer; renal failure; cardiac surgery; or trauma. In many instances the precise cause is idiopathic (unknown).
Symptoms: Chest pain that varies with respiration is a hallmark of pericarditis. The pain often worsens when the patient lies down and improves when he or she sits up and leans forward. The pain is usually described as sharp, constant, and located in the mid chest (retrosternally), but it may radiate to the neck, shoulder, and back. Fever, cough, dyspnea, and palpitations are also characteristic. The classic sign of pericarditis is the pericardial rub (found in about 50% of cases), a multicomponent abnormal heart sound that some observers describe as high-pitched, scratchy, raspy, grating, or leathery. It is best heard with the diaphragm of the stethoscope at the left lower sternal border as the patient sits up, leans forward, and holds his or her breath after expiration.
Diagnosis: Diagnosis is usually based on the clinical presentation, electrocardiogram changes, and echocardiography. Pericardiocentesis is used to obtain fluid for analysis in selected patients, e.g. those with high fevers, cardiac tamponade, or evidence of systemic illness. Fluid obtained by pericardiocentesis should be sent for microbiological studies such as tests for Mycobacterium tuberculosis (MTB), fungi, and cytology.
Treatment: Therapy depends on the cause of the syndrome. Uremic pericarditis is treated with dialysis; pyogenic pericarditis requires antibiotic therapy and drainage. Nonsteroidal anti-inflammatory drugs and colchicine improve outcomes in patients with idiopathic disease. Many cases of pericarditis are self-limiting, but without treatment others may progress to chronic constrictive pericarditis or cardiac tamponade.
What is cardiac tamponade?
Cardiac tamponade is a life-threatening condition in which elevated pressures within the pericardium impair the filling of the heart during diastole. Cardiac tamponade may result from injuries to the heart or great vessels, from cardiac rupture, or from other conditions that produce large pericardial effusions. If fluid accumulates rapidly, as little as 150 mL can impair the filling of the heart. Slow accumulation, as in pericardial effusion associated with cancer, may not produce immediate signs and symptoms because the fibrous wall of the pericardial sac can gradually stretch to accommodate as much as 1 to 2 L of fluid.
Etiology: Cardiac tamponade may be idiopathic (Dressler syndrome) or may result from any of the following causes: effusion (in cancer, bacterial infections, tuberculosis, and, rarely, acute rheumatic fever); hemorrhage from trauma (as from gunshot or stab wounds of the chest, perforation by catheter during cardiac or central venous catheterization, or after cardiac surgery); hemorrhage from nontraumatic causes (as from rupture of the heart or great vessels, or anticoagulant therapy in a patient with pericarditis); viral, postirradiation, or idiopathic pericarditis; acute myocardial infarction; chronic renal failure; drug reaction (as from procainamide, hydralazine, minoxidil, isoniazid, penicillin, methysergide, or daunorubicin); or connective tissue disorders, e.g., such as rheumatoid arthritis, systemic lupus erythematosus, rheumatic fever, vasculitis, and scleroderma. Classic signs of tamponade include persistent hypotension despite fluid boluses, muffled heart sounds, distended jugular veins, and paradoxical pulse (a drop in systolic blood pressure of more than 10 mm Hg on inspiration).
Diagnosis: Cardiac tamponade is suggested by chest radiograph (slightly widened mediastinum and enlargement of the cardiac silhouette), ECG (reduced QRS amplitude, electrical alternans of the P wave, QRS complex, and T wave and generalized ST-segment elevation), and pulmonary artery pressure monitoring (increased right atrial pressure, right ventricular diastolic pressure, and central venous pressure). It is definitively diagnosed with echocardiography.
What is Beck triad?
Beck triad is hypotension, distended neck veins, and muffling of heart sounds, the physical finding in cardiac tamponade.
What is hypertrophic cardiomyopathy (HCM)?
Hypertrophic cardiomyopathy (HCM) is an autosomal dominant cardiomyopathy marked by excessive and disorganized growth of myofibrils, impaired filling of the heart (diastolic dysfunction), a reduction in the size of ventricular cavities, and, often, ventricular arrhythmias and sudden death. Examination of the heart by echocardiography or other modalities may show the enlargement of the heart to be most pronounced in the interventricular septum. Hypertrophy in that location may limit the flow of blood (and increase pressure gradients) from the left ventricle to the aorta. Abnormal anterior motion of the mitral valve during systole also may be found. These two findings are often designated on echocardiographic reports of patients with HCM by the abbreviation ASHSAM (asymmetric septal hypertrophy– systolic anterior motion [of the mitral valve]). Other forms of HCM may affect only the cardiac apex or cause diffuse enlargement of the heart muscle.
Symptoms: Although patients may be asymptomatic for many years, they commonly report shortness of breath (particularly on exertion), fatigue, atypical chest pain (at rest and after meals), orthopnea, dizziness, and other symptoms of congestive heart failure after the heart muscle markedly enlarges. An S4 and a harsh crescendo-decrescendo systolic murmur, best heard at the left lower sternal border, may be present. Ventricular arrhythmias are common and may result in palpitations, syncope, or sudden death.
Treatment: Drug therapies include beta blocking and calcium channel blocking drugs (such as verapamil) to slow heart rate, control arrhythmias, and reduce myocardial oxygen demand. Anticoagulants and antiarrhythmic agents are also occasionally used. For patients with marked enlargement of the ventricular septum and high outflow tract pressure gradients , surgical removal of the enlarged muscle or ablation often produces favorable improvements in exercise tolerance and breathing.
Patient care: Strenuous physical exercise should be discouraged because it may produce breathlessness, presyncope, or frank loss of consciousness. If applicable, the patient should be encouraged to lose weight, stop smoking, and limit alcohol intake. An implanted cardioverter/defibrillator (ICD) may be required. The patient should be advised to report symptoms of chest pain, prolonged dyspnea, or syncope promptly. First-degree relatives of those affected should be referred for evaluation.
What is nonbacterial thrombotic endocarditis (NBTE)?
Nonbacterial thrombotic endocarditis (NBTE) is the presence on the heart valves of vegetations that are produced not by bacteria but by sterile collections of platelets in fibrin. NBTE is characteristically found in severe cases of systemic lupus erythematosus, tuberculosis, or malignancy. The vegetations of NBTE readily embolize, causing infarctions in other organs.
What is restrictive cardiomyopathy?
Restricted cardiomyopathy is cardiomyopathy associated with lack of flexibility of the ventricular walls. Common causes include amyloidosis, hemochromatosis, sarcoidosis, and other diseases in which the heart is infiltrated by foreign material or scarred.
What is aortic insufficiency?
Aortic insufficiency is an imperfect closure of the aortic semilunar valve at the junction of the left ventricle and the aorta, due to distortion of the valve leaflets or dilation of the aortic annulus. This causes blood that has been ejected into the aorta to fall back into the left ventricle. It may produce volume overload of the ventricle, leading to left ventricular dilation and hypertrophy, and congestive heart failure. Stroke volume and ejection fraction (EF) fall. Chronic aortic insufficiency produces a gradual volume overload of the heart and eventual congestive heart failure. It may occur in patients with poorly controlled hypertension, tertiary syphilis, Marfan disease, or other disorders that affect aortic valve competence. Management often includes antihypertensive vasodilators such as nifedipine. If con gestive heart failure becomes severe enough, valve replacement may be recommended for patients who are good operative candidates. Surgery usually is recommended to be done before EF falls below 55%.
Symptoms: Chronic AI may be asymptomatic until heart failure (HF) occurs. With HF, patients often report difficulty breathing (such as during exercise or sleep), and lower extremity swelling. Patients may occasionally report palpitations or a subjective awareness of their heart beating.
Physical findings: The murmur of AI occurs in diastole, is high-pitched (best heard using the diaphragm of the stethoscope), and is usually described as “blowing” and “decrescendo.” It is best heard at the left second to fourth intercostal spaces, radiating to the apex and sometimes the right sternal border, after the patient exhales and sits leaning forward, holding his or her breath. Patients with AI often have a widened pulse pressure with a waterhammer pulse and may have head bobbing, bobbing of the uvula, or visible movement of blood under the nails when the tips of the nails are gently compressed (Quincke pulse). The patient may experience dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and fatigue.
