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Patient history of painless joint deformity and underlying primary disease suggests neurogenic arthropathy. Physical examination may reveal bone fragmentation in advanced disease. X-rays confirm diagnosis and assess severity of joint damage. In the early stage of the disease, soft-tissue swelling or effusion may be the only overt effect; in the advanced stage, articular fracture, subluxation, erosion of articular cartilage, periosteal new bone formation, and excessive growth of marginal loose bodies (osteophytosis) or resorption may be seen. Computed tomography scan helps define the extent of disease.
Other diagnostic measures include:
❑ vertebral examination: narrowing of disk spaces, deterioration of vertebrae, and osteophyte formation, leading to ankylosis and deforming kyphoscoliosis
❑ synovial biopsy: bony fragments and bits of calcified cartilage.
Source: Professional Guide to Diseases (Eighth Edition), 2005
Because pericarditis commonly coexists with other conditions, diagnosis of acute pericarditis depends on typical clinical features and elimination of other possible causes. The pericardial friction rub, a classic symptom, is a grating sound heard as the heart moves. It can usually be auscultated best during forced expiration, while the patient leans forward or is on his hands and knees in bed. It may have up to three components, corresponding to the timing of atrial systole, ventricular systole, and the rapid-filling phase of ventricular diastole. Occasionally, this friction rub is heard only briefly or not at all. Nevertheless, its presence, together with other characteristic features, is diagnostic of acute pericarditis. In addition, if acute pericarditis has caused very large pericardial effusions, physical examination reveals increased cardiac dullness and diminished or absent apical impulse and distant heart sounds.
Chest X-ray, echocardiogram, chest magnetic resonance imaging (MRI), heart MRI, heart computed tomography scan, and radionuclide scanning can detect fluid that has accumulated in the pericardial sac. They may also show enlargement of the heart and signs of inflammation or scarring, depending on the cause of pericarditis.
In patients with chronic pericarditis, acute inflammation or effusions don’t occur — only restricted cardiac filling.
Laboratory results reflect inflammation and may identify its cause:
❑ normal or elevated white blood cell count, especially in infectious pericarditis
❑ elevated erythrocyte sedimentation rate
❑ slightly elevated cardiac enzyme levels with associated myocarditis
❑ culture of pericardial fluid obtained by open surgical drainage or cardiocentesis (sometimes identifies a causative organism in bacterial or fungal pericarditis)
❑ electrocardiography showing the following changes in acute pericarditis: elevation of ST segments in the standard limb leads and most precordial leads without significant changes in QRS morphology that occur with MI, atrial ectopic rhythms such as atrial fibrillation and, in pericardial effusion, diminished QRS voltage.
Other pertinent laboratory data include blood urea nitrogen levels to check for uremia, antistreptolysin-O titers to detect rheumatic fever, and a purified protein derivative skin test to check for tuberculosis. In pericardial effusion, echocardiography is diagnostic when it shows an echo-free space between the ventricular wall and the pericardium.
Source: Professional Guide to Diseases (Eighth Edition), 2005
A patient history of painless joint deformity and underlying primary disease suggests neurogenic arthropathy. The physical examination may reveal bone fragmentation in advanced disease. X-rays help confirm the diagnosis and help assess the severity of joint damage.
In the early stage of the disease, soft-tissue swelling or effusion may be the only overt effect; in the advanced stage, articular fracture, subluxation, erosion of articular cartilage, periosteal new bone formation, and excessive growth of marginal loose bodies (osteophytosis) or resorption may be seen.
Other diagnostic measures include:
❑ vertebral examination:narrowing of disk spaces, deterioration of vertebrae, and osteophyte formation, leading to ankylosis and deforming kyphoscoliosis
❑ synovial biopsy: bony fragments and bits of calcified cartilage.
Source: Handbook of Diseases, 2003
Because pericarditis often coexists with other conditions, diagnosis of acute pericarditis depends on typical clinical features and elimination of other possible causes. It may be detected with X-ray, echocardiogram, magnetic resonance imaging, computed tomography, and coronary angiography. These tests may show scarring, contracture of the pericardium, or enlargement of the heart.
CLINICAL TIP: A classic symptom, the pericardial friction rub, is a grating sound heard as the heart moves. It can usually be auscultated best during forced expiration, with the patient leaning forward or resting on his hands and knees in the bed.
Pericardial friction rub may have up to three components, corresponding to the timing of atrial systole, ventricular systole, and the rapid-filling phase of ventricular diastole, Occasionally, it’s heard only briefly or not at all. Nevertheless, its presence, together with other characteristic features, is diagnostic of acute pericarditis.
In addition, if acute pericarditis has caused large pericardial effusions, the physical examination reveals increased cardiac dullness and diminished or absent apical impulse and distant heart sounds. Acute inflammation or effusions don’t occur in patients with chronic pericarditis — only those with restricted cardiac filling.
Laboratory results reflect inflammation and may identify its cause:
❑ normal or elevated white blood cell count, especially in infectious pericarditis
❑ slightly elevated cardiac enzyme levels with associated myocarditis
❑ culture of pericardial fluid obtained by open surgical drainage or cardiocentesis (sometimes identifies a causative organism in bacterial or fungal pericarditis).
Electrocardiography shows the following changes in acute pericarditis: elevation of ST segments in the standard limb leads and most precordial leads without the significant changes in QRS-complex morphology that occur with an MI, atrial ectopic rhythms such as atrial fibrillation, and diminished QRS complex in pericardial effusion.
Other pertinent laboratory studies include blood urea nitrogen level to check for uremia, antistreptolysin O titers to detect rheumatic fever, and a purified protein derivative skin test to check for tuberculosis. In pericardial effusion, echocardiography is diagnostic when it shows an echo-free space between the ventricular wall and the pericardium.
Source: Handbook of Diseases, 2003
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