28)Acute thracheobronchitis and bronchitis Definition: inflammation of the bronchi.

Ethyiology; virus or bacterial infection, air pollution Symptoms:Cough (obligatory) dry in the beginning, later with sputum; Fever, weakness, fatigue, loss of appetite; Retrosternal pain during cough as a sign of tracheitis. Shortness of breath in bronchiolitis Physical examination Intoxicated face if the patient is with fever; Coarse or decreased vesicular breathing with snoring wheezes and ronchi. Whistling wheezes in spastic bronchitis. Lab test: Occasionally increased WBC(3.5-5.5) and sedimentation rate(in men 5-15; in women 8-20) Microbiology Sputum culture for bacterial infection Serological test for viral infections Radiology Increased lung markings Spirometry Restrictive type respiratory failure in bronchiolitis Blood gases hypoxemia often with hypercapnia Complications Pneumonia Chronic bronchitis acute thrachea bronchitis definition :is an common inflammation afflicting the lower respiratory tract,composed of tracheitis and bronchitis. etiology:virus ,bacteria infection,chemical and physical irratants symptoms: dry cough(obligatory)later with sputum (sometime with blood) fever weakness fatigue shortness of breath ronchi phsycal examinaton: -intoxicated face if the patient is with fever -coarse or decreased vesicular breathing with snoring wheezes and ronchi lab test: occasionally increased WBC(3.5-10.5) sedimentation rate (in men 5-15in women 8-20) microbiology: -sputum culture for bacterial infection -serological test for viral infection radiology: incread lung margines spirometry: restrictive type respiratory failure in bronchiolitis(decreased) blood gases hypoxemia often with hypercapnia

Complications: pneumonia ,chronic bronchitis. 29)Chronic Obstructive Pulmonary Diesease Definition: cough three months in a row, during two consecutive years Predisposition factors Frequent respiratory infections, especially bronchitis and sinusitis, smoking, polluted environment, cold Symptoms Occasionally slight morning cough, during exacerbation same as acute bronchitis phsycal examinaton: -intoxicated face if the patient is with fever -coarse or decreased vesicular breathing with snoring wheezes and ronchi lab test: occasionally increased WBC(3.5-10.5) sedimentation rate (in men 5-15in women 8-20) microbiology: -sputum culture for bacterial infection -serological test for viral infection radiology: incread lung margines spirometry: restrictive type respiratory failure in bronchiolitis(decreased) blood gases hypoxemia often with hypercapnia Complications Bronchiaectases Pulmonary emphysema Pneumofibrosis Pulmonary emphysema Definition anatomical condition of the lungs with constant enlargement of the airspaces distally from the terminal bronchioli and destruction of the alveoli membranes. Ethyology, pathogenesis and predisposition factors Main pathogenic factor is bronchial obstruction in few cases congenital factor deficiency of alpha-1-antitrypsin. Pulmonary emphysema is a complication of chronic bronchitis, bronchiectasis, and bronchial asthma Symptoms: shortness of breath, initially during exercise, later at rest, but it is not relieved significantly in sitting position. Easy tiredness, fatigue, often cough with sputum. Physical examination In patient with respiratory failure general cyanosis and polycythaemia Short neck, sometimes high neck veins Emphysema type chest Decreased vocal fremitus, box-like percussion sound, lower position of lung bases,

reduced respiratory mobility, decreased vesicular breathing with prolonged exhale, often whistling and snoring wheezes. Lab tests Increased HB(120-180), RBC(3,5-5,5), HTC(35-55) and low sedimentation rate(in men 5-15inwomen 8-20) in patients with respiratory failure and polycytaemia. Radiography More air in the lung, dilated intercostal spaces, often increased lung markings for concomitant chronic bronchitis and bronchiectasis. Spirometry - restrictive type respiratory failure. Blood gazes hypoxemia and hypercapnia, decreased oxygen saturation. Complications Right heart failure very rare pneumothorax. Pulmonary emphysema, chronic bronchitis and bronchiectasis Bronchiectases Definition: local dilatation of the bronchi Predisposition factors Chronic bronchitis, pneumonia, congenital (cystic fibrosis) Symptoms Cough with much sputum, especially in the morning and breath odor. The sputum is in three levels upper foam-like, middle mucous, lower purulent, occasionally haemoptysis (blood in the sputum) During exacerbation the same as in acute bronchitis, but more severe, nearer to pneumonia Physical examination Mainly in auscultation - decreased vesicular breathing with ronchi, which are resonant, when there is inflammation of the parenchyma Occasionally clubbing of the fingers Lab tests Increased WBC(3,5-5,5) and sedimentation rate(in men 5-15-in women 8-20) Microbiology Sputum culture Radiology Increased lung markings, stretching to the periphery of the lung CAT - cylindrical or sack-like dilatations of the bronchi. Spirometry Occasionally restrictive type respiratory failure Blood gases hypoxemia, sometimes with hypercapnia Complications Acute- Local: pneumonia, pulmonary abscesses General: myocarditis, pericarditis, endocarditis, encephalitis, meningitis, sepsis;

Chronic- Local: pneumofibrosis, pulmonary emphysema General: amyloidosis

30) Bronchiectases

Definition: local dilatation of the bronchi Predisposition factors Chronic bronchitis, pneumonia, congenital (cystic fibrosis) Symptoms Cough with much sputum, especially in the morning and breath odor. The sputum is in three levels upper foam-like, middle mucous, lower purulent, occasionally haemoptysis (blood in the sputum) During exacerbation the same as in acute bronchitis, but more severe, nearer to pneumonia Physical examination Mainly in auscultation - decreased vesicular breathing with ronchi, which are resonant, when there is inflammation of the parenchyma Occasionally clubbing of the fingers Lab tests Increased WBC(3,5-5,5) and sedimentation rate(in men 5-15-in women 820) Microbiology Sputum culture Radiology Increased lung markings, stretching to the periphery of the lung CAT - cylindrical or sack-like dilatations of the bronchi. Spirometry Occasionally restrictive type respiratory failure Blood gases hypoxemia, sometimes with hypercapnia Complications AcuteLocal: pneumonia, pulmonary abscesses General: myocarditis, pericarditis, endocarditis, encephalitis, meningitis, sepsis; ChronicLocal: pneumofibrosis, pulmonary emphysema General: amyloidosis 31)Bronchial Asthma Definition: in most cases allergic disease causing attacks of breathlessness while exhaling Classification: atopic and nonatopic Ethyology and predisposition factors: For the atopic asthma: family predisposition with increased levels of IgE For the non-atopic type: infections - mainly pneumonia or sinusitis in childhood Special types of asthma:

Drug-induced aspirin, NSAID, cholinomimetics, beta-blockers Exercise-induced asthma Asthma provoked by gastro-esophageal reflux Pathogenesis and pathophysiology Allergen-antibody binding reaction inducing release of allergy mediators which cause bronchospasm, edema and increased secretion of the bronchial mucosa In atopic asthma exoallergens pollens, fur, feathers, house mites, mould, dust etc. They bind to EgI fixed on the surface of mast-cells. Most of them cause bronchospasm, edema and increased secretion of the bronchial mucosa The first two release secondary mediators of the allergic reaction which aggravates the inflammation. In non-atopic asthma endoallergens of bacterial origin. In such case in the reaction participates IgG. Increased activity of n. vagus and decreased activity of n. sympaticus can also participate in the pathogenesis. Symptoms: attacks of breathlessness, tightness in the chest, wheeze, cough (at first dry, later with white sputum). Sometimes running nose, sneezing, scratching in the throat, symptoms warning the patient about the oncoming attack. Most frequent factors which provoke the attacks: Contact with exoallergens, infection, strong smells, drugs (beta-blockers, aspirin ) physical exercise or stress. Status asthmaticus continuous attack of asthma with only partially relief by the treatment. Physical examination: During attack: severely impaired general condition, sitting position, wheezing, often slight general cyanosis, high neck veins. Reduced vocal fremitus, box-like percussion sound, low position of the lung bases with reduced respiratory mobility, decreased vesicular breathing with prolonged exhale, diffusely spread whistling wheezes. During periods of remission often there are not any pathological changes. Lab tests No specific changes in the ordinary tests. However tests for concomitant infection are always required. Radiography During attack more air in the lungs Often no significant changes in remission Spirometry During attack restrictive type respiratory failure (decreased ) Blood gazes hypoxemia, often slight hypercapnia, reduced oxygen

saturation. Specific tests Skin tests for allergens, provocation tests, immunological test (IgE). Complications Pulmonary emphysema Pneumothorax (very rear) 32) Lobar(crouposa) Pneumonia Definition inflammation of the lung parenchyma Classification: -Alveolar, afflicting a whole lob or one or more segments usually in the base of one or both lungs. It has four histological stages (congestion, red hepatisation, grey hepatisation, resolution). During the first and the fourth stage the alveolar sacks are only partially filled with fluid, during the second and the third stage they are completely filled with fluid, RBC and WBC respectively. -Bronchopneumonia (lobular), afflicting several lobuli in the base of one (more often the right one) or both lungs -Interstitial pneumonia afflicting the interstitial tissue of the lower part of one or both lungs. Ethyology: Alveolar bacterial (mainly pneumococcus) Bronchopneumonia bacteria (mainly pneumococcus, streptococcus), fungi Interstitial Mycoplasma pneumoniae, Chlamydia pneumoniae, virus Predisposition factors: acute bronchitis, exacerbated chronic bronchitis, bronchiectasis, hypostasis, aspiration of food, stomach fluid, alien objects all of them for bronchopneumonia. Symptoms Alveolar pneumonia is mostly a primary disease. It begins suddenly with high fever (3940), cough with sputum (brick-red sputum during the stage of red hepatisation), tiredness, fatigue, loss of appetite, pain in the chest (usually at the back), provoked by breathing, shortness of breath in severe cases. Physical examination Slightly or severely impaired general condition. Usually high fever, sometimes with herpes labialis. Facies febrilis. In severe cases increased breath and heart rate and low blood pressure. Lobar pneumonia; the afflicted part of the chest is taking lesser part in the breathing, increased vocal fremitus, relatively dull percussion sound, reduced respiratory mobility. Auscultation I and IV stage decreased vesicular breathing with

crepitations (crackles); II and III stage- bronchial breathing with resonant ronchi. Lab tests Lobar and bronchopneumonia increased sedimentation rate (in men 5-15 in women 8-20)and WBC(3,5-10,5) with neutrophylia(%54%63). These changes are usually slight in patients with interstitial pneumonia. Often relative lymphocytosis. Microbiology:Lobar and bronchopneumonia sputum culture for bacteria and fungi. Radiology:Lobar pneumonia tick shadow at the base of one or both lungs, covering one or more segments or a whole lob. Complications :Acute: pleurisy, pulmonary abscess (often caused by staphylococcus) Chronic: pneumofibrosis, bronchiectasis. General: sepsis, pericarditis, myocarditis, endocarditis, meningitis, encephalitis, the last five often in patients with interstitial pneumonia (echo virus, mycoplasma etc.)

33)Bronchopneumonia (lobular) pneumonia

Definition inflammation of the lung parenchyma Classification: -Alveolar ,afflicting a whole lob or one or more segments usually in the base of one or both lungs. It has four histological stages (congestion, redhepatisation, grey hepatisation, resolution). During the first and the fourth stage the alveolar sacks are only partially filled with fluid, during the second and the third stage they are completely filled with fluid, RBC and WBC respectively. -Bronchopneumonia (lobular), afflicting several lobuli in the base of one (more often the right one) or both lungs -Interstitial pneumonia afflicting the interstitial tissue of the lower part of one or both lungs. Ethyology: Alveolar bacterial (mainly pneumococcus) Bronchopneumonia bacteria (mainly pneumococcus, streptococcus), fungi Interstitial Mycoplasma pneumoniae, Chlamydia pneumoniae, virus Predisposition factors: acute bronchitis, exacerbated chronic bronchitis, bronchiectasis, hypostasis, aspiration of food, stomach fluid, alien objects all of them for bronchopneumonia. Symptoms Bronchopneumonia is usually a secondary disease. It develops as a complication of acute bronchitis, infected bronchiectasis or other infection of the upper respiratory tract, or after aspiration and prolonged hypostasis. Running nose, sore throat, fatigue, slight cough and often subfebril temperature for several days. Then suddenly the general condition deteriorates with high fever, increased cough with sputum,

pain in the chest, provoked by breathing, in severe cases shortness of breath. Physical examination Slightly or severely impaired general condition. Usually high fever, sometimes with herpes labialis. Facies febrilis. In severe cases increased breath and heart rate and low blood pressure. Bronchopneumonia palpation, percussion same as lobar pneumonia. Auscultation decreased vesicular breathing with resonant ronchi. Lab tests Lobar and bronchopneumonia increased sedimentation rate (in men 5-15 in women 8-20)and WBC(3,5-10,5) with neutrophylia(%54-%63).These changes are usually slight in patients with interstitial pneumonia. Often relative lymphocytosis. Microbiology Lobar and bronchopneumonia sputum culture for bacteria and fungi. Radiology Bronchopneumonia patchy shadows at the base of one or both lungs. Complications Local: Acute: pleurisy, pulmonary abscess (often caused by staphylococcus); Chronic: pneumofibrosis, bronchiectasis. General: sepsis, pericarditis, myocarditis, endocarditis, meningitis, encephalitis, the last five often in patients with interstitial pneumonia (echo virus, mycoplasma etc.) 34) Interstitial Pneumonia Definition inflammation of the lung parenchyma Classification: -Alveolar, afflicting a whole lob or one or more segments usually in the base of one or both lungs. It has four histological stages (congestion, redhepatisation, grey hepatisation, resolution). During the first and the fourth stage the alveolar sacks are only partially filled with fluid, during the second and the third stage they are completely filled with fluid, RBC and WBC respectively. -Bronchopneumonia (lobular), afflicting several lobuli in the base of one (more often theright one) or both lungs -Interstitial pneumonia afflicting the interstitial tissue of the lower part of one or both lungs. Ethyology: Alveolar bacterial (mainly pneumococcus) Bronchopneumonia bacteria (mainly pneumococcus, streptococcus), fungi Interstitial Mycoplasma pneumoniae, Chlamydia pneumoniae, virus Predisposition factors: acute bronchitis, exacerbated chronic bronchitis, bronchiectasis,hypostasis, aspiration of food, stomach fluid, alien objects all of them for bronchopneumonia. Symptoms

Interstitial pneumonia is mostly a primary disease. High fever, tiredness, fatigue, loss of appetite, headache, often pain in the chest, in severe cases shortness of breath. Cough is not an obligatory symptom. Physical examination Slightly or severely impaired general condition. Usually high fever, sometimes with herpes labialis. Facies febrilis. In severe cases increased breath and heart rate and low blood pressure. Interstitial pneumonia often the only change is reduced respiratory mobility and decreased vesicular breathing. Lab tests Lobar and bronchopneumonia increased sedimentation rate (in men 5-15 in women 8-20)and WBC(3,5-10,5) with neutrophylia(%54%63).These changes are usually slight in patients with interstitial pneumonia. Often relative lymphocytosis. Microbiology Interstitial pneumonia serological test for antibodies, panel chain reaction etc. Radiology Interstitial pneumonia streaky and patchy markings at the base of one or both lungs,usually connected with the hilus. Complications Local: Acute: pleurisy, pulmonary abscess (often caused by staphylococcus); Chronic: pneumofibrosis, bronchiectasis. General: sepsis, pericarditis, myocarditis, endocarditis, meningitis, encephalitis, the last five often in patients with interstitial pneumonia (echo virus, mycoplasma etc.)

35)Lung Thromboembolism definition:obstruction of a blood vessel with thrombotic material carried by the blood from the site of origin to plug another vessel. etiology:fat from within the marrow of a broken bone ,part of a tumor ,air bubbles Symptoms: Shortness of breath Chest pain Cough may produce bloody or blood-streaked sputum. Leg swelling, usually in only one leg

weakness fatigue Physical Examination: Clammy or bluish-colored skin wheezing excessive sweating radip or irregular heart beat light headadness or fainting Lab Tests: total blood count: erythrocytes(3,5-5,5) sedimentation rate(in men 5-15 in women8-20) liver enzyme -AST(0-38) -ALT(0-40) electrolytes Chest x-ray A pulmonary embolism cannot be seen on the chest xray. But, if a part of the lung tissue dies, this can be seen on the x-ray. CT scan of the chest A spiral CT is a special type of CT scan that is able to make tri-dimensional pictures. It is also a very fast scan that can be completed in a very short period of time. It has become popular in diagnosing pulmonary embolism. Pulmonary angiogram x-rays taken after a dye is injected into the blood vessels in the lungs. The test shows areas of blockage in the lungs. It provides a clear picture of blood flow through the arteries. But, this test is associated with relatively high risks. Electrocardiogram In case of pulmonary embolism, tachycardia (rapid heart beat) is frequently seen, as well as several rhythm patterns. These results can help in the diagnosis. D-Dimer (a clot dissolving substance) blood testIncreased levels in the blood may suggest the presence of a clot. This test is nonspecific, though. A lot of conditions may cause the level to be elevated. Treatment: -medication :anticoagulants clot dissolvers(thrombolytics) -surgical Complications: -embolism -brain ambolism -leg embolism -kidney embolism -gastrointestinal embolism -death

36)Lung Cancer Definition: Lung cancer is a disease in which the cells of lung tissues grow uncontrollably and form tumors. A tumor is a mass or lump of tissue made of abnormal cells. etiology: smoke are over the age of 50 work in industries where substances such as asbestos, nickel, chloromethyl ether, chromium, beryllium and arsenic are used have or have had a lung disease have a family history of lung cancer are former smokers have been exposed to secondhand smoke over many years have been exposed to radon. There are four main types of lung cancer -adenocarcinoma, -squamous cell carcinoma, -small cell carcinoma and -large cell carcinoma. The type of lung cancer is determined by the appearance of the cancerous cells under amicroscope. Small cell lung cancer is sometimes called oat cell cancer, because the cancer cells look like oats when they are viewed under a microscope. It develops most often in the bronchial submucosa and is found predominately in people who are heavy smokers Squamous cell carcinoma, makes up 25 to 30 percent of all lung cancer cases. When viewed under a microscope, the squamous cells look like fish scales. This type of lung cancer often begins in the bronchi and may remain in the chest Adenocarcinoma accounts for about 25 to 30 percent of all lung cancers. When viewed under a microscope, the cancerous cells are cube or column shaped, and they grow in patterns that are usually seen in the glands. Large cell carcinomas make up about 10 to 20 percent of all lung cancer cases. Cells that are not diagnosed as squamous, adenocarcinoma or SCLC, are categorized under this heading. These cancers are found most often in the smaller bronchi. Symptoms: A new cough that doesn't go away Changes in a chronic cough or "smoker's cough" Coughing up blood, even a small amount Shortness of breath Chest pain Wheezing Hoarseness Losing weight without trying Bone pain Headache

Physical examination: Take your temperature and weight to check for a fever or weight loss. Examine your ears, eyes, nose, and throat for signs of infection. Listen to your heart and lungs with a stethoscope. He or she will listen for abnormal air movement through your lungs that may indicate pneumonia or other respiratory problems. Examine your chest for areas of pain in your ribs or muscles. Press or tap on your belly (abdominal palpation) to check for pain, fluid buildup, or an enlarged liver. Examine your neck, armpits, groin, and other areas of your body to check for enlarged lymph nodes. Lab Tests: serotonn(101-283 (ng/mL). ) total blood count etc. chest x-ray to look for growths a sputum test to detect cancerous cells Biopsy (the surgical removal of a small piece of tissue for microscopic examination). ultrasound or a CT scan, Spirometry. Using a machine called a spirometer, the doctor is able to record the rate at which a person exhales air from the lungs and the total volume exhaled, thus indicating a narrowing or obstruction in the airways. Treatment:surgery chemotherapy radiation therapy immunotherapy vaccine therapy Complications: -chemotherapy complication constipation diarrhea hair loss -radiation complication difficulty swalling headache and nausea and vomiting -surgery complication: chest pain pleural effusion pneumonia pneumothorax 37) Pleurisy (pleuritis) Definition inflammation of the pleura.

Classification; fibrinous and exudative Ethyology: a secondary disease, usually complication of pneumonia, tuberculosis,cancer ,pulmonary embolism ,colagenosis ,trauma, pancreatitis, uremia. Causes right heart failure, hypoproteinemia cirrhosis, chronic pancreatitis, etc. Haemothorax blood in the pleural cavity, usually complication of chest trauma and broken ribs. Hilothorax accumulation of lymph in the pleural cavity. Empyema when an abscess near the chest wall opens and the purulent fluid pours out into the pleural cavity. Symptoms: Fibrinous pleuritis sharp stabbing pain provoked by breathing, cough, movement. Also symptoms of the primary disease (cough, fever, fatigue etc.) Exudative pleuritis: It is often second stage of fibrinous pleuritis. The pain becomes dull,more like heaviness, shortness of breath if there is much fluid and especially if the patient is lying on the healthy side. Also the symptoms of the primary disease. Mediastinal pleuritis retrosternal pain, shortness of breath, often disphagia and disphonia; diaphragmal pleuritis paroxysms of chest pain. Physical examination The patient is lying on the afflicted side. The breathing is superficial. palpitation and low blood pressure, often high neck veins. Decreased vocal fremitus. Absolutely dull percussion sound, no respiratory mobility Lab tests are determined by the primary disease.

Radiography Fibrinous pleuritis veiled lower part of the afflicted lung. Exudative pleuritis thick homogenous shadow covering the lower part of the afflicted lung. The upper line is not horizontal (line of Damoisot). The mediastinum is slightly displaced towards the healthy lung. (contrary pleural fibrosis and atelectasis) Spirometry: Restrictive type respiratory failure in exudative pleuritis, hydrothorax and haemothorax with much fluid. In such cases usually hypoxemia and rarely with hypercapnia the last

depends on the primary disease. Specific test for exudative pleurisy toracentesis. It is performed over the upper edge of the rib, where the level of the fluid is at its highest point (between scapular and posterior axillar line) The fluid is tested for protein level, blood and tumor cells,culture for bacteria, including tuberculosis and fungi. Complications: Acute usually caused by toracentesis - pneumothorax, hemorrhage with hemothorax,pulmonary edema. Chronic pleurofibrosis (especially in patients with tuberculosis) 38)pulmonary tuberculosis primary form
Pulmonary tuberculosis (TB) is a contagious bacterial infection that involves the lungs, but may spread to other organs. Pulmonary tuberculosis (TB) is caused by the bacteria Mycobacterium tuberculosis .You can get TB by breathing in air droplets from a cough or sneeze of an infected person. This is called primary TB. The following people are at higher risk for active TB:Elderly ,Infants,,People with weakened immune systems, for example due to AIDS, chemotherapy, diabetes, or certain medications Primary tuberculosis: seen as an initial infection, usually in children. The initial focus of infection is a small subpleural granuloma accompanied by granulomatous hilar lymph node infection. Except for the rare intestinal (bovine) tuberculosis and the even more uncommon skin, oropharyngeal, and lymphoidal primary sites, the lungsare the usual location of primary infections. As detailed earlier , the initial focus of primary infection is the Ghon complex, which consists of a parenchymal subpleural lesion, often just above or just below the interlobar fissure between the upper and the lower lobes, and enlarged caseous lymph nodes draining the parenchymal focus. Primary TB can also present as a lower lobe pneumonia. The course and fate of this initial infection is variable, but in most cases patients are asymptomatic, and the lesions undergo fibrosis and calcification. Secondary tb refers to all forms of tuberculosis that occur after the first few weeks of primary infection when immunity to the mycobacterium has developed. The primary stage of TB usually doesn't cause symptoms. When symptoms of pulmonary TB occur, they may include: Cough (usually cough up mucus) Coughing up blood Excessive sweating, especially at night Fatigue Fever Unintentional weight loss Other symptoms that may occur with this disease: Breathing difficulty Chest pain Wheezing The doctor or nurse will perform a physical exam. This may show:Clubbing of the fingers or toes (in people with advanced disease) Swollen or tender lymph nodes in the neck or other areas Fluid around a lung (pleural effusion) Unusual breath sounds (crackles)

Tests may include: Biopsy of the affected tissue (rare) Bronchoscopy Chest CT scan Chest x-ray Interferon-gamma blood test such as the QFT-Gold test to test for TB infection Sputum examination and cultures Thoracentesis Tuberculin skin test (also called a PPD test) treatment:The goal of treatment is to cure the infection with drugs that fight the TB bacteria. Treatment of active pulmonary TB will always involve a combination of many drugs (usually four drugs). All of the drugs are continued until lab tests show which medicines work best. The most commonly used drugs include: Isoniazid Rifampin Pyrazinamide Complications: Pulmonary TB can cause permanent lung damage if not treated early. Medicines used to treat TB may cause side effects, including liver problems. Other side effects include: Changes in vision Orange- or brown-colored tears and urine Rash

39)pulmonary tuberculosis secondary form

Pulmonary tuberculosis (TB) is a contagious bacterial infection that involves the lungs, but may spread to other organs. Pulmonary tuberculosis (TB) is caused by the bacteria Mycobacterium tuberculosis .You can get TB by breathing in air droplets from a cough or sneeze of an infected person. This is called primary TB. Secondary tb refers to all forms of tuberculosis that occur after the first few weeks of primary infection when immunity to the mycobacterium has developed. Most cases of secondary pulmonary tuberculosis represent reactivation of an old, possibly subclinical infection. During primary infection, bacilli may disseminate, without producing symptoms, and establish themselves in sites with high oxygen tension, particularly the lung apices. Reactivation in such sites occurs in no more than 5 to 10% of the cases of primary infection. Secondary tuberculosis, however, tends to produce more damage to the lungs than does

primary tuberculosis.
Most cases of secondary pulmonary tuberculosis represent reactivation of an old, possibly subclinical infection. During primary infection, bacilli may disseminate, without producing symptoms, and establish themselves in sites with high oxygen tension, particularly the lung apices. Reactivation in such sites occurs in no more than 5 to 10% of the cases of primary infection.Secondary tuberculosis, however, tends to produce more damage to the lungs than does primary tuberculosis The primary stage of TB usually doesn't cause symptoms. When symptoms of pulmonary TB occur, they may include: Cough (usually cough up mucus)

Coughing up blood Excessive sweating, especially at night Fatigue Fever Unintentional weight loss Other symptoms that may occur with this disease: Breathing difficulty Chest pain Wheezing The doctor or nurse will perform a physical exam. This may show: Clubbing of the fingers or toes (in people with advanced disease) Swollen or tender lymph nodes in the neck or other areas Fluid around a lung (pleural effusion) Unusual breath sounds (crackles) Tests may include: Biopsy of the affected tissue (rare) Bronchoscopy Chest CT scan Chest x-ray Interferon-gamma blood test such as the QFT-Gold test to test for TB infection Sputum examination and cultures Thoracentesis Tuberculin skin test (also called a PPD test) Treatment:The goal of treatment is to cure the infection with drugs that fight the TB bacteria. Treatment of active pulmonary TB will always involve a combination of many drugs (usually four drugs). All of the drugs are continued until lab tests show which medicines work best. The most commonly used drugs include: Isoniazid Rifampin Pyrazinamide Complications: Pulmonary TB can cause permanent lung damage if not treated early. Medicines used to treat TB may cause side effects, including liver problems. Other side effects include: Changes in vision Orange- or brown-colored tears and urine Rash

40)Heart failure
Definition syndrome in which the pumping action of the heart cant provide adequate supplies of blood and respectively oxygen to the tissues. Classification Acute and chronic. Etiology and pathogenesis: Impaired contractility of the myocardium ischemic heart disease, myocarditis,cardiomyopathia, end-stage of valve diseases Obstruction in the blood-flow arterial hypertension, coarctation of the aorta,

stenosis of aortic valve pulmonary embolism ,pulmonary valve stenosis ,Reduced loading of the ventricles: pericarditis (total heart failure), mitral and tricuspidal stenosis;Extreme tachycardia or tachyarrhythmia. Symptoms: Left heart failure: shortness of breath (in acute cases it compels the patient to take orthopnoeic position), easy tiredness, fatigue, sometimes cough in pulmonary edema with pink sputum; Stages according to NYHA I class - no shortness of breath II class shortness of breath during higher than the usual physical exercises III class shortness of breath during ordinary physical exercises IV class shortness of breath at rest Right heart failure: tiredness, fatigue, swollen legs, in severe cases generalized edema (dropsy); Physical examination: Left-side heart failure: Acute forms: pulmonary edema: orthopnoeic position, skin pale and sweating,tachydyspnoea,decreased vesicular breathing with crepitations tachycardia, tachyarrhythmia or extreme bradycardia, often third sound high or low blood pressure; Chronic form: slightly impaired general condition, usually sleeps on two or more pillows,decreased vesicular breathing with crepitations;murmur of mitral insufficiency;swollen legs, high neck veins, enlarged lever, painful during palpation; Lungs: right or both sides hydrothorax; Lab tests: obligatory control of creatinine(0.7 to 1.3 mg/dL for men and 0.6 to 1.1 mg/dL for women). and electrolytes (especially potassium because of the diuretic therapy.( 3.7 to 5.2 mEq/L.potassium) Radiology: Left-side heart failure: congestion in the lungs I stage increased markings in the apical regions; II increased markings in the middle regions; III - dilatations of the hiluses; IV patchy shadows in the lower and middle areas of both lungs Right-side heart failure: effusion in the right or both pleural cavities, enlargement of the right side of the heart. ECG Left-side heart failure: left type ECG often atrial fibrillation, hypertrophy of the left ventricle,sometimes with left bundle branch block, often changes in the repolarization Right-side heart failure: right type ECG hypertrophy of the right ventricle ,sometimes right bundle branch block, often changes in the repolarization.

Echocardiography Left-side heart failure: ejection fraction under 50, dilatation of the left ventricle end-diastole diameter over 50 mm, end-systole diameter over 35 mm and of the left atrium end-diastole diameter over 35 mm; Right-side heart failure: dilatation of the right ventricle and of the right atrium, increased systolic pulmonary pressure (over 30 mmHg); Factors provoking the exacerbation of the heart failure: physical exercise, much salt in the food, infections, changes in the rhythm and the frequency (severe bradycardia and tachycardia and arrhythmia), high blood pressure;

41)Cardiac Shock Definition :Cardiogenic shock is a state in which the heart has been damaged
so much that it is unable to supply enough blood to the organs of the body. Causes Shock occurs whenever the heart is unable to pump as much blood as the body needs. The most common causes are serious heart complications. Many of these occur during or after a heart attack(myocardial infarction). These complications include:

A large section of heart muscle that no longer moves well or does not move at all Breaking open (rupture) of the heart muscle due to damage from the heart attack Dangerous heart rhythms, such as ventricular tachycardia, ventricular fibrillation, or supraventricular tachycardia Tear or rupture of the muscles or tendons that support the heart valves, especially the mitral valve Tear or rupture of the wall (septum) between the left and right ventricles (lower heart chambers) Very slow heart rhythm (bradycardia) or problem with the electrical system of the heart (heart block)

Symptoms

Chest pain or pressure Fast breathing Fast pulse Heavy sweating, moist skin Restlessness, agitation, confusion Shortness of breath Skin that feels cool to the touch Pale skin color or blotchy skin Weak (thready) pulse

Decreased mental ability o Loss of ability to concentrate o Loss of alertness Coma (loss of consciousness)

Exams and Tests An examination will show:

Low blood pressure (usually less than 90 systolic) Blood pressure drop of more than 10 points when you stand up after lying down (orthostatic hypotension) Weak (thready) pulse

To diagnose cardiogenic shock, a catheter (tube) may be placed in the lung artery (right heart catheterization). Tests may show that blood is backing up into the lungs and the heart is not pumping properly. Tests include:

Cardiac catheterization Chest x-ray Coronary angiography Echocardiogram Electrocardiogram Nuclear scans

Other studies may be done to find out why the heart is not working properly. Lab tests include:

Arterial blood gas-arterial oxygen partial pressure 75-100 -arterial carbondioxide partial pressure 35- 40 Blood chemistry (chem-7, chem-20, electrolytes) Cardiac enzymes (troponin-0-2), (CKMB 0-3) Complete blood count (CBC)

Treatment :Cardiogenic shock is a medical emergency. You will need to stay in the hospital, usually in the Intensive Care Unit. The goal of treatment is to find and treat the cause of shock to save your life. You may need medicines to increase blood pressure and improve heart function, including:

Dobutamine Dopamine Epinephrine Norepinephrine

When a heart rhythm disturbance (dysrhythmia) is serious, urgent treatment may be needed to restore a normal heart rhythm. This may include:

Electrical "shock" therapy (defibrillation or cardioversion) Implanting a temporary pacemaker Medications given through a vein (intravenous)

Other treatments for shock may include:

Cardiac catheterization with coronary angioplasty and stenting Heart monitoring to guide treatment Heart surgery (coronary artery bypass surgery, heart valve replacement, left ventricular assist device) Intra-aortic balloon counterpulsation (IABP) to improve heart and blood vessel function Pacemaker

Possible Complications: Brain damage Kidney damage Liver damage

42) Acute Endocarditis

Endocarditis, is an infection and inflammation of the heart valves and the inner lining of the heart chambers, which is called the endocardium. Endocarditis occurs when infectious organisms, such as bacteria or fungi, enter the bloodstream and settle in the heart. In most cases, these organisms are streptococci ,staphylococci or species of bacteria that normally live on body surfaces. Depending on the aggressiveness (virulence) of the infecting germ, the heart damage caused by endocarditis can be swift and severe (acute endocarditis) or slower and less dramatic (subacute endocarditis). Acute endocarditis - Acute endocarditis most often occurs when an aggressive species of skin bacteria, especially a staphylococcus, enters the bloodstream and attacks a heart valve. Once staph bacteria begin to multiply inside the heart, they may send small clumps of bacteria called septic emboli into the bloodstream. Subacute endocarditis - This form of endocarditis most often is caused by one of the viridans group of streptococci (Streptococcus sanguis, mutans, mitis or milleri) that normally live in the mouth and throat. Streptococcus bovis or Streptococcus equinus also can cause subacute endocarditis, typically in patients who have a gastrointestinal problem, Subacute endocarditis tends to involve heart valves that are abnormal, such as narrowed or leaky heart valves. Etiology: A congenital (present at birth) malformation of the heart or a heart valve, or mitral valve prolapse with mitral valve regurgitation
A heart valve damaged by rheumatic fever or by age-related valve

thickening with calcium deposits

An implanted device in the heart (pacemaker wire, artificial heart valve)

Symptoms Symptoms of acute endocarditis include:

High fever Chest pain Shortness of breath Cough Extreme fatigue

-Symptoms of acute endocarditis usually begin suddenly and get worse quickly. It is an infection that can develop dramatically over a few days Phsycal examination:Your doctor will examine you, and will check for fever; skin symptoms of endocarditis (tiny hemorrhages in the skin, tender nodules on finger and toes); and a heart murmur, which indicates possible heart valve damage. Additional testing includes: Blood cultures : These blood samples will be added to culture bottles that contain special nutrients to aid bacterial growth. Echocardiography:check for abnormal growths that contain infecting organisms (vegetations) inside the heart. Serological tests - These are blood tests that look for evidence of increased immune system activity, which is a sign of infection. These tests may be helpful when blood cultures do not show bacterial growth. treatment: with antibiotics surgical complications of endocarditis include:Congestive heart failure,Floating blood clots, called emboli, in the bloodstream that lodge in the brain, lungs or coronary arteries,Kidney problems.

43)subacute endocarditis
Endocarditis, is an infection and inflammation of the heart valves and the inner lining of the heart chambers, which is called the endocardium. Endocarditis occurs when infectious organisms, such as bacteria or fungi, enter the bloodstream and settle in the heart. In most cases, these organisms are streptococci ,staphylococci or species of bacteria that normally live on body surfaces. Depending on the aggressiveness (virulence) of the infecting germ, the heart damage caused by endocarditis can be swift and severe (acute endocarditis) or slower and less dramatic (subacute endocarditis). Acute endocarditis - Acute endocarditis most often occurs when an aggressive species of skin bacteria, especially a staphylococcus, enters the bloodstream and attacks a heart valve. Once staph bacteria begin to multiply inside the heart, they may send small clumps of bacteria called septic emboli into the bloodstream. Subacute endocarditis - This form of endocarditis most often is caused by one of the viridans group of streptococci (Streptococcus

sanguis, mutans, mitis or milleri) that normally live in the mouth and throat. Streptococcus bovis or Streptococcus equinus also can cause subacute endocarditis, typically in patients who have a gastrointestinal problem, Subacute endocarditis tends to involve heart valves that are abnormal, such as narrowed or leaky heart valves. Etiology: A congenital (present at birth) malformation of the heart or a heart valve, or mitral valve prolapse with mitral valve regurgitation. A heart valve damaged by rheumatic fever or by age-related valve thickening with calcium deposits An implanted device in the heart (pacemaker wire, artificial heart valve) Symptoms of subacute endocarditis include: Low-grade fever (less than 102.9 degrees Fahrenheit) Chills Night sweats Pain in muscles and joints A persistent tired feeling Headache Shortness of breath Poor appetite Weight loss Small, tender nodules on the fingers or toes Tiny broken blood vessels on the whites of the eyes, the palate, inside the cheeks, on the chest, or on the fingers and toes. Subacute endocarditis develops more slowly, and its milder symptoms can be present for weeks or months before the illness is suspected. Phsycal examination:Your doctor will examine you, and will check for fever; skin symptoms of endocarditis (tiny hemorrhages in the skin, tender nodules on finger and toes); and a heart murmur, which indicates possible heart valve damage. Additional testing includes: Blood cultures : These blood samples will be added to culture bottles that contain special nutrients to aid bacterial growth. Echocardiography:check for abnormal growths that contain infecting organisms (vegetations) inside the heart. Serological tests - These are blood tests that look for evidence of increased immune system activity, which is a sign of infection. These tests may be helpful when blood cultures do not show bacterial growth. treatment: with antibiotics surgical Complications of endocarditis include: Congestive heart failure Floating blood clots, called emboli, in the bloodstream that lodge in the brain, lungs or coronary arteries Kidney problems

44)Myocarditis Definition: Myocarditis is an inflammation of the myocardium, the middle layer of the
heart wall. etiology: there are numerous potential causes of myocarditis, such as: Viruses. Viruses commonly associated with myocarditis include coxsackievirus B,

which can cause symptoms similar to a mild case of flu; Bacteria. Numerous bacteria may cause myocarditis, including staphylococcus, streptococcus, Parasites. Among these are such parasites as Trypanosoma cruzi and toxoplasma, i Fungi. Some yeast infections (such as candida), molds (such as aspergillus) and other fungi

Symptoms: In mild cases, myocarditis may have no noticeable symptoms. You may
feel ill and have general symptoms of a viral infection and never realize your heart is affected. in serious cases, Common myocarditis symptoms include: Chest pain A rapid or abnormal heartbeat (arrhythmia) Shortness of breath, at rest or during physical activity Fluid retention with swelling of your legs, ankles and feet Fatigue Other signs and symptoms you'd have with a viral infection, such as a headache, body aches, joint pain, fever, a sore throat or diarrhea

Lab tests:
WBC(3,5-10,5) sedimentation rate(in men 5-15,inwomen 8-20) RBC(3,5-5,5) Electrocardiogram (ECG). This noninvasive test shows your heart's electrical patterns and can detect abnormal rhythms, Chest X-ray. An X-ray image of your chest allows your doctor to check the size and shape of your heart, as well as look for fluid in or around the heart that might indicate heart failure. Echocardiogram. Sound waves, or ultrasound, can create moving images of the beating heart. complications: Heart failure. Heart attack or stroke. Irregular heartbeats (arrhythmias) Sudden death.

45)myocardiopathias
definition: Cardiomyopathy is a condition in which your heart muscle becomes

inflamed and enlarged. Because it is enlarged, your heart muscle is stretched and becomes weak. This means it cant pump blood as fast as it should. Common types of cardiomyopathy include:

Dilated cardiomyopathy is a condition in which the heart becomes weak and large. It cannot pump blood well enough. Many different medical problems can cause this type of cardiomyopathy. Hypertrophic cardiomyopathy (HCM) is a condition in which the heart muscle becomes thick. This thickening makes it harder for blood to leave the heart. This type of cardiomyopathy is usually passed down through families. Ischemic cardiomyopathy is caused by narrowing of the arteries that supply the heart with blood. Restrictive cardiomyopathy is a group of disorders in which the heart chambers are unable to properly fill with blood because the heart muscle is stiff.

Peripartum cardiomyopathy occurs during pregnancy or in the first 5 months afterward. Common causes of cardiomyopathy are: Alcoholism and cocaine use Amyloidosis Chemotherapy drugs Coronary artery disease -- most common cause End-stage kidney disease Genetic defects High blood pressure (hypertension) Infections due to viruses -- HIV, Lyme disease, Chagas disease

Symptoms: Breathlessness with exertion or even at rest Swelling of the legs, ankles and feet Bloating of the abdomen due to fluid buildup Fatigue Irregular heartbeats that feel rapid, pounding or fluttering Dizziness, lightheadedness and fainting Physical Examination: high blood pressure, high cholesterol, and diabetes.thyroid disorders,respiratory rate, and oxygen saturation,lung examination listening for fluid and from listening to the heart sounds. Murmurs may provide information about leaking heart valves. Examination of the jugular veins in the neck and swelling or fluid in the feet and ankles can be clues to the diagnosis of heart failure. Lab Tests: Blood tests may be helpful in screening for anemia, abnormalities in electrolytes, and kidney and liver function. Other blood tests and lab work may be ordered depending upon the clinical situation. Chest X-ray. An image of your heart will show whether it's enlarged.
Echocardiogram. An echocardiogram uses sound waves to produce images of the heart. Your doctor can use these images to examine the size and function of your

heart and its motions as it beats. Electrocardiogram (ECG). An ECG can show disturbances in the electrical activity of your heart, which can detect abnormal heart rhythms and areas of injury. Cardiac catheterization and biopsy. In this procedure, a thin tube (catheter) is inserted in your groin and threaded through your blood vessels to your heart, where a small sample (biopsy) of your heart can be extracted for analysis in the laboratory. treatment: The conditions that cause dilated cardiomyopathy are treated. Heart failure is treated by: Taking medicines Making important changes in your lifestyle (dieting, exercising, stopping smoking, stopping alcohol use or using it only in moderation, and stopping the use of other substances such as illegal drugs) Knowing your body and the symptoms of heart failure Wearing a pacemaker to treat a slow heart rate or to help both sides of your heart beat at the same time Wearing a defibrillator that sends an electrical pulse to stop life-threatening, abnormal heart rhythms Complications: Heart failure Blood clots. Valve problems. Cardiac arrest and sudden death.

46)Pericarditis:
definition: Pericarditis is a swelling and irritation of the pericardium, the thin sac-like membrane that surrounds your heart. Pericarditis can be classified according to the composition of the inflammatory exudate or in other words the composition of the fluid that accumulates around the heart.[1] Types include:

serous purulent fibrinous caseous hemorrhagic Post infarction

Depending on the time of presentation and duration, pericarditis is divided into "acute" and "chronic" forms. Acute pericarditis is more common than chronic pericarditis, and can occur as a complication of infections, immunologic conditions, or even as a result of a heart attack Chronic pericarditis however is less common, a form of which is constrictive pericarditis.

Symptom:Sharp, piercing chest pain over the center or left side of your chest
Shortness of breath when reclining Low-grade fever An overall sense of weakness, fatigue or feeling sick Dry cough Abdominal or leg swelling Physical examinations The classic sign of pericarditis is a friction rub auscultated on the cardiovascular examination usually on the lower left sternal border.[ Other physical signs include a patient in distress, positional chest pain, diaphoresis (excessive sweating), and possibility of heart failure in form of precardial tamponade causing pulsus paradoxus, and the Beck's triad of hypotension ,distant (muffled) heart sounds, and JVD (jugular vein distention). Electrocardiogram (ECG). In this test, patches with wires (electrodes) are attached to your skin to measure the electrical impulses given off by your heart chest x-ray. Images of your heart may show an enlarged heart if excess fluid has accumulated in the pericardium. Echocardiogram. This test uses high-frequency sound waves to create an image of your heart and its structures, including fluid accumulation in the pericardium. Magnetic resonance imaging (MRI). This technique uses a magnetic field and radio waves to create cross-sectional images of your heart that can reveal thickening or other changes in the pericardium. Treatment: -medication: Medications to reduce the inflammation and swelling associated with pericarditis are often prescribed, including: Narcotic pain relievers,Colchicine (Colcrys), Corticosteroids. -Pericardiocentesis. In this procedure, a doctor uses a sterile needle or a small tube (catheter) to remove and drain the excess fluid from the pericardial cavity. - Pericardiectomy. If you're diagnosed with constrictive pericarditis, you may need to undergo a surgical procedure (pericardiectomy) to remove the entire pericardium that has become rigid and is making it hard for your heart to pump. Complications may include: Constrictive pericarditis Cardiac tamponade

47)Rheumatism
Definition systemic immune-inflammatory disease afflicting mainly the big joints, the heart, the skin and the central nervous system. The disease affects mainly children and young adults (under 30 years old)

Etiology infection mostly of the upper respiratory tract (tonsillitis) with betahaemolytic streptococci group A. Pathogenesis and pathology immune complexes (antigen-antibody complexes), which include streptococci antigens are causing inflammation of the synovial membrane,myocardium etc. Classification and symptoms: General symptoms for all forms: fever, fatigue, loss of appetite; 1 Arthritis affecting mainly the big joints (knees, ankles, wrists,). The disease usually affects only one joint at a time with pain, redness, edema, increased local temperature and impaired movement. 2 Carditis it can affect the myocardium (myocarditis), endocardium (the valves, most often the mitral valve - endocarditis), pericardium (pericarditis). The myocardium is always afflicted, but the lesions can affect also the valves and the pericardium. The symptoms of myocarditis are easy tiredness, in severe cases shortness of breath (left-side heart failure), often rhythm disorders, mainly premature beats, very rare pain in case of coronaritis . The symptoms of valvulitis appear later, caused by the fibrous deformation of the valves during the process of healing. The main symptom of pericarditis is the pain which is not related to the breathing. In rheumatic fever the effusion into the pericardial cavity is not so large to cause shortness of breath and other symptoms. 3 Neurological form it is caused by damages of the corpus striatum in the basal ganglia (in the brain) due to autoimmune response against the streptococci antigens. 4 Erythema marginatum presented by reddish circular patches on the trunk and the inner surfaces of the limbs. 5 Rheumatic subcutaneous nodules small painless nodules formed on bony prominences such as elbows, knees etc. Physical examination General inspection: possible orthopnoeic position; Lungs possible congestion (decreased vesicular breathing with crepitations) in myocarditis and endocarditis. Patient with pericarditis often sit in bed, bowed forward. Heart: Myocarditis possible increased area of the relative dullness to the left, tachycardia,often premature beats, possible third sound with gallop rhythm, Endocarditis similar to that of myocarditis but the murmurs correspond to the afflicted valve; Pericarditis pericardial friction rub in dry pericarditis, increased area of absolute dullness and decreased sounds in exudative pericarditis; Lab tests: Specific for streptococci infection: AST , smear from the throat for beta-hemolytic streptococci; Increased WBC(3,5-10,5), especially neutrophils(2-7.5), sedimentation rate(in men 5-15,in women8-20), CRP ,,increased fibrinogen, alpha-2 globulin, Instrumental tests:

ECG the changes are typical for myocarditis, always present when the heart is affected usually tachycardia, often premature beats ,prolonged duration of PQ segment, repolarization changes in ST segment and T wave. In pericarditis possible elevation of ST segment; Echocardiography dilatation of the left ventricle and the left atrium, which is causing relative mitral-valve insufficiency, diskinesia of the myocardium; In pericarditis possible thickening of the pericardium or fluid in the pericardial cavity. Radiography enlargement of the heart, in severe cases - lung congestion. Complication rheumatic valve diseases (most often the mitral valve), very rear chronic glomerulonephritis or pulmonitis with pneumofibrosis. 48)-Mitral insufficiency Definition - inability of the mitral valve to close completely during systole. Pathogenesis, patophysiology, symptoms:The mitral valve is unable to close completely during systole which is causing reflux of blood from the left ventricle into the left atrium. Other causes for mitral valve insufficiency are the prolapse (congenital disease), rupture of chorda tendinaea or papillary muscle ,endocarditis and all cases with excessive enlargement of the left ventricle causing relative mitral insufficiency such as myocarditis,cardiomyopathy, ischemic heart disease etc.. Symptoms: ventricular and supraventricular extrasystoli, atrial fibrillation or flutter, Increased pressure in the pulmonary veins and congestion in the lungs,shortness of breath. Physical examination Heart enlarged area of relative dullness to the left, displaced ictus cordis to VI or even VII intercostals space left of the medioclavicular line. Often absolute arrhythmia, but extrasystolic arrhythmia is also possible. Decreased I sound with holosystolic murmur. The later is best heard on the apex, but also on the Erb point (left III and IV intercostals space next to the sternum and propagates toward the left armpit. The lab tests are directed to find eventual rheumatic activity, endocarditis, and estimation of the renal function (creatinine) and electrolytes (potassium).Estimation of respiratory function is required. ECG more often found P-mitrale, because the patients are longer in sinus rhythm. Later they also develop atrial fibrillation with absolute arrhythmia and ventricular extrasystoli are also common. Hypertrophy of both ventricles. Radiography two photos are required face and profile, the later with contrast in the oesophagus. Both show enlargement of the left atrium with normal left ventricle. Later - enlargement of right ventricle and atrium. the left ventricle is also dilated

Echocardiography dilatation of both ventricles and atria, insufficiency of both mitral and later of the tricuspidal valve, later decreased ejection fraction, increased pulmonary pressure. Catheterization left measurement of the mitral valve Insufficiency and estimation of the function of the left ventricle; right measurement of the pulmonary pressure and the tricuspidal insufficiency.

Complications - thrombembolism in patient with atrial fibrillation, bacterial endocarditis,cardiac cirrhosis, pulmonary fibrosis. 49)-Mitral valve stenosis Definition narrowing of the mitral valve opening (normal size 3-6 cm2). Clinically significant stenosis when the opening is narrower then 1.5 cm2. The mitral stenosis could be also congenital. Pathogenesis, pathophysiology and symptoms Impairment of the blood-flow through the narrowed mitral valve opening during diastole. I stage: Hypertrophy, soon followed by dilatation of the left atrium. Symptoms: supraventricular extrasystoli, soon followed by atrial fibrillation or flutter; Peripheral hypoperfusion: Symptoms: easy tiredness, fatigue; Increased pressure in the pulmonary veins and lung congestion: Symptoms: shortness of breath, often cardiac asthma. II stage: Increased pressure in the pulmonary artery, causing hypertrophy and dilatation of the right ventricle with relative tricuspidal valve insufficiency, followed by dilatation of the right atrium and congestion in the peripheral circulation. Symptoms: heaviness in the right hypochondrium due to congestion in the lever, swollen legs, in severe cases generalized edema (dropsy), peripheral cyanosis. However the breathlessness is a little bit relieved. General examination I stage: Facies mitralis (dilated cyanotic capillaries on the chicks) II stage: added peripheral cyanosis, high neck veins, enlarged and painful lever in severe cases ascites . Lungs: I stage: congestion decreased vesicular breathing with crepitations (ronchi in pulmonary edema). II stage: added pleural effusion in the right or both sides. The lab tests are directed to find eventual rheumatic activity, endocarditis, and estimation of the renal function (creatinine) and electrolytes (potassium).Estimation of respiratory function is required. Spirometry restrictive type respiratory failure; Blood gases hypoxemia with normo- or hypocapnia. ECG usually tachyarrhythmia due to atrial fibrillation with hypertrophy of the right ventricle. Radiography - two photos are required face and profile, the later with contrast in the oesophagus. Both show enlargement of the left atrium with normal left ventricle. Later -enlargement of right ventricle and atrium. Echocardiography - .dilated left atrium, right ventricle and right atrium, narrowed mitral valve opening often with calcinosis, insufficiency of the tricuspidal valve (with doppler technique), increased pressure in the left atrium and in the pulmonary artery, Catheterization usually through the right femoral vein, measuring the pressure in the pulmonary artery and the tricusidal insufficiency. Left side catheterization can also be performed for measuring the gradient of the mitral valve. Complications: thrombembolism in patient with atrial fibrillation, (in the lungs from the right atrium,in the brain, limbs, kidneys etc, from the left atrium), bacterial endocarditis, cardiac cirrhosis, pulmonary fibrosis.

50)Aortic Insufficiency
Definition incomplete closing of the artic valve during diastole, followed by regurgitation of blood from the aorta back to the left ventricle. Etiology: rheumatic fever, atherosclerosis, endocarditis, syphilis, connective tissue diseases ,congenital (Marfan syndrome); Pathogenesis, pathophysiology and symptoms: Because of the incomplete closing of the aortic valve during diastole there is a reflux of large portion of blood (in significant regurgitation) from the aorta back to the left ventricle. This regurgitation blood flow and the one normally coming from the left atrium are causing a progressive dilatation of the left ventricle followed by left-side heart failure; I stage: Dilatation of the left ventricle; Symptoms: ventricular extrasystoles; Peripheral hypoperfusion: Symptoms: Chest and high blood pressure; Easy tiredness, fatigue; II stage - relative mitral insufficiency, lung congestion; Symptoms same as in aortic stenosis, the atrial fibrillation Physical examination: Pale aortic face, high systolic and low diastolic blood pressure Heart displacement of the apex beat to VI or VII intercostals space to the left of the medioclavicular line, enlargement of the area of relative dullness; tachycardia ECG sinus rhythm, but sometimes atrial fibrillation, often ventricular extrasystoles,the left bundle branch block Radiography enlargement only of the left ventricle in the first stage, enlargement of the left atrium in the second stage with lung congestion; enlargement of the right ventricle and atrium in third stage; Echocardiography aortic valve regurgitation, measuring of the regurgitation jet to determine the grade and dilatation of the left ventricle; mitral valve regurgitation and dilatation of the left atrium, reduced ejection fraction (second stage); increased pressure in the pulmonary artery, Catheterization trough the left femoral artery measuring the aortic and in the later stage the mitral regurgitation, estimating the function of the left ventricle; coronary angiography is also required in most cases; Complications most common bacterial endocarditis;

51) AORTIC STENOSIS

Definition narrowing of the opening of the aortic valve, which is smaller than 3 cm2, clinically significant under 1.5 cm2 Etiology: most common causes - atherosclerosis, rheumatic fever, congenital Pathogenesis and symptoms: I stage hypertrophy of the left ventricle which pumps out blood against increased resistance Symptoms: Ventricular extrasystoles ,Peripheral hypoperfusion,Chest pain due to ischemia of the myocardium during physical exercise, tachycardia and high blood

pressure,Vertigo, lightheadedness, dizziness during physical exercise, tachycardia or high blood pressureEasy tiredness, fatigue... II stage dilatation of the left ventricle, followed by relative mitral insufficiency and lung congestion Symptoms: shortness of breath during physical exercise; cardiac asthma, possible pulmonary edema often provoked by tachycardia or tachyarrhythmia, high blood pressure, physical exercise III stage hypertension in the pulmonary artery followed by hypertrophy and dilatation of the right ventricle with relative tricuspid insufficiency; Symptoms: edema Physical examination: I stage: pale face, low blood pressure with small pulse amplitude (around 110/80 mmHg), low and slow pulse; cold feet Examination of the heart: apex beat with enlarged area; systolic fremisman; often extrasystolic arrhythmia with coarse systolic murmur, best heard on the aortic valve II stage: Appearance of signs of lung congestion decreased vesicular breathing with crepitations, systolic murmur at the apex III stage: Appearance of signs of right-side heart failure (peripheral cyanosis, high neck veins,enlarged and painful lever, swollen legs; systolic murmur at the tricuspid valve point due to tricuspid valve insufficiency.. Lab tests same as in mitral valve diseases; ECG sinus rhythm often with ventricular extrasystoles, hypertrophy of the left ventricle, usually left bundle branch block, often ST-T depression; Radiography; I phase often no significant changes; II phase lung congestion, dilatation of the left ventricle and the left atrium; III phase plus dilatation of the right ventricle and the right atrium, possible rightside hydrothorax; The most frequent complication, as in all valve diseases is bacterial endocarditis.

52) ARTERIAL HYPERTENSION

Hypertension is sustained elevation of resting systolic BP ( 140 mm Hg), diastolic BP ( 90 mm Hg), or both. Etiology:Hypertension may be primary (85 to 95% of cases) or secondary. Primary hypertension: Hemodynamics and physiologic components (eg, plasma volume, activity of the renin-angiotensin system) vary, indicating that primary hypertension is unlikely to have a single cause. Heredity is a predisposing factor, but the exact mechanism is unclear. Environmental factors (eg, dietary Na, obesity, stress) seem to affect only genetically susceptible people.

Secondary hypertension: Causes include renal parenchymal disease (eg, chronic glomerulonephritis, polycystic renal disease, connective tissue disorders, obstructive uropathy), renovascular disease pheochromocytoma, Cushing's syndrome, primary aldosteronism, congenital adrenal hyperplasia, hyperthyroidism, myxedema, and coarctation of the aorta. Excessive alcohol
intake and use of oral contraceptives are common causes of curable hypertension. Use of sympathomimetics, NSAIDs, corticosteroids, cocaine, or licorice commonly contributes to hypertension. Pathology and complications: No pathologic changes occur early in hypertension. Severe or prolonged hypertension damages target organs (primarily

the cardiovascular system, brain, and kidneys), increasing risk of coronary artery disease (CAD), MI, stroke, and renal failure. The mechanism involves development of generalized arteriolosclerosis and acceleration of atherogenesis. Because of increased afterload, the left ventricle gradually hypertrophies, causing diastolic dysfunction. The ventricle eventually dilates, causing dilated cardiomyopathy and heart failure (HF) due to systolic dysfunction. Symptoms: Dizziness, flushed facies, headache, fatigue, epistaxis, and nervousness are not caused by uncomplicated hypertension. Severe hypertension can cause severe cardiovascular, neurologic, renal, and retinal symptoms. A 4th heart sound is one of the earliest signs of hypertensive heart disease.Retinal changes may include arteriolar narrowing, hemorrhages, exudates, and in patients with encephalopathy, papilledema. Diagnosis: Hypertension is diagnosed and classified by sphygmomanometry. 1. Multiple measurements of BP to confirm 2. Urinalysis and urinary albumin:creatinine ratio; if abnormal, consider renal ultrasonography 3. Blood tests: Fasting lipids, creatinine, K 4. Renal ultrasonography if creatinine increased 5. Evaluate for aldosteronism if K decreased 6. ECG: If left ventricular hypertrophy, consider echocardiography 7. Sometimes thyroid-stimulating hormone measurement 8. Evaluate for pheochromocytoma if BP elevation sudden and labile or severe Physical examination: includes measurement of height, weight, and waist circumference; funduscopic examination for retinopathy; auscultation for bruits in the neck and abdomen; and a full cardiac, respiratory, and neurologic examination. The abdomen is palpated for kidney enlargement and abdominal masses. Peripheral arterial pulses are evaluated; diminished or delayed femoral pulses suggest aortic coarctation, particularly in patients < 30. Thyroid-stimulating hormone is often measured. If urinalysis detects albuminuria (proteinuria), cylindruria, or microhematuria or if serum creatinine is elevated ( 1.4 mg/dL in men; 1.2 mg/dL in women), renal ultrasonography to evaluate kidney size may provide useful information. On ECG, a broad, notched P-wave indicates atrial hypertrophy. Left ventricular hypertrophy, indicated by a sustained apical thrust and abnormal QRS voltage with or without evidence of ischemia.

Treatment 1. Weight loss and exercise 2. Smoking cessation 3. Diet: Increased fruits and vegetables, decreased salt, limited alcohol

4. Drugs if BP is initially high (> 160/100 mm Hg) or unresponsive to lifestyle

modifications Primary hypertension has no cure.

53) Ischemic heart disease stable and unstable angina;:

Definition inability of the coronary arteries to provide adequate amount of blood and respectively oxygen to the myocardium. Etiology and pathogenesis: Narrowing of the lumen of the coronaries Atherosclerosis of the coronary arteries Thrombosis or embolism of the coronaries Spasm of the coronaries Inflammation of the coronaries Increased need of oxygen due to hypertrophy of the myocardium, or tachycardia or tachyarrhythmia Reduced cardiac output; Aortic valve diseases Predisposition factors: Arterial hypertension; Hyperlipidaemia; Diabetes; Hypothyroidism; Gout; Obesity; Stress; Smoking; Drugs (cocaine); Inactivity; Hypercoagulation; Vasculitis Classification: stable angina, unstable angina, myocardial infarction Symptoms: Asymptomatic form is mainly caused by mild atherosclerosis of the coronaries and is randomly discovered by ECG or veloergometry. Stable angina: is usually caused by atherosclerosis of the coronaries. Symptoms: Pain, tightness or discomfort in the chest. It often propagates toward the last two fingers of the left arm. the duration usually 5-15 minutes. As a rule pain which is located in one point or takesThe pain is provoked by increased need of oxygen by the myocardium and is usually relieved at rest and by nitroglycerin, or when the blood pressure, the hearts rate or the blood sugar are normalized. Unstable angina: is caused by ulceration and thrombosis of an atherosclerotic plaque in the coronary wall or coronary spasm. Chest pain which appears for first time or with accelerated frequency are also considered as unstable angina. Symptoms: Pain in the chest, which appears at rest and is not relieved by nitroglycerin. Its duration is usually between 15 and 30 min.

Physical examination In asymptomatic patients or in those with stable and unstable angina there are not specific changes except for predisposition factors as obesity, cholesterol yellow lesions or plaques on the skin, high blood pressure, changes in the heart rate or the rhythm etc Lab tests: often increased levels of cholesterol (high LDL, low HDL)
Cholesterol (total) Cholesterol (HDL) Cholesterol (LDL) Less than 200 mg/dL desirable 30 - 75 mg/dL Less than 130 mg/dL desirable

and triglycerides (high VLDL)

Triglycerides (Male) Triglycerides (Female) Greater than 40 - 170 mg/dL Greater than 35 - 135 mg/dL

blood sugar, (4.4 to 6.1 mmol/L (82 to 110 mg/dL) uric acid (240 - 755 mg / 24 hr) ECG: Asymptomatic patients negative T wave or/and depression of ST-segment, possible disorders of the conduction. Stable angina usually no changes; the diagnosis is proven by veloergometry and other cardiac stress tests, or coronary angiography. Unstable angina persisting ischemic changes negative T wave or/and ST depression. The catheterization is the most important for the diagnosis of all forms of ischemic heart disease and is often used in the treatment of the patients.Computer tomography is a useful alternative. In some patients scintigraphy can be also performed.

54) Ischemic heart disease myocardial infarction:

Definition inability of the coronary arteries to provide adequate amount of blood and respectively oxygen to the myocardium. Etiology and pathogenesis: Narrowing or obstruction of the lumen of the coronaries Atherosclerosis of the coronary arteries Thrombosis or embolism of the coronaries Spasm of the coronaries Inflammation of the coronaries Increased need of oxygen due to hypertrophy of the myocardium, or/and tachycardia or tachyarrhythmia;Reduced cardiac output; Aortic valve diseases Predisposition factors:Arterial hypertension; Hyperlipidaemia; Diabetes; Hypothyroidism; Gout; Obesity; Stress; Smoking; Drugs (cocaine); Inactivity;

Hypercoagulation; Vasculitis Classification: stable angina, unstable angina, myocardial infarction Symptoms:Asymptomatic form is mainly caused by mild atherosclerosis of the coronaries and is randomly discovered by ECG or veloergometry. Myocardial infarction is necrosis of the myocardium due to ischemia. It is usually a consequence of unstable angina. If the pain continues more than 30 min. The stable angina can also lead to infarction. Symptoms: cold sweat and nausea, not so often vomiting, shortness of breath sometimes cardiac asthma or cardiac shock, premature beats, fear. Physical examination: In patients with myocardial infarction the skin is with cold sweat, the face often pale. The blood pressure is high or low, the heart rate usually high sometimes irregular. Auscultation of the lung sometimes with signs of left-side heart failure. Lab tests: Specific tests: increased troponin (0 - 0.1 ng/ml (onset: 4-6 hrs, peak: 12-24 hrs, return to normal: 4-7 days), ASAT (aspartate transaminase)
AST, SGOT (Male) AST, SGOT (Female) 7 - 21 U/L 6 - 18 U/L

LDH (lactate dehydrogenase) (56-194 IU/L) Unspecific: WBC, sedimentation rate, CRP, blood sugar Veloergometry is contraindicated in such cases; Myocardial infarction most important is the elevation of the ST segment, which shows the lesions zones, appearance of Q deeper than 2 mm shows necrosis. Radiology is not relevant to the ischemic heart disease. However lung congestion due to left-side heart failure or enlargement of the heart are often found especially in patients with acute myocardial infarction. The catheterization is the most important for the diagnosis of all forms of ischemic heart disease and is often used in the treatment of the patients. Computer tomography is a useful alternative. In some patients scintigraphy can be also performed. Complications of the myocardial infarction:ventricle fibrillation and cardiac arrest. Left-side heart failure, including pulmonary edema or cardiac shock; Rupture of papillary muscle or chorda tendinea Rupture of the myocardial wall with haemopericardium Cardiac aneurism

55) Acute renal failure:

Definition sudden reversible impairment of the renal function causing retention of nitrogen-containing substances, hypervolemia, electrolyte and acid-base misbalance Classification prerenal, renal and postrenal

Etiology and pathogenesis;Prerenal causes Hypovolemic or other types of shock (cardiac, septic etc) and hepatorenal syndrome; causing arteriolar constriction and increased absorption of sodium; the secretion of ADH is also increased; Massive hemolysis, Massive muscular damage. Renal causes embolism or thrombosis of the renal artery or thrombosis of the renal vein, DIC syndrome (disseminated intravascular coagulation), TTP (thrombotic thrombocytopenic purpura), HUS (Hemolytic uremic syndrome), preeclampsia, acute glomerulonephritis Postrenal causes It is not real acute renal failure but retention of the urine due to obstruction of the urinary tract . Stages oligoanuric, polyuric, recovery Symptoms Main symptom is oligoanuria (diuresis under 500 and 100 ml) Nausea, vomiting, possibly diarrhea Fatigue, exhaustion, loss of appetite and of weight; shortness of breath Physical examination Kussmaul (deep acidotic) breathing, pale skin often with cold sweat; often slight tremor; In severe cases anxiety, confusion, drowsiness or coma; The tongue is often with yellow-brownish surface and there is uremic odor Lab tests Urine proteinuria and erythrocyteuria; leukocyteuria in cases with infection; the osmolality of the urine gives a clue to the form of renal failure osmolality of the urine over 500 mosm/l suggest prerenal cause; when under 300 mosm/l renal cause usually acute tubular necrosis; Increased creatinine (A normal result is 0.7 to 1.3 mg/dL for men and 0.6 to 1.1 mg/dL for women), urea (Normal urea levels in healthy adults are between 10 and 20 mg/dL.); ncreased potassium (The normal range is 3.7 to 5.2 mEq/L);complete blood count Instrumental tests Abdominal ultrasound is urgently required to exclude retention; Renal biopsy is seldom performed in acute renal failure; ECG, X ray of the lungs, sometimes echocardiography Complications Uremic coma; Pulmonary and cerebral edema; Heart arrest Pericarditis; Gastrointestinal bleeding

56) Chronic renal failure

Definition progressive irreversible impairment of the renal function causing progressively reduced clearance of nitrogen and other products including hormones, leading to general intoxication , misbalance in the electrolyte and acid-base homeostasis, Etiology and pathogenesis All forms of chronic glomerulonephritis and

nephropathies, chronic tubulointerstitial nephritis ,uncontrolled arterial hypertension, continuous retention of the urine, hereditary diseases Symptoms Fatigue, exhaustion, headache, muscular weakness, loss of appetite and, Itching without rush Pain in the bones Physical examination; Kussmaul breathing, possible slight tremor, reduced muscle and fat tissue; Dirty pale color of the skin Arterial hypertension Lab tests;Increased levels of creatinine (A normal result is 0.7 to 1.3 mg/dL for men and 0.6 to 1.1 mg/dL for women), urea (Normal urea levels in healthy adults are between 10 and 20 mg/dL.)Hypocalcaemia and hyperphosphatemia

Urine : pH Na K Cl Protein

4.6 - 8.0 10 - 40 mEq/L Less than 8 mEq/L Less than 8 mEq/L 1 - 15 mg/dL

Total protein and albumin are increased; Sedimentation rate and alpha amylase are usually increased; Instrumental tests Abdominal ultrasound; Renal biopsy ECG, echocardiography and X ray Complications Uremic coma Pulmonary and cerebral edema Pericarditis Heart arrest Gastrointestinal bleeding due to erosive gastritis

57 Acute diffuse glomerulonephritis

Classification acute, rapidly progressive (subacute) and chronic; Acute glomerulonephritis Definition acute, diffuse immune inflammation of both kidneys affecting the glomerular basement membrane, the mesangium and the capillary endothelium; Etiology beta hemolytic streptococci group A (acute poststreptoccocal glomerulonephritis); the usual sources of infection are pharyngeal infection and tonsillitis, but other locations are also possible;

Pathogenesis formation of immune complexes of streptococci antigen and antibodies which are deposited or formed in situ on the glomerular basal membrane (hunchlike subepithelial depositions) and in the mesangium causing local inflammation with stasis and proliferation of endothelial and mesangial cells and infiltration with polymorphonuclear leukocytes and monocytes; Symptoms The symptoms appear usually 10-14 days after streptococcal pharyngitis (initial phase); Olygo-anuric phase (duration usually about a week); Olyguria (urine under 500 ml/24h) or anuria (under 100 ml) due to reduced glomerular filtration rate (GFR); The consequences are: 1 Hypervolemia causing Edema, Arterial hypertension ,left-side heart failure with cardiac asthma and even pulmonary edema or cerebral edema; diarrhea and loss of weight; the hyperkalaemia may lead to cardiac arrest; Recovery phase (usual duration 3 6 months) during which the changes in the urine (proteinuria, hematuria) disappear completely and the GFR is normalized; Physical examination Oligo-anuric phase orthopnoeic position; periorbital edema, swollen legs, yellow-brownish surface of the tongue, odor; deep acidotic brathing; Lungs decreased vesicular breathing with crepitations in patients with cardiac asthma; Heart the heart rate is variable, often normal or bradycardia; increased blood pressure; Percussion of kidneys often slightly positive sucussio renalis; Polyuric phase possible signs of dehydration; Lab tests Slightly increased WBC(3.5-10.5) increased sedimentation rate(in women 8-20, in man 5-15 ) and CRP, possible presence of cryoglobulins; Urine- (10-20) Typical for the oliguric phase lab constellation of acute renal failure increased levels of creatinin, urea, uric acid and potassium; decompensated metabolite acidosis (decreased both pH of the blood below 7.35 and BE below 2.5); Increased AST (above 200); In polyuric phase potassium(3.7-5.2) may be decreased; Instrumental tests abdominal ultrasound the kidneys are slightly enlarged with diffuse structural changes; ECG and X ray of CT- scan Renal biopsy Complications Pulmonary and cerebral edema; uremic coma, chronic glomerulonephritis usually

mesangioproliferative type;

58) Chronic glomerulonephritis:

Definition - chronic progressive diffuse autoimmune inflammations of both kidneys, damaging mainly the glomerular basement membrane and the mesangium Classification 1-Idiopathic nephrotic syndrome Etiology and pathogenesis in most cases idiopathic; infections (mononucleosis, HIV), vaccination, drugs and toxicity (NSAID, antibiotics, interferon, mercury, lithium), allergy (insects, etc), tumors (lymphomas) Pathogenesis - disorder of T cells. Idiopathic nephrotic syndrome with IGM depositions Focal segmental glomerulosclerosis and hyalinosis Symptoms edema, arterial hypertension chronic renal failure malaise, fatigue, exhaustion, heaviness in the abdomen, indigestion, bloating iron deficiency anemia Physical examination Edema in all forms of the disease and in severe cases the general condition may be impaired; in case of anemia - pale skin and mucosa; often tachycardia. Lab tests urine excessive proteinuria (over 3.5 g/l), erythrocyturia Reduced levels of plasma total protein (5 - 9 gm/dL) and albumin (3.5 - 5.0 gm/dL) and increased cholesterol (normal value=Less than 200 mg/dL desirable) slight anemia Instrumental tests Abdominal ultrasound Renal biopsy X ray of the chest and echocardiography Complications: hypovolemic shock; pulmonary or cerebral edema and coma 2-Chronic membranous glomerulonephritis: Etiology infections (including chronic hepatitis B and C, malaria, bacterial endocarditis), tumors (cancer, lymphoma), autoimmune diseases (thyreotoxicosis, Hashimoto disease), drugs (gold, lithium, mercury, penicillamine, captopril) Symptoms: severe edema, same as idiopathic nephrotic syndrome The biopsy is crucial for the diagnosis Complications are same as idiopathic nephrotic syndrome 3-Chronic mesangioproliferative glomerulonephritis: Etiology and pathogenesis IGA nephropathy is usually a consequence of pathological immune reaction of the mucosa; immune complexes with IGA and C3 are deposited in the mesangium; develop hematuria, arterial hypertension and chronic renal failure; IGA levels are also increased in liver cirrhosis, Schonlein-Henoch disease, HIV infection Symptoms arterial hypertension and hematuria Physical examination Arterial hypertension usually without signs of edema Lab tests Urine-massive hematuria and moderate proteinuria (usually between 1-3 g/l)

Increased sedimentation rate (8-20 for women,5-15 for men), often AST(7 - 21 U/L for men, 6 - 18 U/L for women), mild iron deficiency anemia is found; specific for Berger disease is elevation of IGA. Test for estimation of the renal function including creatinin clearance Instrumental tests Abdominal ultrasound Biopsy is crucial for the diagnosis ECG and echocardiography are required 4-Mesangiocapillar (membranoproliferative) glomerulonephritis:

Etiology infections (chronic B and C hepatitis, Mycoplasma, malaria), tumors (lymphoma, leukemia), vaccines, liver cirrhosis, sickle cell anemia, thrombotic thrombocytopenic purpura (TTP),hemolytic uremic syndrome (HUS) Pathogenesis subendothelial deposition or formation in situ of immune complexes with IGG and C3 on the glomerular basement membrane and in the mesangium causing severe
proteinuria with hypoproteinemia and edema Symptoms, physical examination and tests are similar to progressive glomerulonephritis Complications predisposition to infections and thromboembolic incidents, pulmonary and brain edema

59) Nephrolithiasis;
Definition formation of stones in the pyelon, calices or bladder in one or both kidneys; Classifications of the stones oxalates, uric acid stones, phosphates,cystein; Predisposition factors;Metabolite disorders - hyperuricemia and hyperuricosuria; hyperoxaluria; cysteinuria hypercalciuria, distal tubular acidosis, hypocitraruria, etc; Endocrine disorders hyperparathyroidism; Dehydration Infections of the kidney and the bladder; Family predisposition; Symptoms The typical clinic form is the renal colic sudden harsh pain usually in one of the lumbar regions, propagating toward the bladder and the groin; Hematuria; Nausea and vomiting, fatigue; Pain and burning during urinating fever Lab tests Urine erythrocytes and even RBC(3.5-5.5) casts, mild proteinuria; WBC (normal range up to 4-5) in case of concomitant infection; Blood count and sedimentations rate Instrumental tests Abdominal ultrasound would show the stones Native X ray of abdomen may show only roentgen-positive stones Roentgen-negative stones are visualized by venous urography CT and MRI hydronephrotuc curve; Chemical analysis of the stone must be performed when it is eliminated spontaneously or instrumentally; Measurement of the ph of the urine is also important due to treatment and prophylaxis of

nephrolithiasis... Complications Hydronephrosis in some cases followed by pyonephrosis; in prolonged hydronephrosis the renal function may be irreversibly damaged and even the kidney may be totally lost Infections-when both ureters are obstructed retention of the urine and acute renal failure

60) Renal colic

Definition: Renal colic is a type of pain caused by kidney stones. A stone may block the flow of urine and can cause pain if it travels down the tubes of the urinary tract. Symptoms: Abnormally colored urine Fever with or without chills Foul-smelling urine Nausea Pain in the side, back, abdomen Etiology: Renal colic is triggered by the buildup of crystals, or stones, in the kidneys. When these stones interfere with the flow of urine, they can cause the kidneys to swell Treatment: Allopurinol Alpha-blocker medications to help stones pass Antibiotics to clear infections Cystine control medications to reduce cystine levels in urine Diuretics Pain medications Heat therapy Lithotripsy Surgery to remove large stones Ureteral stent placement Ureteroscopy Complications: Blockage of the urinary tract Kidney damage Loss of kidney function Recurrence of stones Urinary tract infection

61) Acute and chronic tubulointerstitial nephritis:

Definition bilateral, acute or chronic inflammation of kidneys tubules, interstitium and pyelon Etiology Infectious usually gram negative bacteria (E. coli, Enterobacter, Klebsiela, Proteus, Pseudomonas); the infection may spread through blood, lymph or from the lower urinary tract Toxic or allergic mechanism - caused by heavy metals (cadmium, mercury with direct toxicity); drugs - antibiotics as amino glycosides (direct toxicity); penicillin (allergy), sulfonamides, NSAID, analgesics, cyclosporine Metabolite hyperuricaemia (gout); Genetic Alport syndrome, hereditary polycystosi Cryptogenic Balkan endemic nephropathy

Acute tubulointerstitial nephritis: Pathogenesis acute tubulo-interstitial inflammation followed by reversible tubular dysfunction Symptoms Pain in one or both lumbar regions Fever Pain and burning during urinating Fatigue, weakness, loss of appetite Physical examination fever; tachycardia, often hypotension positive sucussio renalis Lab tests Specific urine mild proteinuria(1 - 15 mg/dL), leukocyteuria(Negative), bacteriuria; Required urine culture Blood count increased WBC(3.5-10.5), sedimentation rate(8-20 for men, 5-15 for women) Instrumental tests Abdominal ultrasound irregular contour of one or both kidneys with asymmetrical parenchyma changes CT or MRI are often required Complications Abscess, plegmon, carbuncul; sepsis; Pyonephrosis in patients with hydronephrosis; Acute renal failure

Chronic tubulointerstitial nephritis: Pathogenesis chronic tubulo-interstitial inflammation followed by fibrosis and tubular atrophy with irreversible damage of the tubules Symptoms: in early stages there may be pain in the joints in patients with gout; In later stages, appear fatigue, weakness, loss of appetite and weight, possibly arterial hypertension, anemia Lab tests Urine mild selective proteinuria (about 1 g/l) which is slightly increased during exacerbation with leukocyteuria(normal=Negative) and bacteriuria; Cultures of urine are required WBC(3.5-10.5) are increased only during exacerbations but sedimentation(5-15 for women, 820 for men) rate is elevated; Instrumental tests Abdominal ultrasound - irregular contour of the kidneys, usually asymmetric narrowed peripheral zone, the size of the kidneys is often asymmetrically reduced Venous urography Complications Chronic renal failure Nephrolithiasis
62) Gastroesophageal reflux disease (GERD) Definition reflux of fluids from the stomach into the esophagus which damages the esophageal mucosa causing

inflammation often with erosions; Etiology Abnormal relaxation of the lower esophageal sphincter; Hiatal hernia Predisposition factors obesity, visceroptosis, all causes for hyperacidity, sclerodermia; Symptoms Main symptoms heartburn (pyrosis), acids, regurgitation; Possible dysphagia (difficulty to swallow), odynophagia (pain during swallowing), retrosternal pain, increased salivation, bleaching, nausea; In some cases chronic cough, even asthmatic attacks or dental hypersensitivity; Iron deficiency anemia is often found in patients with hiatal hernia; Heaviness in the chest, shortness of breath, palpitations and premature beats also in patients with hiatal hernia; Physical examination White surface of the tongue, possible odor; Lab and instrumental tests There are not specific lab tests for GERD; In patients with hiatal hernia may be found reduced levels of HB(14-18 g/dL (erkek); 12-16 g/dL (kadin), Ht % 42-52 (erkek); %36-46 (kadin), RBC(3,5-5,5) and iron; Diagnosis is established by EGD (gastroscopy) and esophageal pH monitoring (during reflux ph in the esophagus decreases to or under 4); X-ray with Barium contrast and esophageal manometry are also used; Complications Erosions or ulcer with bleeding; Esophageal cancer (precursor factor intestinal metaplasia in the esophageal mucosa); Chronic pharyngitis, chronic laryngitis, bronchial asthma sinusitis; 63) Acute and chronic gastritis Definition inflammation of the lining of the stomach. Etiology and pathogenesis 1 Infections: most common in chronic gastritis - helicobacter pylori Could be also bacterial, viral, fungal, parasitic 2 Toxicity: Alcoholic very common; Drug induced NSAID, corticosteroids, antibiotics, digoxin etc Bile reflux in patients with diskinesia of the gall bladder as a secondary symptom in other diseases uremia, diabetes, hypercorticism, hyperparathyroidism congestive heart failure, respiratory failure in pernicious anemia, Crohns disease, coeliac disease, Symptoms Acute gastritis: Sharp epigastrial pain increased by eating Often nausea and vomiting Fatigue, exhaustion Possibly fever Diarrhea in gastroenterocolitis Chronic atrophic gastritis:

tachycardia due to iron deficiency or vitamin B 12 anemia Sometimes dysphagia Physical examination: Acute gastritis: White or yellow-white surface of tongue Possible fever, tachycardia, hypotension Palpation severe or moderate pain in the epigastria without stiffness, negative Chronic superficial gastritis: White surface of the tongue Palpation usually mild pain in the epigastria Chronic atrophic gastritis: Pale skin Polished tongue Sometimes rhagades in the mouths angles Palpation usually without pain Lab tests: Acute gastritis: Possible increased WBC(3.5-10,5), Gastroscopy. Chronic superficial gastritis: has no specific lab tests. Gastroscopy is performed to establish the presence of helicobacter pylori, X-ray would show increased volume of fluid in the stomach before swallowing of the contrast. Chronic atrophic gastritis: Often decreased RBC(4.2-5.6 M/L for men, 3.8 - 5.1 M/L for women), HB(14-18 g/dL for men, 11-16 g/dL for women), Ht (39 - 54% for men, 34 - 47% for women) Complications Acute gastritis: ulcerous-hemorrhagic gastritis with bleeding, phlegmon of the stomach Chronic superficial gastritis: erosions with bleeding, ulcer, chronic atrophic gastritis Chronic atrophic gastritis: iron deficiency or vitamin B 12 deficiency anemia, funicular myelosis, cancer ..

64) Gastric and duodenal ulcer:

A gastric ulcer is a break in the normal tissue that lines the stomach.
Etiology: gastric ulcers are caused by an imbalance between stomach acid, an enzyme called pepsin, and the natural defenses of the stomach''s lining.

Use of aspirin and NSAIDs Helicobacter pylori infection Chronic gastritis Smoking ncreasing age Mechanical ventilation (being put on a breathing machine) Certain blood clotting problems Symptoms Abdominal pain Nausea Abdominal indigestion Vomiting, especially vomiting blood Blood in stools or black, tarry stools Unintentional weight loss Fatigue Tests: EGD (esophagogastroduodenoscopy) and biopsy showing a benign gastric ulcer

Upper GI series showing a gastric ulcer Treatment H2 receptor antagonist such as famotidine (Pepcid) or nizatidine (Axid) or a proton pump inhibitor such as omeprazole (Prilosec) or esomeprazole (Nexium) to suppress acid, combined with two antibiotics. If the ulcer bleeds, endoscopy can control bleeding in most cases. Surgical procedures include: Vagotomy - cuts the vagus nerve, which controls the stomach's production of gastric acid Partial gastrectomy -removes part of the stomach Complications Bleeding from the ulcer Perforation in the stomach Blockage in the stomach that prevents movement of stomach contents DUODENAL ULCER: pathologically exceeded secretion of hydrochloric acid Symptoms: Pain in the epigastria Acids Often heartburn, bleaching, heaviness in the abdomen; Sometimes constipation Loss of weight, although the appetite is normal Nausea and vomiting Physical examination Slightly impaired general condition Often reduced muscle and fat tissue Tongue with white or yellow-white surface Often odor Palpation pain in the epigastria without signs of peritoneal irritation Lab tests No specific changes in the lab tests Esophagogastroduodenoscopy is most important for the diagnosis. X-rays in patients refusing EGD will show a defect in the lining of the stomach Complications Bleeding when the ulcer erodes a blood vessel in the duodenum often on the posterior wall Predisposition factors Drugs Aspirin and other NSAID, corticosteroids, anticoagulants and antiagregants; Severe physical exercise Wrong food or alcohol

65) Gastric cancer:

Definition malignant tumor of the stomach, 90% adenocarcinoma Predisposition factors and diseases: Family predisposition Helicobacter pylori Polypus of the stomach Chronic atrophic gastritis with intestinal metaplasia Autoimmune atrophic gastritis with pernicious anemia Gastric ulcer Symptoms

early symptoms are abdominal discomfort or heaviness after meal often with loss of appetite Later usually appears abdominal pain; If it is malignant ulcer there is change in the characteristic of the pain Nausea and vomiting Fatigue, exhaustion, anemia and loss of weight, possible bleeding Peritoneum ascites Lungs shortness of breath, mantel pneumonia Invasion of the pancreas pancreatitis Ovarial metastases Physical examination Reduced fat and muscular tissue, loss of weight Pale skin White surface of the tongue Often tachycardia due to anemia Palpation pain in the epigastria Lab tests: Reduced HB (14 - 18 g/dL for men, 11 - 16 g/dL for women), Ht (39 - 54% for men, 34 - 47% for women), RBC (4.2 - 5.6 M/L for men, 3.8 - 5.1 M/L for women), Iron (52 - 169 g/dL), increased sedimentation rate (5-15 for women, 8-20 for men); the WBC(3.5-10.5) are increased in patients with necrosis of the tumor; Instrumental tests EGD with biopsy is crucial for the diagnosis; For eventual metastases ultrasound and CAT of the abdomen is required, X-ray or CAT of the lungs; Complications Bleeding Pulmonary tromboembolism

66) Acute and chronic enteritis; gluten enteropathy:

Definition inflammation of the mucosa of the small intestine Etiology: Infectious-Bacterial - usually caused by consuming contaminated food Viral usually acute but in rare cases chronic (HIV); in most cases caused by consumption of contaminated food, (enterovirus, rotavirus, norovirus, etc.) but also as a symptom of a general viral infection ass grippe, hepatitis, HIV Fungi most common Candida Protozoa amoebiasis Helminthiasis ascaridosis Pathogenesis Diarrhea increased secretion and motility Constipation caused either by reduced motility or spasm of the colon; Acute enteritis (staphylococcus, E. coli, Campylobacter, rotavirus, norovirus) Symptoms Pain in the epigastria or in the whole abdomen Nausea and vomiting mainly of gastric fluid Diarrhea without blood Fever in patients with infections Dehydration, fatigue, exhaustion, occasionally headache, muscle pain and cough Physical examination pale and dry skin possible fever; white surface of the tongue, often odor

increased heart rate with low blood pressure Palpation pain in the epigastria and in the umbilical region Auscultation increased peristaltic Lab tests possible increased levels of leukocytes(3.5-10.5) and increased sedimentation rate(5-15 for women, 8-20 for men), possible decreased potassium (normal=Less than 8 mEq/L) culture of feces; PCR (polymerase chain reaction) for viruses Complications erosions of the stomach and duodenum with bleeding Chronic enteritis (gluten enteropathy, lactase deficiency) Symptoms: Diarrhea Heaviness in the abdomen, bloating, meteorism, flatulence In severe cases weakness, fatigue, loss of weight, anemia Physical examination In untreated cases of gluten enteropathy the general condition is impaired, the bodyweight is reduced and the abdomen enlarged, the children are with retarded growth; Slight periumbilical pain and increased peristaltic are found during exacerbation of the symptoms In patients with gluten enteropathy the biopsy of the jejunum is crucial for the diagnosis immune tests for anti-gliadin antibodies are performed The deficiency of lactase may be proved by excluding milk from the meals

67) Chronic ulcerous colitis:

Definition: is a chronic inflammation of the large intestine Etiology: Genetic factors, Environmental factors (Diet, Breastfeeding), Autoimmune disease Mild form diarrhea usually 5-6 defecations daily sometimes with blood and mucus, mixed with the feces, heaviness in the abdomen, mild or moderate pain often during defecation, fatigue Severe form diarrhea up to 15-16 defecations daily with blood and mucus, possible fever, abdominal pain often during defecation, loss of weight, fatigue, weakness even exhaustion, anemia Fulminating form sudden onset, diarrhea up 20 and more defecations daily with much blood and mucus, septic fever, abdominal pain, loss of weight, fatigue, weakness even exhaustion, anemia Physical examination pale skin, lips, and conjunctives, possible dry skin with reduced turgor Tachycardia and low blood pressure Often pain over the colon, usually on the left side, increased peristaltic Lab tests: increase of sedimentation rate(5-15 for women, 8-20 for men), CRP; possible elevated WBC (3.5-10.5) and platelets(150,000 - 400,000 mcL) Reduced HB(14 - 18 g/dL for men, 11 - 16 g/dL for women), Ht (39 - 54% for men, 34 - 47% for women), RBC(4.2 - 5.6 M/L for men, 3.8 - 5.1 M/L for women), Iron (52 - 169 g/dL);

Necessary control of cholestatic lever enzymes (GGT 1 - 94 U/L for men, 1 - 70 U/L for women) and bilirubine(0.2 - 1.4 mg/dL); culture of feces Instrumental tests crucial fibroconoscopy alternative Barium enema X ray Ultrasound of the abdomen Complications: Local - severe bleeding; abscesses; anal, rectovaginal or other fistulas Pseudopolyposis and malignant degeneration General eye inflammation; arthritis; sepsis, hemolytic anemia, venous thrombosis Treatment: aminosalicylates such as sulfasalazine corticosteroids such as prednisone immunosuppressive medications such asazathioprine biological agents such as infliximab colectomy

68) Colonic and rectal cancer

Predisposition factors polyps, chronic ulcerous colitis, Crohn disease, constipation; eventually hemorrhoids Symptoms: Proximal type:Easy tiredness, fatigue due to anemia; fever, later loss of weight with reduced appetite, eventually abdominal pain in cases with obstruction of the passage Distal type constipation and rectorrhagia, often painful or very frequent defecation; later fatigue, easy tiredness, loss of weight with reduced appetite End stage symptoms from the metastases, In the liver jaundice, possible pain; In the peritoneum acites Physical examination:Pale skin, white surface of the tongue, reduced bodyweight Palpation pain the rectum enlarged inguinal lymphatic nodes and liver or ascites in the metastases stage Auscultation loud, cracking peristaltic Lab tests: Decreased levels of HB (14 - 18 g/dL for men, 11 - 16 g/dL for women), Ht(39 - 54% for men, 34 - 47% for women), RBC (4.2 - 5.6 M/L for men, 3.8 - 5.1 M/L for women), Iron(52 - 169 g/dL); lymphocytes(14 - 44%); increased sedimentation rate(5-15 for women, 8-20 for men), CRP(Low risk: less than 1.0 mg/L, Average risk: 1.0 to 3.0 mg/l, High risk: above 3.0 mg/L), Increased liver enzymes (GGT-1 - 94 U/L for men, 1 - 70 U/L for women), bilirubin (0.2 - 1.4 mg/dL) Instrumental tests: Fibrooscopy crucial for the diagnosis; Barium enema X-ray as alternative, PET or CAT. Ultrasound of the abdomen and X-ray of the chest as a general screening for metastases Complications: Bleeding; Obstruction with ileus Rectovesical, rectovaginal or other fistulas Treatment: Surgery, Chemotherapy, Radiation, Palliative care

69) Irritable bowel syndrome:

Definition: a symptom-based diagnosis characterized by chronic abdominal pain, discomfort, bloating, and alteration of bowel habits.

Classification: IBS can be classified as either diarrhea-predominant (IBSD), constipation-predominant (IBS-C) or IBS with alternating stool pattern (IBS-A). Symptoms: abdominal pain or discomfort in association with frequent diarrhea or constipation,a feeling of incomplete evacuation, bloating or abdominal distention Etiology: prolonged fever, anxiety, and depression Diagnosis: involves excluding conditions that produce IBS-like symptoms, and then following a procedure to categorize the patient's symptoms. Ruling out parasitic infections, lactose intolerance, small intestinal bacterial overgrowth and celiac disease is recommended for all patients before a diagnosis of irritable bowel syndrome is made. Tests: Stool microscopy and culture Blood tests: Full blood examination, Liver function tests, Erythrocyte sedimentation rate, serological testing for coeliac disease Instrumantel Tests: Abdominal ultrasound ,Endoscopy and biopsies (to exclude peptic ulcer disease, coeliac disease, inflammatory bowel disease, malignancies), Hydrogen breath testing (to exclude fructose and lactose malabsorption) Treatment: Diet, fiber supplementation, Laxatives, Antispasmodics, Tricyclic antidepressants, Serotonin agonists, Serotonin antagonists, Psychotherapy.

70) Acute viral hepatitis:

Acute viral hepatitis is inflammation of the liver caused by infection with one of the five hepatitis viruses. In most people, the inflammation begins suddenly and lasts only a few weeks. Etiology: many different viruses. Hepatitis A is the most common cause, followed by hepatitis B. Blood transfusion, multiple sex, using drug iv. Symptoms: it can cause anything from a minor flu-like illness to fatal liver failure. Sometimes there are no symptoms. Symptoms usually begin suddenly. They include a poor appetite, nausea, vomiting, and often a fever and pain in the upper right of the abdomen. In people who smoke, a distaste for cigarettes is a typical symptom. Typically, after a few days, the urine becomes dark, and jaundice (a yellowish discoloration of the skin and whites of the eyes) develops. Diagnosis: During the physical examination, a doctor presses on the abdomen above the liver, which is tender and somewhat enlarged. Blood tests to evaluate liver function are done. These tests can detect parts of the viruses or specific antibodies produced by the body to fight the viruses. Occasionally, if the diagnosis is unclear, a biopsy is done. Complications: Endogenic hepatic encephalopathy (in fulminant cases, often hepatitis A, B or E); Chronic hepatitis (in infections with B, B and D, and C virus); Chronic persistent hepatitis

Prevention: Vaccines, given by injection into muscle, are available to prevent hepatitis A, B, and E infections. No vaccines against hepatitis C or D virus are available. However,
vaccination against hepatitis B virus also reduces the risk of infection with hepatitis D virus. Other preventive measures: 1. Washing hands thoroughly before handling food 2. Not sharing needles to inject drugs

3. Not sharing toothbrushes, razors, or other items that could get blood on them 4. Practicing safe sexfor example, using barrier protection such as a condom 5. Limiting the number of sex partners Treatment: the initial treatment consists of relieving the symptoms of nausea, vomiting, and abdominal pain. Careful attention should be given to medications which can have adverse effects in patients with abnormal liver function. The patient must abstain from drinking alcohol since alcohol is toxic to the liver.

71) Chronic hepatitis B:

Hepatitis B is an infectious inflammatory illness of the liver caused by the hepatitis B virus. Etiology:The virus is transmitted by exposure to infectious blood or body fluids such as semen and vaginal fluids, while viral DNA has been detected in the saliva, tears, and urine of chronic carriers. Other risk factors for developing HBV infection include working in a healthcare setting, transfusions, and dialysis, acupuncture, tattooing, extended overseas travel and residence in an institution. Symptoms: chronic inflammation of the liver, leading to cirrhosis, increases the incidence of hepatocellular carcinoma, development of Membranous glomerulonephritis. Diagnosis: The tests, called assays, involve serum or blood tests that detect either viral antigens or antibodies. The hepatitis B surface antigen (HBsAg) is most frequently used to screen for the presence of this infection. Shortly after the appearance of the HBsAg, another antigen called hepatitis B e antigen (HBeAg) will appear. Individuals who remain HBsAg positive for at least six months are considered to be hepatitis B carriers. Carriers of the virus may have chronic hepatitis B, which would be reflected by elevated serum alanine aminotransferase (7 - 56 U/L) levels and inflammation of the liver, as revealed by biopsy. PCR tests have been developed to detect and measure the amount of HBV DNA, called the viral load, in clinical specimens. Prevention: Several vaccines have been developed for the prevention of hepatitis B virus infection. The risk of transmission from mother to newborn can be reduced from 2090% to 510% by administering to the newborn hepatitis B vaccine (HBV 1) and hepatitis B immune globulin (HBIG) within 12 hours of birth, followed by a second dose of hepatitis B vaccine (HBV 2) at 12 months and a third dose at and no earlier than 6 months (24 weeks). Treatment:The hepatitis B infection does not usually require treatment because most adults clear the infection spontaneously. On the other hand, treatment of chronic infection may be necessary to reduce the risk of cirrhosis and liver cancer. Chronically infected individuals with persistently elevated serum alanine aminotransferase, a marker of liver damage, and HBV DNA levels are candidates for therapy.Although none of the available drugs can clear the infection, they can stop the virus from replicating,include antiviral drugs lamivudine (Epivir), adefovir (Hepsera), tenofovir (Viread), telbivudine (Tyzeka) and entecavir.

72) Chronic hepatitis C:

Definition:an infectious disease affecting primarily the liver, caused by the hepatitis C virus. Etiology: HCV is spread primarily by blood-to-blood contact associated with intravenous drug use, poorly sterilized medical equipment and transfusions,

Sexual intercourse, Body piercings, Shared personal items Symptoms: fatigue, cirrhosis , hepatocellular carcinoma, portal hypertension, ascites , easy bruising or bleeding, varices, jaundice. Diagnosis: HCV antibody enzyme immunoassay or ELISA, recombinant immunoblot assay, and quantitative HCV RNA polymerase chain reaction (PCR). Liver biopsies are used to determine the degree of liver damage present. Prevent: A combination of harm reductionstrategies, such as the provision of new needles and syringes and treatment of substance use, decrease the risk of hepatitis C. Treatment: Those with chronichepatitis C are advised to avoid alcohol and medications toxic to the liver, and to be vaccinated for hepatitis A and hepatitis B. Ultrasound surveillance for hepatocellular carcinoma is recommended in those with accompanying cirrhosis. The medication is a combination pegylated interferon alpha and the antiviral drug ribavirin for a period of 24 or 48 weeks, depending on HCV genotype.

73) Liver cirrhosis portal hypertension, ascites:

Cirrhosis is scarring of the liver and poor liver function. It is the final phase of chronic liver disease. Causes Hepatitis C infection (long-term infection) Long-term alcohol abuse Autoimmune inflammation of the liver Disorders of the drainage system of the liver, such as primary biliary cirrhosis and primary sclerosing cholangitis Hepatitis B (long-term infection) Medications Metabolic disorders of iron and copper (hemochromatosis and Wilson's disease) Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) Symptoms
1. Confusion or problems thinking 2. Impotence, loss of interest in sex, and breast development in men 3. Loss of appetite 4. Nausea and vomiting 5. Nosebleeds or bleeding gums 6. Pale or clay-colored stools 7. Small, red spider-like blood vessels on the skin 8. Swelling or fluid buildup of the legs (edema) and in the abdomen (ascites) 9. Vomiting blood or blood in stools 10. Weakness 11. Weight loss 12. Yellow color in the skin, mucus membranes, or eyes (jaundice)

Exams and Tests

1. 2. 3. 4. 5. 6.

An enlarged liver or spleen Excess breast tissue Expanded abdomen, as a result of too much fluid Reddened palms Red spider-like blood vessels on the skin Small testicles

7. Widened veins in the abdomen wall 8. Yellow eyes or skin 9. Anemia 10. Clotting problems 11. Liver function problems 12. Low blood albumin 13. Computed tomography (CT) of the abdomen 14. Magnetic resonance imaging (MRI) of the abdomen 15. Endoscopy to check for abnormal veins in the esophagus or stomach 16. Ultrasound of the abdomen

A liver biopsy confirms cirrhosis. Treatment Stop drinking alcohol. Limit salt in the diet. Eat a nutritious diet. Get vaccinated for influenza, hepatitis A and hepatitis B, and pneumococcal pneumonia A procedure called transjugular intrahepatic portosystemic shunt (TIPS) is sometimes needed for bleeding varices or ascites.When cirrhosis progresses to end-stage liver disease, patients may be candidates for a liver transplant. Complications Bleeding disorders Buildup of fluid in the abdomen (ascites) and infection of the fluid Enlarged veins in the esophagus, stomach, or intestines that bleed easily Increased pressure in the blood vessels of the liver (portal hypertension) Kidney failure (hepatorenal syndrome) Liver cancer (hepatocellular carcinoma) Mental confusion, change in the level of consciousness, or coma (hepatic encephalopathy) PORTAL HYPERTENSION:an increase in the blood pressure within a system of veins called the portal venous system. Etiology: cirrhosis of the liver(scarring of a liver injury caused by hepatitis, alcohol abuse) blood clots in the portal vein. Symptoms: Gastrointestinal bleeding: Black, tarry stools or blood in the stools; or vomiting of blood ,Ascites ,Encephalopathy ,Reduced levels of platelets. Diagnosis: based on the presence of ascites or of dilated veins or varices as seen on physical exam of the abdomen or the anus. Various lab tests, X-ray tests, and endoscopic examinations may also be used. Treatment: Endoscopic therapy, Medications (Nonselective beta blockers nadolol or propranolol- to reduce the pressure in varices and further reduce the risk of re-bleeding), Transjugular intrahepatic portosystemic shunt (TIPS). ASCITES:Ascites is excess fluid in the space between the tissues lining the abdomen and abdominal organs (the peritoneal cavity). Causes liver disease, high pressure in the blood vessels of the liver (portal hypertension) and low albumin(3.5 - 5.0 gm/dL) levels, Cirrhosis , Long-term infections with hepatitis C or B and long-term alcohol abuse.

Clots in the veins of the liver (portal vein thrombosis) Congestive heart failure Pancreatitis Thickening and scarring of the sac like covering of the heart Symptoms:When just a small amount of fluid has collected in the belly, there may be no symptoms. As more fluid collects, abdominal pain and bloating may occur. When a large amount of ascites is present shortness of breath may develop. Exams and Tests A physical examination may reveal a swollen abdomen, or belly. Test to evaluate the liver may be done, including: 24-hour urine collection Creatinine and electrolytes Kidney function tests Liver enzyme, bilirubin, coagulation, and serum protein tests Urinalysis Paracentesis or abdominal tap may be performed. This procedure involves using a thin needle to pull fluid from the abdomen. Treatment Diuretics to help remove the fluid; usually, spironolactone (Aldactone) is used first, and then furosemide (Lasix) will be added Antibiotics, if an infection develops Limiting salt in the diet (no more than 1,500 mg/day of sodium) Avoiding drinking alcohol Procedures used for ascites that do not respond to medical treatment include: Placing a tube into the area to remove large volumes of fluid Transjugular intrahepatic portosystemic shunt (TIPS), which helps reroute blood around the liver Patients who develop end-stage liver disease, and whose ascites no longer respond to treatment will need a liver transplant. Possible Complications Spontaneous bacterial peritonitis Hepatorenal syndrome (kidney failure) Weight loss and protein malnutrition Mental confusion, change in the level of alertness, or coma (hepatic encephalopathy) 5. Other complications of liver cirrhosis
1. 2. 3. 4.

74) Liver cirrhosis hepatic encephalopathy and coma:

Cirrhosis is scarring of the liver and poor liver function. It is the final phase of chronic liver disease. Causes Hepatitis C infection (long-term infection) Long-term alcohol abuse Autoimmune inflammation of the liver Disorders of the drainage system of the liver, such as primary biliary cirrhosis and primary sclerosing cholangitis Hepatitis B (long-term infection) Medications Metabolic disorders of iron and copper (hemochromatosis and Wilson's disease) Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) Symptoms

Confusion or problems thinking Impotence, loss of interest in sex, and breast development in men Loss of appetite Nausea and vomiting Nosebleeds or bleeding gums Pale or clay-colored stools Small, red spider-like blood vessels on the skin Swelling or fluid buildup of the legs (edema) and in the abdomen (ascites) Vomiting blood or blood in stools Weakness Weight loss Yellow color in the skin, mucus membranes, or eyes (jaundice) Exams and Tests An enlarged liver or spleen Excess breast tissue Expanded abdomen, as a result of too much fluid Reddened palms Red spider-like blood vessels on the skin Small testicles Widened veins in the abdomen wall Yellow eyes or skin Anemia Clotting problems Liver function problems Low blood albumin Computed tomography (CT) of the abdomen Magnetic resonance imaging (MRI) of the abdomen Endoscopy to check for abnormal veins in the esophagus or stomach Ultrasound of the abdomen A liver biopsy confirms cirrhosis. Treatment Stop drinking alcohol. Limit salt in the diet. Eat a nutritious diet. Get vaccinated for influenza, hepatitis A and hepatitis B, and pneumococcal pneumonia A procedure called transjugular intrahepatic portosystemic shunt (TIPS) is sometimes needed for bleeding varices or ascites.When cirrhosis progresses to end-stage liver disease, patients may be candidates for a liver transplant. Complications Bleeding disorders Buildup of fluid in the abdomen (ascites) and infection of the fluid Enlarged veins in the esophagus, stomach, or intestines that bleed easily Increased pressure in the blood vessels of the liver (portal hypertension) Kidney failure (hepatorenal syndrome) Liver cancer (hepatocellular carcinoma) Mental confusion, change in the level of consciousness, or coma (hepatic encephalopathy) HEPATIC ENCEPHALOPATHY:Hepatic encephalopathy is a worsening of brain function that occurs when the liver is no longer able to remove toxic substances in the blood. Causes:disorders that reduce liver function (such as cirrhosis or hepatitis) and conditions in which blood circulation does not enter the liver. The exact cause of

hepatic encephalopathy is unknown. Hepatic encephalopathy may be triggered by: Dehydration Eating too much protein Bleeding from the intestines, stomach, or esophagus Kidney problems Low oxygen levels in the body Use of medications that suppress the central nervous system (such as barbiturates) Alcohol intoxication Meningitis Metabolic abnormalities such as low blood glucose Subdural hematoma (bleeding under the skull) Wernicke-Korsakoff syndrome

Symptoms Breath with a musty or sweet odor Change in sleep patterns Changes in thinking Confusion that is mild Forgetfulness Poor concentration Worsening of handwriting or loss of other small hand movements Abnormal movements or shaking of hands or arms Disorientation Drowsiness or confusion Inappropriate behavior or severe personality changes Slurred speech

Exams and Tests Coarse, "flapping" shaking of the hands when attempting to hold the arms out in front of the body and lift the hands Abnormal mental status Signs of liver disease, such as yellow skin and eyes and fluid collection in the abdomen (ascites) Tests may include: Complete blood count or hematocrit to check for anemia CT scan of the head or MRI EEG Liver function tests Prothrombin time Serum ammonia levels Sodium level in the blood(135 - 148 mEq/L) Potassium level in the blood(3.5 - 5.5 mEq/L) BUN and creatinine to see how the kidneys are working Treatment:Gastrointestinal bleeding must be stopped. The intestines must be emptied of blood. Infections, kidney failure, and electrolyte abnormalities need to be treated.Lactulose may be given to prevent intestinal bacteria from creating ammonia, and as a laxative to remove blood from the intestines. Neomycin may also be used to reduce ammonia production by intestinal bacteria. Rifaximin, a new antibiotic, is also effective in hepatic encephalopathy. Possible Complications Brain herniation Brain swelling Increased risk of: *Cardiovascular collapse *Kidney failure *Respiratory failure *Sepsis Permanent nervous system damage Progressive, irreversible coma COMA: is a profound or deep state of unconsciousness. The affected individual is alive but is not able to react or respond to life. Etiology: intoxication ,metabolic abnormalities, central nervous system diseases, acute neurologic injuries such as strokes, hypoxia, hypothermia, hypoglycemia, drug poisoning, lack of oxygen, side effects of a stroke,trauma, bleeding, malnutrition, hypothermia or hyperthermia. Symptoms: Generally, a patient who is unable to voluntarily open the eyes, does not have a sleep-wake cycle, is unresponsive in spite of strong tactile, or verbal stimuli and who generally scores between 3 to 8 on the Glasgow Coma Scale is considered to be in coma. It therefore could be a compensatory state in which the body's expenditure of energy is not superfluous. For instance, severe hypoglycemia (low blood sugar) or hypercapnia (increased carbon dioxide levels in the blood) initially cause mild agitation and confusion, but progress to obtundation, stupor and finally complete unconsciousness. Physical examination: Perform basic CPR if person is not breathing or has absent pulse Determine the level of consciousness using the Glasgow com scale Note general skin color - e.g. cyanosis, bruising, jaundice, rashes, hyperpigmentation of Addison's disease

Look for evidence of injury to head Examine for neck stiffness which may indicate meningitis or subarachnoid hemorrhage Look for injection marks signifying drug addicts or diabetics Breath odor may be a feature of alcohol, diabetes, kidney or liver failure Temperature - if fever suggests severe infection; if low temperature consider hypothyroidism. Blood pressure - if low may suggest shock due to blood loss, dehydration, anaphylaxis, heart failure or septicemia. Examine heart and lungs for signs of disease Examine abdomen for tenderness and masses Look for papilledema (swelling of the optic disc) - would indicate brain tumor, brain abscess or subdural haematoma. Blood tests: Full blood count ESR (Female: 1-25 mm/hr, Male: 0-17 mm/hr) Electrolytes and kidney function tests Blood sugar (before meals hover around 70 to 80 mg/dL) Liver function tests Thyroid function tests Pregnancy test Serum cortisol Blood alcohol Urine tests: Urinalysis Urine microscopy and culture Urine drug screen Electrocardiograph Radiological investigations CT scan of brain Treatment: hospitals usually place comatose patients in an Intensive Care Unit immediately. In the ICU, the hospital monitors a patients breathing and brain activity through CT scans. Attention must first be directed to maintaining the patient's respiration and circulation, using intubation and ventilation, administration of intravenous fluids. The nursing staff will move the patient every 23 hours from side to side and depending on the state of consciousness sometimes to a chair. The goal is to move the patient as much as possible to try to avoid bedsores, atelectasis and pneumonia. Pneumonia can occur from the persons inability to swallow leading to aspiration, lack of gag reflex or from feeding tube.Medicine may be given to calm the patients. Inducing hypothermia on comatose patients provides one of the main treatments for patients after suffering from cardiac arrest. In this treatment, medical personal expose patients to external or intravascular cooling at 3234 C for 24 h.; this treatment cools patients down about 2-3 C less than normal body temperature.

75) Primary hepatic cancer:

Primary liver cancer means that the cancer started in the liver. It occurs most commonly in people over 65 years. There are different types of primary liver cancer: Hepatoma. This is the most common type. It is sometimes called hepatocellular carcinoma. This type of cancer originates from a hepatocyte which becomes cancerous. Fibrolamellar hepatoma develops in a liver which was previously healthy. Cholangiocarcinoma develops from cells which line the bile duct.

Hepatoblastoma is a very rare cancer which occurs in some young children. Angiosarcoma develops from cells of blood vessels within the liver. Etiology:A cancerous tumour starts from one abnormal cell. The exact reason why a cell becomes cancerous is unclear. It is thought that something damages or alters certain genes in the cell. Most people who develop a primary liver cancer have one or more of the following 'risk factors' which seem to make liver cells more prone to becoming cancerous: Cirrhosis. Long-term infection with the hepatitis B or C virus Ingesting some poisons or toxins. Some conditions which cause persistent inflammation of the gut increase the risk slightly of developing a cholangiocarcinoma smoking can increase the risk of developing primary liver cancer Symptoms:There may be no symptoms in the early stage of the disease. As the cancer grows, the symptoms are feeling generally unwell, feeling sick, loss of appetite, weight loss and tiredness. Many people who develop primary liver cancer will already have symptoms associated with cirrhosis. As the cancer develops further, symptoms include:
1. 2. 3. 4.

Abdominal pain over the liver area. Jaundice. Itch Swelling of the abdomen.

Diagnosis: Initial assessment Assess the stage of the cancer. That is, how much of the liver is affected and whether the cancer has spread to other parts of the body. Assess the state of your liver function and your general health. Scans such as ultrasound scan, CT scan or MRI scan can help to show the exact location and extent of the cancer. A liver biopsy is usually done to confirm the type of cancer. Blood tests help to assess the liver function and your general health. Treatment: Surgery:If the cancer is small, has not spread outside the liver, and the rest of the liver is healthy, then it may be possible to cut out the part of the liver which contains the cancer. A liver transplant is another option. Surgery also has a role in palliative care. For example, if jaundice is severe, it may be possible to relieve the blockage of the bile by inserting a 'stent'. This is a narrow tube which allows the bile to drain into the gut. Chemotherapy:Chemotherapy is a treatment which uses anti-cancer drugs to kill cancer cells, or to stop them from multiplying. It is not likely to be curative for primary liver cancer, but may shrink the tumour down to slow the progression of the disease.

76-Cholelithiasis Cholelithiasis Definition metabolite disease characterized with formation of stones in the gall bladder or/and the bile ducts; Etiology and pathogenesis

The change in the compositions of the bile is the main factor responsible for the formation of the stones; it is due either to changed ratio of its usual ingredients (increased level of cholesterol and decreased level of phospholipids and bile acids) or appearance of substances alien to the bile (indirect bilirubin or calcium); the condition is called dyscoloidocholia; Predisposition factors due to increased level of cholesterol hereditary hypercholesterolemia, diabetes, hypothyroidism, treatment with hormonal contraceptive drugs and other causes of increased level of estrogen; impaired metabolism of cholesterol in the liver due to hereditary enzyme deficiency (cholesterol-7alpha- hydroxilase participating in the synthesis of bile acids) or consequence of hepatitis and cirrhosis; obesity and female sex may be also included in this group; Indirect bilrirubin in the bile hemolytic anemia, Gilberts disease; Increased level of calcium hyperparathyroidism; Additional predisposition factors Obstructed drainage of the gall bladder or the bile ducts (dyskinesia, atonia, stenosis, etc.); Chronic cholecystitis; Type of stones cholesterol, bilirubin, mixed; Clinical forms and symptoms 1 Latent form no symptoms; the stone is discovered accidentally by abdominal ultrasound or on X ray; 2 Dyspeptic form the main symptoms are nausea, sometimes vomiting, biter taste in the mouth, heaviness or dull pain in the right hypogastria, usually provoked by fatty and fried food, eggs, chocolate, coffee, alcohol, meteorism; 3 Biliary colic (gallstone attack, when the stone is obstructing ductus cysticus or ductus choledochus known as common bile duct) severe pain in the right hypogastria propagating toward the back and the right shoulder (the attack often occurs in the night), nausea, vomiting of green fluid (bile) with biter taste; brownish urine and jaundice (if ductus choledochus is obstructed), possible intermittent fever even without concomitant infection; the colic is caused by the same provoking factors to which must be included stress; Physical examination of patient with bile colic Impaired general condition; possible icter or subicter; tongue with white surface; possible fever and tachycardia; palpation severe pain in the right hypogastria, but without signs of peritoneal irritation; usually slightly enlarged and tender liver; signs of predisposition factors female, obesity, cholesterol skin deposits (xantomas or xantelasmas); Lab tests Blood count possibly slightly increased WBC (even without infection) but normal sedimentation rate; Often increased liver enzymes; usually ASAT and ALAT (reactive hepatitis) and also GGT, AP, direct bilirubin (cholestsis); For possible pancreatitis as complication an alpha-amylase test is also required; In the urine possible increase of urobilinogen and presence of direct bilirubin in patient with choledocholithiasis; Lab tests for predisposition factors cholesterol, calcium, etc; Instrumental tests During bile colic abdominal ultrasound enlarged ductus cysticus or d. choledochus, or the stone or stones may be seen; the lever is also enlarged and there may be changes in the pancreatic gland; Radiology the stones may be seen on native X ray, however cholecystography with contrast is usually performed; in patients with choledocholithiasis ERCP (endoscpic retrograde cholangiocholecystopancreatography) or MRI (MRCP) are required (in patient with cholestasis

and increased levels of bilirubin the ordinary cholangiocholecystography with contrast is contraindicated); Complications Acute or chronic cholecystitis; Cholestatic icter in patients with choledocholithiasis; Hydrops of the gall bladder (when the stone is in ductus cysticus and the bile is moving only in one direction, into the gall bladder, causing its enlargement); Reactive hepatitis or/and pancreatitis; Very rare perforation of the gall bladder with biliar peritonitis; Cancer of the gall bladder;
Choledocholithiasis is the presence of at least one gallstone in the common bile duct. The stone may be made up of bile pigments or calcium and cholesterol salts. Causes :About 15% of people with gallstones will develop stones in the common bile duct, the small tube that carries bile from the gallbladder to the intestine.Risk factors include a history of gallstones. However, choledocholithiasis can occur in people who have had their gallbladder removed. Symptoms : Symptoms usually do not occur unless the stone blocks the common bile duct. Symptoms that may occur include: Abdominal pain in the right upper or middle upper abdomen that may: +Be steady +Be sharp, cramping, or dull +Spread to the back or below the right shoulder blade Fever Loss of appetite Jaundice (yellowing of skin and whites of eyes) Nausea andvomiting Lab Tests:Bilirubin,Complete blood count (CBC),Liver function tests,Pancreatic enzymes Instrumental Tests: Tests that show the location of stones in the bile duct include the following: Abdominal CT scan Abdominal ultrasound Endoscopic retrograde cholangiography (ERCP) Endoscopic ultrasound Magnetic resonance cholangiopancreatography (MRCP) Percutaneous transhepatic cholangiogram (PTCA) Complications:Biliary cirrhosis,Cholangitis,Pancreatitis

77) Jaundice:
Jaundice is a yellow color of the skin, mucus membranes, or eyes. The yellow coloring comes from bilirubin, a byproduct of old red blood cells. Causes: Too many red blood cells are dying or breaking down and going to the liver The liver is overloaded or damaged The bilirubin from the liver is unable to move through the digestive tract properly Acute hepatitis Obstruction of the bile ducts, Gallstones Hemolytic anemia Gilbert's syndrome Cirrhosis Cancer of the pancreas Symptoms:Jaundice may appear suddenly or develop slowly over time. Yellow skin and the white part of the eyes - when jaundice is more severe, these

areas may look brown Yellow color inside the mouth Dark or brown-colored urine light-colored stools itching of the skin Other symptoms depend on the disorder causing the jaundice: Cancers may produce no symptoms, or there may be fatigue, weight loss, or other symptoms Hepatitis may produce nausea, vomiting, fatigue, or other symptoms Exams and Tests:physical exam may reveal liver swelling.

A bilirubin blood test will be done.

Hepatitis virus panel to look for infection of the liver Liver function tests to determine how well the liver is working Complete blood count to check for low blood count or anemia Abdominal ultrasound Abdominal CT scan Endoscopic retrograde cholangiopancreatography (ERCP) Percutaneous transhepatic cholangiogram (PTCA) Liver biopsy Cholesterol level(Less than 200 mg/dL desirable) Prothrombin time Treatment:Treatment depends on the cause of the underlying condition leading to jaundice.Treatment may consist of expectant management (watchful waiting) at home with rest. Medical treatment with intravenous fluids, medications, antibiotics, or blood transfusions may be required.If a drug/toxin is the cause, these must be discontinued. In certain cases of newborn jaundice, exposing the baby to special colored lights or exchange blood transfusions may be required to decrease elevated bilirubin levels. Surgical treatment may be required.

78-)Cholecystitis Definition acute or chronic inflammation of the gall bladder and eventually the bile ducts (cholangitis, choledochitis); Etiology Usually bacterial (from the intestinal flora) E. coli, Enterobacter, Klebsiela, etc; Protozoa Lamblia intestinalis; Predisposition factors Obstructed drainage of the bile; Stones in the gall bladder; Chronic colitis, ulcer, pyelonephritis or other infections; Diabetes or other diseases or conditions causing decrease of immunity; Acute cholecystitis Symptoms Harsh pain in the right hypogastria often propagating toward the back and the right shoulder; High fever usually with shivers; Nausea and vomiting; Fatigue, exhaustion, loss of appetite; Often jaundice and brownish urine; Physical examination Impaired general condition, possible compelled position in bed, fever often with facies febrilis, usually icter; tongue with white surface; tachycardia, possibly hypotension;

Palpation severe pain in the right hypogastria but without symptoms of peritoneal irritation; usually enlarged and tender liver; Lab tests increased WBC and especially neutrophil granulocytes; increased sedimentation rate and CRP; usually increased ASAT, ALAT, bilirubil; possible elevation of GGT, AP, alphaamylase; Urine elevated urobilinogen, presence of direct bilirubin in patients with cholestasis; In some cases blood culture may be required; Instrumental tests Abdominal ultrasound and in some cases CT scan or MRI; specific for acute cholecystitis is thickening (more than 3 mm) and doubling of the gall bladders wall; Complications Phlegmon of the gall bladder or/and sepsis; Perforation of the gall bladder and peritonitis; Fistula toward the small intestine; Cholangiohepatitis; Acute pancreatitis; Chronic cholecystitis; Chronic cholecystitis Symptoms Dull pain or heaviness in the right hypogastria; usually subfebrile temperature; nausea, fatigue, loss of appetite, possible brownish urine but jaundice is rare; Physical examination Palpation - positive sign of Murphy indicating pain in the right hypogastria during inhaling; possibly n. phrenicus sign (increased sensitivity in the right side during palpation between the two branches of m. sternocleidomastoideus); often enlarged liver; the general condition is usually satisfactory, often subfebrile temperature but jaundice is rare; Lab tests Possibly slightly increased WBC, elevated sedimentation rate; liver enzymes, bilirubin, alphaamylase and urine have to be checked; Instrumental tests Specific test for diagnosis is duodenal intubation with investigation of the three types of bile fluid (A from the bile duct, B from the gall bladder, C from the liver) for culture, microscopy for Lamblia (Lamblia cysts may be found in the feces); and cytology for leukocytes and tumor cells; Abdominal ultrasound - visualization of thickened wall of the gall bladder; changes in the liver and the pancreatic gland are often found; Cholangiocholecystography or CT may also be performed; Complications Chronic hepatitis; Acute or chronic pancreatitis; Cholelithiasis; Cancer of the gall bladder; Development of peritonitis is possible during exacerbation; 79 Acute pancreatitis
Definition acute or chronic inflammation of the pancreatic gland; Acute pancreatitis Etiology and pathogenesis The main pathogenic factor is the premature activation of the pancreatic enzymes (trypsinogen, chymotrypsinogen, lipase, amylase, maltase, which are normally activated in the duodenum) in the gland, which is severely damaged by them; they

cause auto-digestion of the gland with congestion, hemorrhagic and necrotic lesions; Provoking factors Penetration of non-conjugated bile salts and lisolecitin into the gland usually caused by increased pressure in the bile ducts and bacterial metabolism (E. coli); Toxicity, mainly by alcohol or drugs (steroids, sulfonamides, diuretics), causing inflammation and edema of the gland and premature activation of the enzymes; Infection viral or bacterial (mumps, Coxsackie virus, Mycoplasma pneumoniae); Inflammation of adjacent organs mainly cholecystitis or penetration of duodenal ulcer; Abdominal trauma; Symptoms Severe pain in the epigastria, with encircling propagation toward both hypogastria and the back but mostly on the left side; Nausea and vomiting; Fever, possibly with rigors; Severe weakness and possibly shock; Appearance of jaundice is frequent; Physical examination Severely impaired general condition; possibly compelled (embryonic or sitting) position; pale and sweating skin, possibly with subicter or icter; tongue with white surface; Tachycardia and low blood pressure possibly even under 70/40 (shock); Harsh pain in the upper part of the abdomen, mainly in the epigastria but without signs of peritoneal irritation; liver is often enlarged and tender; In rare cases small ascites and left side hydrothorax may also be found; Lab tests Elevated WBC, sedimentation rate, CRP; Specific for the diagnosis are the increased levels of alpha-amylase, lipase and decreased level of calcium; blood sugar is usually slightly elevated and glycosuria is often present; Decreased levels of HB, Ht, RBC, total protein and albumin are common; Liver enzymes and bilirubin are usually elevated as is the urobilinogen in the urine; Measurement of creatinine, potassium and sodium are also required; Instrumental tests Abdominal ultrasound edema of the pancreatic gland, a small volume of mobile fluid in the abdominal cavity may also be found as in the left pleural cavity on X ray; In severe cases MRI or CT may be required; Complications Peritonitis; Sepsis and shock and acute renal failure; Relapsing pancreatitis (repeated episodes of acute pancreatitis with somewhat milder symptoms); Chronic pancreatitis;

80-)Chronic pancreatitis
Etiology and pathogenesis fibrous changes in the gland possibly with formation of pseudocystsosis causing impairment of its exocrine and eventually endocrine functions; Etiological factors Acute or relapsing pancreatitis; Factors causing primary chronic pancreatitis;

Toxicity alcoholism; drugs; Metabolite and hormonal disorders - hypercholesterolemia; hyperparathyroidism; Infections of adjacent organs usually chronic cholecystitis; Cystic fibrosis; Idiopathic; Symptoms The exocrine insufficiency is causing malabsorption syndrome with diarrhea (soft stinking stool with steatorrhoea and cratorrhoea), heaviness in the abdomen, meteorism, flatulence, fatigue, weakness; the symptoms are exacerbated by fatty food and alcohol; its consequences are loss of weight, hypoproteinemia often with edema, anemia; The exocrine insufficiency is causing diabetes usually in mild form; Pain in the epigastria and the left hypogastria, propagating toward the back may also be present (provoked by fatty food, alcohol, etc), usually in patients with pseudocystosis which also may have jaundice; Physical examination The skin may be pale or with subicter (icter is rare), often dry with reduced turgor; rhagadas at the mouths angles, possible aphtous stomatitis and heilitis, tongue often with white surface; Reduced bodyweight and possible edema (usually swollen legs); Palpation positive signs of Grot, indicating pain in the left hypogastria, laterally of m. rectus abdominis; possibly reduced obesity in the left paraumbilical region; the liver may also be slightly enlarged; Lab tests Possibly reduced levels of HB, RBC, Ht, iron; slightly increased sedimentation rate; decreased total protein and albumin; liver enzymes and bilirubin may be elevated; blood sugar is increased in patients with secondary diabetes; cholesterol, calcium, potassium and sodium must also be checked; amylase is rarely slightly elevated; Specific for the diagnosis is stool tests for steatorrhea and creatorrhea; Instrumental tests Abdominal ultrasound diffuse structural changes in the pancreatic gland, possibly with pseudocystosis and calcifications; in the later case CT scan is often required; Secretin stimulation test, PABA test or triolein test may be performed to evaluate the exocrine function of the gland (the first measures the secretion of sodium bicarbonate and enzymes from the gland after stimulation and requires duodenal intubation); Complications Pseudocystosis; Pancreatic cancer; painless jaundice is the main symptom when the tumor is localized in the head of the gland with witching, hemorrhagic diathesis and palpation of the enlarged gall bladder (Curvoisiers sign); pain and often feeling of fear are the main symptoms when the tumor develops in the tail of the gland; Chronic hepatitis;

81-) Pancreatic cancer

Pancreatic cancer begins in the tissues of your pancreas an organ in your abdomen that lies horizontally behind the lower part of your stomach. Your pancreas secretes enzymes that aid digestion and hormones that help regulate the metabolism of sugars.Pancreatic cancer often has a poor prognosis, even when diagnosed early. Pancreatic cancer typically spreads rapidly and is seldom detected in its early stages, which is a major reason why it's a leading cause of cancer death. Signs and symptoms may not appear until pancreatic cancer is quite advanced and surgical removal isn't possible.

How pancreatic cancer forms Pancreatic cancer occurs when cells in your pancreas develop mutations in their DNA. These mutations cause cells to grow uncontrollably and to continue living after normal cells would die. These accumulating cells can form a tumor.Most pancreatic cancer begins in the cells that line the ducts of the pancreas. This type of cancer is called pancreatic adenocarcinoma or pancreatic exocrine cancer.Rarely, cancer can form in the hormone-producing cells of the pancreas. This type of cancer is called islet cell cancer or pancreatic endocrine cancer. Factors that may increase your risk of pancreatic cancer include: Being African-American,Being overweight or obese,Chronic inflammation of the pancreas (pancreatitis),Diabetes,Family history of genetic syndromes that can increase cancer risk, including a BRCA2 gene mutation, Lynch syndrome and familial atypical mole-malignant melanoma (FAMMM),Personal or family history of pancreatic cancer,Smoking. Sympthoms :Upper abdominal pain that may radiate to your back,Yellowing of your skin and the whites of your eyes (jaundice),Loss of appetite,Weight loss,Depression,Blood clots... Physical Examination : During the physical exam, the doctor will typically:Check for signs of disease, such as lumps or anything else that seems unusual.Check for ascites (an abnormal buildup of fluid in the abdomen).Examine the skin and the eyes for signs of jaundice. The medical history will entail an assessment of the patient's health habits, medical conditions, and a family history of any medical conditions, past illnesses, and treatments. Lab Tests :Unfortunately, there are no laboratory tests available for the early detection or diagnosis of pancreatic cancer. Diagnosis is usually made after the cancer has already spread, using imaging tests and biopsy.Laboratory tests that may be abnormal but are not diagnostic of pancreatic cancer include: Amylase: the blood level of amylase is usually significantly elevated Comprehensive metabolic panel: a group of tests that may be used to evaluate why someone is jaundiced, to detect elevated levels of bilirubin and liver enzymes, and to monitor liver and kidney function CA 19-9 (Cancer Antigen 19-9): a tumor marker for pancreatic cancer; it may be used to monitor for cancer recurrence but is not useful for detection or diagnosis CEA (Carcinoembryonic antigen): a tumor marker used as a monitoring tool Other tests, such as fecal fat, stool trypsin, trypsinogen, and lipase, may be ordered to help evaluate how well the pancreas is functioning and to determine whether pancreatic enzyme supplementation is necessary. Instrumental Tests : Computed tomography (CT) scan: useful for detecting pancreatic masses and checking for metastasized cancer Biopsy: used to confirm diagnosis of cancer, often in conjunction with CT scan Endoscopic retrograde cholangiopancreatography (ERCP): a test that uses a flexible scope inserted through the mouth and threaded through the esophagus to allow the pancreas to be examined; may be used to introduce a dye for X-rays or to place a stent (a metal or plastic tube that can help keep a duct open and functioning) Transabdominal ultrasound Magnetic resonance cholangiopancreatography (MRCP): a type of magnetic resonance imaging (MRI) used to see the pancreas, its ducts, and the bile ducts more clearly; often used before or instead of ERCP. Stages of pancreatic cancer Using information from staging tests, your doctor assigns your pancreatic cancer a

stage. Stage I. Cancer is confined to the pancreas. Stage II. Cancer has spread beyond the pancreas to nearby tissues and organs and may have spread to the lymph nodes. Stage III. Cancer has spread beyond the pancreas to the major blood vessels around the pancreas and may have spread to the lymph nodes. Stage IV. Cancer has spread to distant sites beyond the pancreas, such as the liver, lungs and the lining that surrounds your abdominal organs (peritoneum). Complications : Jaundice. Pancreatic cancer that blocks the liver's bile duct can cause jaundice. Signs include yellow skin and eyes, dark-colored urine, and pale-colored stools. Pain. A growing tumor may press on nerves in your abdomen, causing pain that can become severe. Pain medications can help you feel more comfortable Bowel obstruction. Pancreatic cancer that grows into or presses on the small intestine (duodenum) can block the flow of digested food from your stomach into your intestines. Weight loss. A number of factors may cause weight loss in people with pancreatic cancer. Nausea

82 -)Iron deficiency anemia

Definition lack of iron or inability to be used in erythropoiesis causing reduced synthesis of hemoglobin; Etiology and pathogenesis Absolutely (babies which after the third month are still fed only by milk but not with fruit and vegetable juice) and diet without meat and vegetables; or relatively insufficient intake of iron (pregnancy, lactation, etc); Reduced absorption of iron on two levels Atrophy of the stomachs mucosa or resection of the stomach; the result is hypoacidity or achlorhydria causing reduced absorption of iron (the hydrochloric acid transforms the bivalent iron from the food into trivalent and so it can be absorbed by the intestinal mucosa); Chronic diarrhea (chronic enterocolitis, chronic pancreatitis, gluten enteropathy (celiac disease), etc) causing reduced absorption of the iron in the small intestine; Sideroachrestic anemia conditions in which the iron is used by tumor or inflammatory cells and in the bone marrow for synthesis of hemoglobin (tumors, tuberculosis and other chronic infectious diseases, autoimmune diseases, etc; Increased loss of iron acute or chronic hemorrhage (ulcer, erosive gastritis, hypermenorrhea (excessive menstruation) or metrorrhagia, epistaxis, etc), some types of parasite infections (Ankylostoma duodenale); Loss of iron transporting proteins (transferin) nephrotic syndrome; Symptoms - typical for all forms of anemia Fatigue, easy tiredness, tachycardia, headache, noise in the ears, vertigo; Symptoms of the main disease causing the anemia bleeding, inflammation, tumors, etc; Physical examination Pale skin and visible mucosa; possible ulcerations (ragadas) at he mouths angles (angular stomatitis); possible polished tongue in patients with atrophic gastritis; often changes in the nails (koilonychia), Heart tachycardia, systolic murmur at the apex, Signs of bleeding or of the main disease causing the anemia; Lab tests

Blood count - reduced levels of HB (mainly), erythrocytes, and Ht, with low mean corpuscular volume (MCV) and mean corpuscular hemoglobin concentration (MCHC); however the WBC and platelets are usually normal; On a smear microcytosis, (small erythrocytes) and hypochromia (less colored because they contain less hemoglobin; in severe cases anulocytes (erythrocytes whose hemoglobin is spread only in the periphery in a shape of a ring); Reduced iron; the iron binding capacity is increased in anemia due to decreased intake and absorption or increased loss; it is normal or even elevated in patients with sideroachrestic anemia (chronic inflammation, tumor, etc); Reticulocytes (young erythrocytes) are low; Slightly increased sedimentation rate, the higher values are determined by the main disease causing the anemia; Test for occult bleeding in the stool; Test for establishing the primary disease; Instrumental tests usually directed to establish the etiology (gastroscopy, colonoscopy, etc); Complications All types of anemia cause exacerbation of ischemic heart disease, cardiac or respiratory failure, cerebral atherosclerosis, etc;

83 -)Vitamin B 12 and folic acid deficiency anemia

Definition anemia caused by lack of vitamin B 12 (and folic acid) leading to impaired DNA replication and mitosis of the hemopoietic cells (erythroblasts, myelocytes, megacaryocytes which are bigger than usual), epithelial and neuroepithelial cells; it cause also peripheral neuropathy and dorsal and lateral spinal column degeneration (funicular myelosis); Etiology and pathogenesis Absolutely (insufficient intake of meat) or relatively (pregnancy, lactation, etc) reduced intake of vitamin B12; Decreased absorption of vitamin B 12 on two levels; Autoimmune gastritis (pernicious anemia with autoantibodies against the parietal gastric cells producing intrinsic factor or against the intrinsic factor itself; the later facilitates the absorption of vitamin B 12 by the intestinal mucosa and protects it from the local bacterial flora; chronic atrophic gastritis or resection of the stomach; Lack of pancreatic enzymes (chronic pancreatitis); Chronic diarrhea and inflammatory bowel disease; Vitamin B 12 achrestic anemia increased use of vitamin B 12 by tumor or inflammatory cells; Increased loss of vitamin B 12 caused by a intestinal parasite Diphyllobothrium latum; Drugs purine analogs (6-mercaptopurine, acyclovir), pyrimidine analogs (5fluorouracil), metformin, etc, Symptoms Besides the typical symptoms of the iron deficiency anemia these patients have also burning of the tongue (due to Hunters glossitis), dysphagia (difficulty, sometimes pain (odynophagia) during swallowing), paraesthesiae (spontaneous sensations of pinching, shivering, etc) of the limbs, ataxia, lose proprioceptive and vibratory senses, depression, loss of memory, psychosis; Symptoms from the primary disease causing the anemia; Physical examination Pale skin often with subicter (because the megalocytes are easily destructed in the spleen, which leads to increase of the non-conjugated bilirubin); polished tongue (Hunters glossitis); tachycardia and systolic murmur at the apex are also present, change in the sensitivity of the limbs, etc;

Lab tests Blood count - reduced levels of HB, erythrocytes (mainly) and Ht, but MCV and MCHC are increased: leukocytes and platelets are also reduced; Decreased reticulocytes; On a smear megalocytosis with normochromia (large erythrocytes with normal hemoglobin load); large granulocytes with hypersegmentation of the nucleus; Slightly increased iron and non-conjugated bilirubin and LDH due to hemolysis; as is the urobilinogen in the urine; Decreased plasma level of vitamin B 12 and often of folic acid; Slightly increased sedimentation rate; Instrumental tests Gastroscopy is usually required; Other tests depend on the primary disease; Smear of bone marrow (with aspiration biopsy) is often performed showing megaloblastic erythropesis with hypercellularity and erythroid hyperplasia; Complications Cancer of the stomach; Funicular myelosis; Exacerbation of cardiovascular, brain and pulmonary diseases as in the other forms of anemia);

84-) Acute leukemia

Definition malignant disease in which a cell clone from the myeloid, lymphoid or erythroblast chain in the bone marrow becomes malignant; it has accelerated reproduction and proliferates, suppressing the growth of the normal hemopoiesis in the bone marrow and spreads like metastases in different organs and tissues; Classification: acute myeloid leukemia M0 - undifferentiated leukemia; M1 myeloblastic without differentiation; M2 - myeloblastic with differentiation; M3 promyelocytic; M4 myelomonocytic; M5 - monoblastic leukemia; M6 erythroleukemia; M7 - megakaryoblastic leukemia; other types - acute lymphoblastic leukemia (B cell or T cell); Acute (blastic) leukemia is a malignant (clonal) disease of the bone marrow in which early lymphoid or myeloid precursors proliferate and replace the normal hematopoietic cells of the marrow; they may be distinguished from other malignant lymphoid and myeloid disorders by the immunophenotype of the cells, which is similar to B- or T-precursor cells; immunochemistry, cytochemistry, and cytogenetic markers may also aid in categorizing the malignant lymphoid clone. The malignant cells of acute lymphoblastic and myelogenous leukemia are lymphoid and myeloid precursor cells (ie, lymphoblasts and myeloblasts) that are arrested in an early stage of development; Etiology unclear; several existing theories genetic (due to chromosomal abnormalities - an abnormal expression of genes, often as a result of chromosomal translocations) Down syndrome, Fanconi anemia, etc, infectious (Epstein-Bar virus responsible for lymphoblast leukemia and Hodgkin disease); radioactive or other types of toxicity including cytostatic drugs; for the acute myeloid leukemia specific factors are antecedent hematologic disorders as myelodisplastic syndrome (which manifests with progressive cytopenia), aplastic anemia, myelofibrosis, paroxysmal nocturnal hemoglobinuria and polycythemia vera; Pathogenesis the malignant cell branch spread uncontrolled in the bone marrow suppressing the growth of the normal cells from the myeloid, erythroblast and megacariocyte (thrombocyte) chains; the result is refractory to treatment aplastic anemia; hemorrhagic diathesis due to thrombocytopenia; frequent serious infections due to hypo- or agranulocytosis (the malignant myeloid cells can not perform the protective functions of the normal leukocytes); the other symptoms

are caused by spreading of malignant cells infiltrates like metastases in different tissues and organs; Symptoms The two main initial symptoms of the disease are fatigue and exhaustion, due to refractory to treatment anemia and infection (usually pneumonia or other respiratory infection) with fever, etc; (fever may be present without active infection); Additional symptoms may be bleeding (from the gums, epistaxis, etc), pain in the joints and the bones (usually at rest, in the night); enlargement of the lymphatic nodes (in cases with lymphoblastic leukemia) with shortness of breath when the mediastium is engaged; loss of appetite and bodyweight; headache and other symptoms due leukemic infiltrates damaging the central nervous system; Physical examination Usually impaired general condition; wax-like pallor of the skin and the visible mucosa; possible hemorrhagic rush (petechiae, ecchymoses, hematoma, etc) or leukemids (skin infiltrates of leukemic cells); enlarged lymphatic nodes and possibly spleen in patients with lymphoblastic leukemia; possibly enlarged liver and spleen in patients with myeloid leukemia; Lab tests Blood count normocyte, normochrome anemia, the number of the WBC may be increased, reduced or even normal, but neutropenia (decreased number of neutrophil granulocytes is always present; the number of platelets is often increased in the early stages, and reduced later; Blood smear specific for the diagnosis is the presence of blast cell (atypical leukocytes originated from some malignized cell from the myeloid, lymphoid, erythroblast or magacaryocyte hemepoietic chains); sometimes these cells are so deformed that it is impossible to determine their origin; in such cases cytochemical test are required (by measuring the different enzymes (AP of granulocytes, esterase, etc) in the blast cells could be established the level of their maturation and so the original cell which had malignant transformation); often hiatus leukemikus phenomenon is found (paraleukoblasts and matured leukocytes are found but not the intermediary forms); Additional tests increased sedimentation rate, CRP, LDH, uric acid due to cell destruction, often liver enzymes (ASAT, ALAT, GGT, AP); Instrumental tests Specific for the diagnosis is smear from the bone marrow (obtained by bone marrow aspiration and biopsy with different type of staining, cytometric and cytogenetic tests) it presents invasion of blast cells which are suppressing the normal erythropoiesis, granulocytopoiesis and thrombocytopoiesis; Abdominal ultrasound, CAT, X ray of the chest may be useful to establish enlargement of liver, spleen and lymphatic nodes or infiltrates and tumor masses in the lungs and mediastinum; In cases with neurological symptoms cytological examination of spinal fluid is required (the fluid is obtained by lumbar punction) and sometimes ophthalmoscopy for leukemic infiltrates; Complications Vulnerability to infections, sepsis; Hemorrhage (gastrointestinal, gynecological, etc); Disseminated intravascular coagulation syndrome; Brain damage due to leukemic infiltration or increased intracranial pressure;

85- Chronic myeloid leukemia

Definition myeloproliferative disorder with increased uncontrolled proliferation of the granulocytic cell line without the loss of their capacity to differentiate; it

suppress the other cell lines (erythrocyte and thrombocyte) in the bone marrow and causes even extramedular hemopoiesis; Etiology often the cause is radiation, other possible cause toxicity (benzene); there is an acquired abnormality of the hematopoietic stem cell. It is characterized by a cytogenetic aberration consisting of a reciprocal translocation between the long arms of chromosomes 22 and 9; The translocation results in a shortened chromosome 22 (Philadelphia (Ph1) chromosome);. This translocation relocates an oncogene from the long arm of chromosome 9 to a specific breakpoint cluster region in the long arm of chromosome 22; Pathogenesis The uncontrolled proliferation of the myeloid cell branch is suppressing at first the erythropoiesis, causing anemia, and later the thrombocytopoiesis, causing hemorrhagic diathesis; The myeloid cell proliferation spreads to other organs, including, liver, spleen, etc; The excessive number of myeloid cells in the circulations is predisposition for thrombosis and thrombembolism; Symptoms The disease has three stages chronic, accelerated and blastic (leukemic); the first symptoms usually are fatigue and easy tiredness due to aplastic anemia; and heaviness in the abdomen caused by excessive enlargement of liver and spleen; thrombotic and thromembolic incidents may also be among the first symptoms (including pain in the left hypogastria due to infarction of the spleen); fever and sweating, loss of appetite and body weight, pain in bones and joints are also possible; hemorrhagic diathesis or symptoms from other organs (due to infiltration) appear in the later stages of the disease; Physical examination At the early stages the general condition is satisfactory; possible pallor due to anemia, leukemids on the skin; specific for the diagnosis is the excessive hepatosplenomegalia; in case of infarction of the spleen, the organ is painful and perisplenal friction rub may be detected; signs of leukostasis; Lab tests Blood count excessive elevation of WBC, usually over 100 000 or 150 000; reduced RBC (normocrome and normocyte anemia); elevated platelets in the early stages, decreased in the late stages; Blood smear specific for the diagnosis is the presence of all immature forms of myeloid cells (down to myeloblasts) in the peripheral blood so it looks like smear from bone marrow; the enzyme test shows severely reduced AP of the granulocytes which may reach 0; Genetic tests may show (in over 90%) the presence of damaged 22nd chromosome, called Philadelphian chromosome also specific for the diagnosis; Increased sedimentation rate, CRP, LDH; The liver enzymes may be elevated; Instrumental tests Smear from bone marrow shows increased myelopoiesis and reduced erythro- and megacaryocytopoiesis; increased ration myeloid cell to erythroblast cell to 7-8:1, normally 3-4:1; Abdominal ultrasound enlarged liver and spleen; Ophtalmoscopy may show papilledema and hemorrhages; Complications Blast crisis in which the chronic myeloid leukemia is transformed in some type of myeloblast leukemia; Thrombosis and thrombembolism (lungs, spleen, etc);

Hemorrhage and severe infections are not so common as in blast leukemia (the platelets are reduced only in the late stages of the disease and the granulocytes still can perform their protective functions against microorganisms);

86- Chronic lymphoid leukemia

Definition is a monoclonal disorder characterized by uncontrolled proliferation of functionally incompetent lymphocytes which suppress the other lines of hemopoiesis; Classification chronic B-cell (including hairy-cell leukemia) and chronic T-cell leukemia; Etiology possible persistent Epstein-Bar virus infection or other factors causing chromosome anomalies; Pathogenesis the uncontrolled proliferation of clonal B cells arrested in the Bcell differentiation pathway, intermediate between pre-B cells and mature B cells. Morphologically, in the peripheral blood, these cells resemble mature lymphocytes; they infiltrate the bone marrow, suppressing the other branches of hemopoiesis; the lymphocytes cant perform their normal protective function, so the patients is with increased vulnerability to infections; Symptoms Anemia, serious infection and general enlargement of the lymphatic nodes are the common symptoms leading to the diagnosis; fatigue, weakness, loss of weight and appetite; sweating often in the night, itching, often fever, possible bleeding from gums, etc; Physical examination The general condition is satisfactory in the early stages; pallor of the skin and visible mucosa, possible leukemoid infiltrates over the skin; specific for the diagnosis is the general enlargement of the lymphatic nodes which are soft and painless; the spleen is also enlarged and possibly the liver; Lab tests Blood count excessive elevation of the lymphocytes (possibly over 100 000), reduced numbers of granulocytes, erythrocytes (normochrome and normocyte anemia) and platelets; Blood smear specific for the diagnosis ix the excessively large number of lymphocytes, including immature cells and Gumpreht shadows (nuclei of degenerated lymphocytes); Increased sedimentation rate, CRP and LDH, often uric acid; decreased iron and iron binding capacity; possibly elevated liver enzymes, Specific tests for phenotype and immunotype are required; Instrumental tests Smear of bone marrow is not always required, specific for the diagnosis is the infiltration of lymphopoietic cells which suppress the other branches of hemopoiesis; Biopsy of a lymph node may be important for the diagnosis; Abdominal ultrasound and CAT are useful to establish the enlargement of the spleen, liver ad lymphatic nodes; Complications Severe infections, including sepsis; Sarcomatisation of the disease (some group of lymphatic nodes degenerates malignantly and is transformed in lymphosarcoma); Hemorrhage;

87 -Multiple myeloma (plasmocytoma)

Multiple myeloma is a type of cancer. Cancer is a group of many related diseases. Myeloma is a cancer that starts in plasma cells, a type of white blood cell. It's the most common type of plasma cell cancer.Most blood cells develop from cells in the

bone marrow called stem cells. Bone marrow is the soft material in the center of most bones. Stem cells mature into different types of blood cells. Each type has a special job: White blood cells help fight infection. There are several types of white blood cells.Red blood cells carry oxygen to tissues throughout the body.Platelets help form blood clots that control bleeding.Plasma cells are white blood cells that make antibodies. Antibodies are part of the immune system. They work with other parts of the immune system to help protect the body from germs and other harmful substances. Each type ofplasma cell makes a different antibody. Myeloma cells Myeloma, like other cancers, begins in cells. In cancer, new cells form when the body doesn't need them, and old or damaged cells don't die when they should. These extra cells can form a mass of tissue called a growth or tumor. Myeloma begins when a plasma cell becomes abnormal. The abnormal cell divides to make copies of itself. The new cells divide again and again, making more and more abnormal cells. These abnormal plasma cells are called myeloma cells. In time, myeloma cells collect in the bone marrow. They may damage the solid part of the bone. When myeloma cells collect in several of your bones, the disease is called "multiple myeloma." This disease may also harm other tissues and organs, such as the kidneys. Myeloma cells make antibodies called M proteins and other proteins. These proteins can collect in the blood, urine, and organs. Age over 65: Growing older increases the chance of developing multiple myeloma. Most people with myeloma are diagnosed after age 65. . Race: The risk of multiple myeloma is highest among African Americans and lowest among Asian Americans. The reason for the difference between racial groups is not known. Being a man: Each year in the United States, about 11,200 men and 8,700 women are diagnosed with multiple myeloma. It is not known why more men are diagnosed with the disease. Personal history of monoclonal gammopathy of undetermined significance (MGUS): MGUS is a benign condition in which abnormal plasma cells make M proteins Family history of multiple myeloma: Studies have found that a person's risk of multiple myeloma may be higher if a close relative had the disease. Symptoms:Common symptoms of multiple myeloma include:Bone pain, usually in the back and ribs,Broken bones, usually in the spine ,Feeling weak and very tired,Feeling very thirsty,Frequent infections and fevers,Weight loss,Nausea or constipation,Frequent urination Physical Examination :Bone tenderness,Numbness and tingling,Pale skin ,Slow wound healing,Swelling over the shoulders,Swelling over the clavicles,Swelling over the ribs,Swelling over the breastbone,Swelling over the skull,Weakness or fatigue,Unintentional weight loss,Eyes fail to move in unison Lab Tests : Blood tests: The lab does several blood tests: Multiple myeloma causes high levels of proteins in the blood. The lab checks the levels of many different proteins, including M protein and other immunoglobulins (antibodies), albumin, and beta-2-microglobulin.Myeloma may also cause anemia and low levels of white blood cells and platelets. The lab does a complete blood count to check the number of white blood cells, red blood cells, and platelets.The lab also checks for high levels of calcium.To see how well the kidneys are working, the lab tests for creatinine. Urine tests: The lab checks for Bence Jones protein, a type of M protein, in urine.

The lab measures the amount of Bence Jones protein in urine collected over a 24hour period. If the lab finds a high level of Bence Jones protein in your urine sample, doctors will monitor your kidneys. Bence Jones protein can clog the kidneys and damage them Instrumental Test : X-rays: You may have x-rays to check for broken or thinning bones. An x-ray of your whole body can be done to see how many bones could be damaged by the myeloma. Biopsy: Your doctor removes tissue to look for cancer cells. A biopsy is the only sure way to know whether myeloma cells are in your bone marrow. Before the sample is taken, local anesthesia is used to numb the area. This helps reduce the pain. Your doctor removes some bone marrow from your hip bone or another large bone. Bone marrow aspiration: The doctor uses a thick, hollow needle to remove samples of bone marrow. Bone marrow biopsy: The doctor uses a very thick, hollow needle to remove a small piece of bone and bone marrow. Complications : Impaired immunity. Myeloma cells inhibit the production of antibodies needed for normal immunity. Having multiple myeloma may make you more likely to develop infections, such as pneumonia, sinusitis, bladder or kidney infections, skin infections, and shingles. Bone problems. Multiple myeloma also can affect your bones, leading to erosion of bone mass and fractures. The condition may cause compression of your spinal cord. Signs of this medical emergency include weakness, or even paralysis, in your legs. Impaired kidney function. Multiple myeloma may cause problems with kidney function, including kidney failure. Higher calcium levels in the blood related to eroding bones can interfere with your kidneys' ability to filter your blood's waste. The proteins produced by the myeloma cells can cause similar problems, especially if you become dehydrated. Anemia. As cancerous cells crowd out normal blood cells, multiple myeloma can also cause anemia and other blood problems.

88- Essential thrombocytopenia; myeloproliferative diseases;

Essential thrombocythemia (ET) is an uncommon disorder in which your body produces too many blood platelets (thrombocytes). It's also known as primary thrombocythemia (throm-bo-sigh-THE-me-uh). Essential thrombocythemia is one of a group of diseases of the blood and bone marrow known as myeloproliferative neoplasms.The most common symptoms of essential thrombocythemia include headache, lightheadedness, vision changes, and tingling, numbness or burning pain in the hands and feet. Essential thrombocythemia most often occurs in people over age 50 and is more common in women.You may not need treatment for essential thrombocythemia if you're not experiencing symptoms. If you have abnormal blood clotting or bleeding, however, medications can help you avoid potentially serious complications. Symptoms : Having too many platelets in the blood may not cause any symptoms, and up to 50% of people (1 in 2) are diagnosed with ET during a routine

blood test, when they have no symptoms.A high number of platelets can cause the blood to clot more easily. It may also cause abnormal bleeding because the platelets are immature and don't work properly.Symptoms can occur because a blood clot (thrombosis) has formed in a vein in the body. Clotting problems are more common in people over 60, or in those who have already had a previous blood clot or have conditions such as high blood pressure or diabetes. The symptoms will depend on where in the body a clot forms. Common sites where a clot may form are; The deep veins of the leg:This can cause symptoms such as pain, swelling, heat and redness of a calf. This is known as deep vein thrombosis or DVT. The brainThis may cause mild symptoms, such as headaches, sight disturbances or dizziness. Blood clots in the brain may also cause symptoms that are more serious, such as a stroke or TIAs (transient ischaemic attacks [mini-strokes]). The heart:A blood clot in the heart may cause chest pain and in severe cases can result in a heart attack. The lungs: A blood clot in a lung may cause breathlessness and chest pain. This is known as a pulmonary embolism.Problems caused by abnormal bleeding are less common than clotting problems. They can include:nose bleeds, bruising, abnormal vaginal bleeding ,bleeding gums. Physical Examination :The major symptoms are bleeding and thrombosis. Other symptoms include epistaxis (nosebleeds) and bleeding from gums and gastrointestinal tract. One characteristic symptom is throbbing and burning of the hands and feet due to the occlusion of small arterioles by platelets (erythromelalgia). An enlarged spleen (splenomegaly) may be found on examination. Lab Tests : Complete blood count (CBC). This test determines the number of platelets in your blood. Blood smear. A small amount of your blood is examined under a microscope to view the condition of your platelets, such as whether they're abnormally large or clumped together. Genetic testing. Special tests can determine whether you have chromosomal abnormalities that can cause a high platelet count and whether you have a JAK2 gene mutation. Other blood tests. Your doctor may check the level of iron in your blood or test for markers of inflammation. If your blood count is above 450,000 platelets per microliter of blood, your doctor will look for an underlying condition. If there's no evident cause of your high

platelet count, and it remains high over time, your doctor may suggest a bone marrow test. The two types of bone marrow tests provide different but complementary information about your blood cells. Often they're done together. Instrumental Tests: Bone marrow aspiration. Your doctor extracts a small amount of your liquid bone marrow through a needle and examines it under a microscope, looking for abnormal cells. Bone marrow biopsy. Your doctor takes a sample of solid bone marrow tissue through a needle for examination under a microscope. If you have ET, your bone marrow has a higher than normal number of the large cells that make platelets (megakaryocytes). Complications : Pregnancy complications. Uncontrolled thrombocythemia can cause miscarriage, premature delivery, high blood pressure (preeclampsia), early separation of the placenta from the uterine wall (placental abruption) and slow fetal growth. If you have ET and become pregnant, be sure your doctor monitors you carefully throughout your pregnancy. Stroke. A clot that blocks blood flow to your brain can cause a stroke. If you develop signs and symptoms of a stroke, get immediate medical attention. Heart attack. A clot that obstructs blood flow to your heart can cause a heart attack. If you develop signs and symptoms of a heart attack, such as pressure, fullness or a squeezing pain in the center of your chest lasting more than a few minutes; pain extending to your shoulder, arm, back, teeth or jaw; shortness of breath; and sweating or clammy skin, get immediate medical attention.Essential thrombocythemia can also cause bleeding (hemorrhage) with significant blood loss. A small minority of people with ET may later develop acute leukemia or myelofibrosis, both of which can be life-threatening: Acute leukemia. Acute myelogenous leukemia is a type of blood and bone marrow cancer that progresses rapidly. Myelofibrosis. This progressive bone marrow disorder results in bone marrow scarring, severe anemia, and enlargement of your liver and spleen.

89-)Hyperthyroidism
Definition increased synthesis and secretion of thyroid hormones causing increased metabolism affecting all systems; thyroid hormones are necessary for normal growth and development, and they regulate cellular metabolism; excess of thyroid hormones cause an increase in the metabolic rate that is associated with increased total body heat production and cardiovascular activity (increased heart contractility, heart rate, vasodilation).with weight loss, tachycardia, intolerance to heath, etc;

Classification diffuse toxic goiter (Grave-Basedow disease), toxic multinodular goiter (Plummers disease), toxic adenoma and subacute thyroiditis are the most common causes over 90% Secondary hyperthyroidism (very rare) caused by pituitary tumors producing YSH or TTH or due to pituitary resistance to thyroid hormones; Graves disease Etiology and pathogenesis It is an immune-mediated disorder that results from the production of thyroidstimulating immunoglobulins (TSI) by stimulated B lymphocytes. These immunoglobulins bind to the thyroid-stimulating hormone (TSH) receptor to mimic the action of TSH and stimulate thyroid growth and thyroid hormone overproduction; Predisposition factors family predisposition, female sex; Provoking factors stress, infection; Symptoms Rapid weight loss in spite of increased appetite; sweating, intolerance to heath, increased heart rate with premature beats or absolute arrhythmia, systolic arterial hypertension, weakness, fatigue, easy tiredness, in some cases secondary diabetes mellitus (usually mild form), anxiety, irritability, restlessness, sleeplessness, attention problems, emotional instability, tremor, frequent defecation with soft stool or diarrhea, menstrual disturbances, sexual impotence in men; if the thyroid gland becomes very large, it may cause pressure symptoms and signs, including difficulty swallowing and hoarseness. Physical examination Reduced body weight and fat tissue; muscle waste and decreased muscle strength; smooth and moist (velvet-like) skin usually with signs of red dermographism; possible pretibial myxedema; tremor (fine and bilateral); bilateral exophtalmus with hyperthyroid stare and positive signs of Grefe (dropping of the eyelids), Moebius (insufficient convergence) and Stelwag (infrequent blinking) and in severe cases with lagophtalm (inability of the eyelid to cover the eye), chemosis (conjunctival edema); the thyroid gland is diffusely enlarged, with tenderness during palpation, often thre may be found audible bruit (systolic drill); increased heart rate often with rhythm disorders and often systolic murmur at the apex; increased systolic blood pressure and celerity of the pulse, liver is often slightly enlarged, hyperactive bowel sound (peristaltis); possible gynecomastia; increased reflexes; Lab tests Specific for the disease decreased cholesterol and triglycerides, slightly increased glucose; often slightly or moderately increased liver enzymes, total protein and albumin may be slightly decreased, mild normochrome and normocyte anemia, slightly decreased platelets and WBC with relative lymphocytosis (in most of the cases caused by the treatment) is also common; Crucial for the diagnosis are the hormonal tests increased FT3 (free triiodthyronin) and FT4 (free thyroxin) and decreased TSH (thyroid stimulating hormone) and TTH (thyrotropin hormone) reverse feedback; assays for thyrotropin-receptor antibodies (particularly TSIs specific for Graves disease) almost always are positive; a high titer of serum antibodies to collagen XIII is associated with active Graves ophthalmopathy Instrumental tests Ultrasound of the thyroid gland which is diffusely enlarged with structural changes; Radioactive iodine scanning and measurements of iodine uptake are useful in differentiating the causes of hyperthyroidism; in Graves disease, the radioactive iodine uptake is increased and the uptake is diffusely distributed over the entire gland (scintigraphy with iodine-123 (123 I) or technetium-99m (99m Tc));

Additional tests increased protein-bonded iod and radioiodcaptation; ECG, HOLTER-ECG, echocardiography are usually required; Complications Thyrotoxic crisis (storm) Provoking factors thyroid or other types of surgery, infections, abrupt ceased thyrostatic treatment, trauma, stress; Excessive weakness, high fever possibly with rigors; excessively increased heart rate or tachyarrhythmia; in severe cases possible coma; Malignant ophtalmopathy; the pathogenesis of ophthalmopathy lies in the deposition of glycosaminoglycans (GAG) in the extraocular muscles and adipose and connective tissue of the retro-orbit, leading to T-cell activation; the TSH receptor antigen is thought to be a key mediator in the process of T-cell activation. Cigarette smoking is a significant risk factor for ophthalmopathy; the symptoms are: tearing, gritty sensation in the eye, photophobia, eye pain, protruding eye, diplopia, and eventually visual loss; Thyrotoxic cardiomyopathy with rhythm disorders and progressive total heart failure; Toxic hepatitis due to increased levels of thyroid hormones or to thyrostatic treatment; Accelerated osteoporosis, especially in women; In patients with toxic adenoma and toxic multinodular goiter (Plummer disease) the leading symptoms are mainly from the heart; in the second case the symptoms of thyrotoxicosis are usually mild, because only a slight elevation of thyroid hormone levels is present, and the signs and symptoms of thyrotoxicosis often are blunted; in this case possible provoking factors are high iodine intake, (ie, with contrast or amiodarone exposure); specific for the diagnosis - a toxic adenoma demonstrates a solitary hot nodule with suppression of function in the surrounding normal thyroid tissue; a toxic multinodular goiter demonstrates an enlarged thyroid with multiple nodules and areas of increased and decreased isotope uptake due to the decreased TSH;. In patient with acute thyroiditis the signs of bacterial infection are crucial for the diagnosis, but in patients with subacute thyroiditis (subacute thyroiditis usually demonstrates very low123 I isotope uptake) and Hashimotos disease the diagnosis is determined by fine-needle aspiration biopsy of the gland and tests for autoantibodies (TAT and MAT) in the later case; increased level of thyroglobulin may suggest thyroid cancer; cold nodules requires biopsy to exclude malignancy;

90- Hypothyroidism - etiology, pathogenesis, symptoms, diagnosis

Definition decreased secretion of thyroid hormones which causes cretinism in children (mentally retarded dwarfs) and in adults decreased metabolism, accelerated atherosclerosis and myxedematous infiltration (ie, accumulation of glucosaminoglycans in the tissues); Classification Primary caused by diseases directly affecting the thyroid gland, most common cause Hashimoto disease; Secondary - lack of thyroid hormone secretion due to inadequate secretion of either thyrotropin (ie, thyroid-stimulating hormone, TSH) from the pituitary gland or thyrotropin-releasing hormone (TRH) from the hypothalamus (secondary or tertiary hypothyroidism); common causes are panhypopituitarism (SimondsSheehan syndrome) or pituitary adenoma; Etiology and pathogenesis of the primary hypothyroidism Autoimmune - the most frequent cause of acquired hypothyroidism is autoimmune thyroiditis (Hashimoto thyroiditis); a chronic immune reaction with production of

antibodies against the thyroid antigens, resulting in lymphocytic infiltration of the gland and progressive destruction of functional thyroid tissue (TSH receptor blocking antibodies in Hashimoto disease chronic lymphocytic thyroiditis); postpartum thyroiditis and subacute granulomatous thyroiditis are relatively rare cases: Other important cases for hypothyroidism are; reduced intake of iodine which is essential fir the synthesis of the thyroid hormones (causing goiter and decreased hormonal secretion); infections; partial or total resection of the gland (due to cancer or toxic adenoma); complication of radioiodine therapy; drugs such as amiodarone, interferon alpha, thalidomide, lithium, etc; idiopathic; Predisposition factors female sex, family predisposition, endemic region with lack of iodide; Symptoms Fatigue, exhaustion, sleepiness, bradylalia and bradypsychia (slowed talking and thinking), confusion, weight gain in spite of decreased appetite, coarse voice; bradycardia, total heart failure, constant sensation of cold, amenorrhea, decreased libido, impotence in men; signs of ischemic heart disease chest pain, shortness of breath; edema; serious constipation, often hypoacidity due to atrophic gastritis; loss of hair; in mild cases hypothyroidism may be asymptomatic; More specific to Hashimoto thyroiditis are: feeling of fullness in the throat or painless thyroid enlargement; sometimes neck pain, sore throat, or both; subfebrile temperature is also possible; Physical examination Bradypsychia and bradylalia with coarse voice, in severe cases the patients are somnolent or disorientated; obesity; the skin is pale, dry with reduced turgor, often edematous (legs, face); dull facial expression (mask-like face); loss of scalp hair, axillary hair, pubic hair, or a combination; periorbital puffiness; macroglossia (enlargement of the tongue); the thyroid gland may be enlarged depending on the etiology; low heart rate and systolic blood pressure, however the diastolic pressure may be increased; signs of total heart failure or/and pericardial effusion; possibly enlarged liver; edema of lower extremities, delayed reflexes; Lab tests Specific for the disease are increased cholesterol and low blood glucose; often mild anemia and slightly increased liver enzymes, is some cases sodium nay be decreased due to dilution; Crucial for the diagnosis are the increased TSH and TTH with decreased FT3 and FT4 reverse feedback; however in patients with secondary hypothyroidism all hormones (including TSH and TRH) are decreased; antimicrosomal or antithyroid peroxidase (anti-TPO) antibodies are found more commonly than antithyroglobulin (anti-Tg) antibodies in patients with Hashimotos disease; in patients with operation of the gland plasma calcium and parathyroid hormone have to be checked to exclude concomitant hypoparathyroidism; Instrumental tests Ultrasound - Hashimoto thyroiditis is usually associated with a heterogeneous ultrasonographic image and fine-needle aspiration biopsy may be performed in some dubious cases; in cases of secondary hypothyroidism MRI of the pituitary gland and possibly perimetria of the vision; ECG bradycardia with low QRS complexes and ST-T changes, echocardiography decreased contractility and ejection fraction, often pericardial effusion; often veloergometry and coronary angiography are required; Doppler of the carotid and vertebral arteries and abdominal ultrasound may also be useful; Complications Ischemic heart disease with myocardial infarction or dilative cardiomyopathy;

Myxedema coma - provoking factors are infections or abruptly ceased hormonal treatment; the main symptoms are serious bradicardia and hypothermia with low blood pressure and often hypoglycemia, hypercarbia, and hyponatremia;

91 Hypocorticism (Adissons disease) - etiology, pathogenesis, symptoms, diagnosis;

Definition decreased synthesis and secretion of corticosteroids and mineralcorticoids (aldosteron) from the suprarenal glands; Classification, etiology and pathogenesis Primary hypoadrenocorticism due to atrophy of the cortex of the suprarenal gland caused by infections (tuberculosis), autoimmune diseases, amyloidosis, after prolonged treatment with corticosteroids, or resection of the glands; The autoimmune causes include polyglandular autoimmune disease I (PGAD I) and polyglandular autoimmune disease II (PGAD II). PGAD I is described as destruction of the adrenal and thyroid glands resulting in adrenal insufficiency, hypothyroidism, and chronic candidiasis. PGAD I may also be associated with type 1 diabetes mellitus, hypogonadism, chronic hepatitis, immunoglobulin A (IgA) deficiency, chronic atopic dermatitis, keratoconjunctivitis, vitiligo, or alopecia. PGAD II, also called Schmidt syndrome, is characterized by autoimmune-mediated adrenal insufficiency and may involve autoimmune-mediated thyroiditis and/or autoimmune-mediated type 1 diabetes mellitus, usually for the autoimmune diseases there is a genetic predisposition and at some time they are triggered by an environmental agent; Secondary hypoadrenocorticism due to tumors or postpartum ischemic infarction (Simond-Sheehan syndrome) of the pituitary gland; Symptoms Excessive weakness, easy tiredness, vertigo, drowsiness, low blood pressure (systolic under 110 mmHg) with orthostatism (sudden drop of the blood pressure when the patient is standing upright), nausea, abdominal pain, sometimes vomiting and diarrhea; loss of appetite and weight, menstrual disturbances; in some cases depression, irritability, and decreased concentration; Physical examining Hyperpigmentation (darkening of the skin and visible mucosa) face, breasts, elbows, lines of the palms, gums, sublingual mucosa, etc (due to increased secretion of melanocyte-stimulating hormone (MSH) in patients with primary hypoadrenocorticism); dry skin with reduced turgor, often vitiligo (local depigmententation of the skin); loss of hair in women in the pubic and axillary regions; reduced fat and muscle tissue, low blood pressure; Lab tests Specific for the disease are increased potassium, low sodium, low blood glucose, usually slight anemia is present; Crucial for the diagnosis are the reduced levels of cortisol and aldosteron with increased ACTH in primary hypocorticism but decreased if the pituitary gland is damaged; The hypothalamic-pituitary axis is usually evaluated by the corticotropin (Cortrosyn) stimulation test; Once the diagnosis of adrenal insufficiency is confirmed, the site of the defect in the hypothalamic-pituitary axis should be determined by using corticotropin sampling, corticotropin provocative testing, or corticotrophin-releasing hormone (CRH) provocative test; Autoantibodies against 21-hydroxylase may be detected in patients with autoimmune polyglandular syndrome; in some cases test for tuberculosis are necessary; Instrumental tests

Both computed tomography (CT) and magnetic resonance imaging (MRI) demonstrate a diminished adrenal gland in patients with autoimmune destruction and an enlarged adrenal gland in patients with infection. CT adequately shows the calcification that occurs in adrenal failure caused by tuberculosis in the chronic phase of the disease; (CT scan, eventually PET scan or MRI for the suprarenal glands and MRI for the pituitary gland; in the later cases consultation with ophthalmologist and additional test are usually required); Complications Addisons crisis and coma most common provoking factors are infections and abrupt cease of the substitute hormonal therapy; physical findings that occur in a patient in adrenal crisis include hypotension, abdominal pain, vomiting, and mental confusion (secondary to low serum sodium or hypotension). Other findings include hypoglycemia, hyperkalemia, hyponatremia, and metabolic acidosis

92- Cushings syndrome and disease (hypercorticism) - etiology, pathogenesis, symptoms, diagnosis;
Cushing's syndrome occurs when your body is exposed to high levels of the hormone cortisol for a long time. The most common cause of Cushing's syndrome, sometimes called hypercortisolism, is the use of oral corticosteroid medication. The condition can also occur when your body makes too much cortisol.Too much cortisol can produce some of the hallmark signs of Cushing's syndrome a fatty hump between your shoulders, a rounded face, and pink or purple stretch marks on your skin. Cushing's syndrome can also result in high blood pressure, bone loss and, on occasion, diabetes.Treatments for Cushing's syndrome can return your body's cortisol production to normal and noticeably improve your symptoms. The earlier treatment begins, the better your chances for recovery. Classification of Cushing's Syndrome ACTH dependent Cushing's disease Ectopic ACTH syndrome Ectopic corticotropin-releasing hormone syndrome* ACTH independent Iatrogenic Adrenal adenoma Micronodular hyperplasia* Macronodular hyperplasia* Symptoms : involve progressive obesity and skin changes, such as: Weight gain and fatty tissue deposits, particularly around the midsection and upper back, in the face (moon face) and between the shoulders (buffalo hump),Pink or purple stretch marks (striae) on the skin of the abdomen, thighs, breasts and arms,Thinning, fragile skin that bruises easily,Slow healing of cuts, insect bites and

infections,Acne, Women with Cushing's syndrome may experience: Thicker or more visible body and facial hair (hirsutism),Irregular or absent menstrual periods Men with Cushing's syndrome may experience: Decreased libido,Decreased fertility,Erectile dysfunction Other signs and symptoms include: Fatigue, Muscle weakness,Depression, anxiety and irritability,Loss of emotional control,Cognitive difficulties,New or worsened high blood pressure,Glucose intolerance that may lead to diabetes,Headache,Bone loss, leading to fractures over time Physical Examination : Take your blood pressure.Examine you for changes in skin thickness; an unusual amount of fat on the back of your neck, on your upper back, and around your waist; bruising; stretch marks; and infected wounds. Check your skin for tanning in places where you would not expect to see a tan, especially in the mouth, around the nipples, and in the creases of your palms. Weigh you. Check the strength of your arms and legs. Examine you carefully for any signs of cancer. rounding of the face (moon face), a pad of fatty tissue between the shoulders and neck (buffalo hump), and thin skin with bruises and stretch marks. Radiology And Lab Tests: X-ray - a diagnostic test which uses invisible electromagnetic energy beams to produce images of internal tissues, bones, and organs onto film. 24-hour urinary test (urine is collected over a 24-hour period to measure for corticosteroid hormones) Computed tomography scan (Also called a CT or CAT scan.) - a diagnostic imaging procedure that uses a combination of x-rays and computer technology to produce cross-sectional images (often called "slices"), both horizontally and vertically, of the body. A CT scan shows detailed images of any part of the body, including the bones, muscles, fat, and organs. CT scans are more detailed than general x-rays. Magnetic resonance imaging (MRI) - a diagnostic procedure that uses a combination of large magnets, radio frequencies, and a computer to produce detailed images of organs and structures within the body. Dexamethasone suppression test (to differentiate whether the excess production of corticotropins are from the pituitary gland or tumors elsewhere) Corticotropin-releasing hormone (CRH) stimulation test (to differentiate whether the cause is a pituitary tumor or an adrenal tumor) If you've been taking a corticosteroid medication for a long time, your doctor may suspect that you've developed Cushing's syndrome as a result of this medication. If you haven't been using a corticosteroid medication, these diagnostic tests may help pinpoint the cause: Urine and blood tests. These tests measure hormone levels in your urine and blood and show whether your body is producing excessive cortisol. For the urine

test, you may be asked to collect your urine over a 24-hour period. Both the urine and blood samples will be sent to a laboratory to be analyzed for cortisol levels. Saliva test. Cortisol levels normally rise and fall throughout the day. In people without Cushing's syndrome, levels of cortisol drop significantly in the evening. By analyzing cortisol levels from a small sample of saliva collected late at night, doctors can see if cortisol levels are too high, suggesting a diagnosis of Cushing's. Complications : If you don't receive prompt treatment for Cushing's syndrome, other complications may occur, such as:Bone loss (osteoporosis), which can result in unusual bone fractures, such as rib fractures and fractures of the bones in the feet,High blood pressure (hypertension),Diabetes,Frequent or unusual infections,Loss of muscle mass and strength.

93 -Diabetes - etiology, pathogenesis, symptoms, diagnosis, complications;

Definition polygene metabolite disorder due to absolute or relative lack of insulin, affecting mainly the carbohydrate metabolism, but also protein and fat metabolism; Classification Type I insulin dependent diabetes mellitus, usually affecting children and young adults under age of 40; Type II non-insulin dependent diabetes mellitus usually affecting elder people (over 40); Secondary diabetes as a consequence or complication of another, usually endocrine disease Cushings syndrome and disease (hyperglucocorticism); hyperthyroidism; acromegaly; hyperparathyroidism, severe form of chronic pancreatitis, iatrogenic (due to prolonged treatment with corticosteroids); Etiology and predisposition factors Family predisposition; Viral infections affecting the pancreatic gland (mumps, rubella, coxsackievirus); Obesity and physical inactivity are the main predisposition factors for type II diebetes; All the causes leading to secondary diabetes mellitus; Provoking factors initiating the clinical manifestation of the disease Stress, infection, corticosteroid therapy; Pathogenesis Absolute lack of insulin (typical for I type diabetes) due to severe damage of the beta cells in the islets of Langernahs in the pancreatic gland (autoimmune destruction, viral, toxic) in which circulating insulin is very low or absent, plasma glucagon is elevated, and the pancreatic beta cells fail to respond to all insulinsecretory stimuli; Combination of resistance to insulin action and inadequate insulin secretion (typical for type II diabetes) which has been attributed to elevated levels of free fatty acids in plasma and often insufficient number of insulin receptors; Other possible causes inactivation of the insulin in the circulation by antibodies, contrainsular hormones, toxic agents; Insulin is a protein hormone with strong anabolic effect which facilitates the penetration of the glucose into the cell; its lack impairs seriously that process and

deprives the cells of sugar which is essential source of energy necessary for its metabolism and synthetic functions; to compensate the lack of energy more glucose is produced from the glycogen in the liver and gluconeogenesis (transformation of amino and fat acids into glucose); fat and amino acids are used as alternative sources of energy, resulting progressive dominance of the catabolic processes over the anabolic; Symptoms The progressively increasing level of blood sugar leads to hyperosmolarity which causes thirst (polydipsia); glycosuria is another consequence of increased blood sugar; this and the increased intake of water causes increased urine volume (polyuria due to osmotic diuresis); the inability of the cells to utilize the glucose is provoking constant hunger (polyphagia); meanwhile the catabolic processes prevail over the anabolic which is followed by weight loss (autophagia);these symptoms are typical for first type diabetes and in some patients the disease make its first appearance with ketoacidosis; In cases with II type diabetes these symptoms are usually mild and the leading complains are caused by skin and urinary tract infections (staphylococcal follicular skin infections, pruritis, oral or genital candidal infections, vulvitis, balanitis, lower urinary tract infections, conjunctivitis, other superficial fungal infections affecting nails, toes, etc) with itching in the genital region, feet, tights, parodontosis (inflammation of the gums, etc; the patients are usually obese and in both types there are blurred vision and menstrual disturbances in women and erectile problems in men; often hemorrhagic diathesis and in some cases muscle cramps due to hypokalemia; A large group of symptoms in both types is connected with the complications due to impairment of the blood vessels; they are divided in two groups diabetic microangiopathy (afflicting the small vessel arterioles and capillaries) and diabetic macroangiopathy (afflicting medium caliber arteries usually heart, brain and limbs); Diabetic microangiopathy pathogenesis deposition of glycoproteins in the walls of arterioles and capillaries; Clinical forms Diabetic retinopathy; three stages: I - microaneurisms of the retinal arterioles; II hemorrhages in the retina; III sclerosis and proliferation of new blood vessels which lead to blindness; cataracts and glaucoma are more common in patients with diabetes; Diabetic nephropathy afflicting the renal arterioles and glomerular basal membrane; it leads to increasing proteinuria, eventually with hypoproteinemia and nephrotic syndrome in the later stages; arterial hypertension and chronic renal failure (the renal biopsy shows arteriolar and glomerular hyalinization Kimmelstiel-Wilson syndrome); acute and chronic tubulointerstitial nephritis are common in patients with diabetes; Diabetic polyneuropathy (four types - sensory and autonomic neuropathy are due to axonal degeneration and segmental demyelination; motor neuropathy and cranial mononeuropathy are due to vascular disease in blood vessels supplying nerves); Peripheral sensory polyneuropathy (distal and symmetrical in a glove-andstocking distribution) is the most common - main symptoms pain in the early stages and paraesthesiae (spontaneously occurring tingling and pinching sensations); latter hyposensitivity and even loss of peripheral sensation (numbness; the decreased sensitivity to pain my lead to painless form of myocardial infarction, tooth gangrene, etc) and paraesthesiae (spontaneously occurring tingling and pinching sensations) are usually affecting the limbs;

Diabetic neurovegetopathy - main symptoms rhythm disorders, enteropathy, retention of urine, etc. Diabetic macroangiopathy pathogenesis accelerated atherosclerosis of medium size arteries; Clinical forms Ischemic heart disease due to atherosclerosis of the coronary arteries angina, myocardial infarction, rhythm disorders, left-side or total heart failure; Ischemic brain disease due to atherosclerosis of the internal carotid and vertebrobasilar arteries and their branches transitory brain ischemia, brain infarction, multi-infarct dementia, etc; Chronic ischemia of the limbs due to atherosclerosis of the iliofemoral and smaller arteries; most affected are the feet and the main complains are freezing and pain usually during movement (claudicatio intermitens) but also at rest; the chronic ischemia and the vulnerability to infections are predisposition factors for another complication gangrene and necrotic osteomyelitis of the toes and even the feet; mycotic infections are also common; compromised protein metabolism, hyperglycemia and acidemia impair the humoral immunity; decreased microvascular perfusion is also a predisposition factor for infections in diabetics; The renal arteries are also afflicted by the atherosclerosis and participate in the pathogenesis of arterial hypertension and nephrosclerosis with chronic renal failure; Physical examination The general condition is impaired in cases with complications; patient with I type diabetes are with reduced body weight, with II type are usually obese; the cheeks are often pink (rubeosis diabetica); the arterial pulsations of the limbs (especially of arteries dorsalis pedis and tibialis posterior) are decreased; the feet are usually cold; often the blood pressure is high and there are premature beats; the liver may be slightly enlarged due to steatosis; Lab tests Blood sugar (n 3.6-5.6 mm/l) - diagnosis diabetes mellitus is certain when the blood sugar before meal is over 7 mm/l; Glucose-tolerance test (measuring the blood sugar after intake of 75 g glucose) the test is positive when the blood sugar at the first hour exceeds 11 mm/l and 8 at the second hour; Glycated hemoglobin (HbA1c) is measured to identify the average plasma glucose concentration for the last two months before the test thus estimating the compensation of the diabetes and evaluation of the treatment (n. under 6.5%); Blood glucose profile usually measuring the blood sugar four times daily (morning, noon and evening before meal and about 2-3 pm after meal) or every three hours in patients with serious complications as ketoacidosis; the object of the test is to estimate the effectiveness of the treatment; Urine test Protein including test for microalbuminuria (n. under 30 mg/d); important for establishing urinary infection or diabetic nephropathy (the test for microambuminuria); Glucose its presence in the urine indicates poor compensation of the diabetes; however if the blood sugar is normal tubular damage and renal diabetes should be considered; Ketones their presence in the urine indicates one of the most serious complications of diabetes; Sediment leukocytes would indicate urinary infection; Cholesterol (n. 3.2-5.2 mm/l) usually increased (exception secondary diabetes in patients with hyperthyroidism); LDL increased over 3 mm/l;

Triglycerides (under 2.2 mm/l) specifically increased in diabetic patients; VLDV over 1.0 mm/l; Additional lab tests include potassium (tendency to hypokalaemia due to polyuria); liver enzymes (ASAT,ALAT, GGT) and alpha amylase, creatinine for evaluation of renal function; sedimentation rate, coagulation status, etc; electrolytes, acid-base balance and creatinine are especially important in cases with ketoacidosis; Immunoreactive insulin (IRI - the portion of insulin in the blood presumed to represent the free (unbound) and biologically active fraction of total blood insulin.) and C-peptide (C-peptide is formed during conversion of proinsulin to insulin) are usually increased in patients with second type diabetes in the early stages of the disease; tests for anti-insulin antibodies or antibodies against the islets beta-cells may be required in some case; high positive titer of glutamic acid decarboxylase antibodies also suggests type I diabetes; when secondary diabetes is observed different hormonal tests are required; Instrumental tests ECG possible disorders in rhythm and conduction and often ischemic changes; Holter ECG, veloergometry, echocardiography are usually required and sometimes coronary angiography; Abdominal ultrasound the liver is often enlarged with steatosis; pancreatic gland is with normal size but increased density; possible changes in the kidneys; Consultation with ophthalmologist and ophtalmoscopy is periodically required as is the consultation with neurologist and eventually EMG (electromyography) and Doppler ultrasound of carotid and vertebrobasilar arteries; When there are circulatory problems with limbs Doppler ultrasound is required and in case of gangrene X-ray of the plants; Complications (beside the vascular, already described)

94 -Gout (podagra) - etiology, pathogenesis, symptoms, diagnosis;

Gout is a disease that results from an overload of uric acid in the body. This overload of uric acid leads to the formation of tiny crystals of urate that deposit in tissues of the body, especially the joints. When crystals form in the joints, it causes recurring attacks of joint inflammation (arthritis). Gout is considered a chronic and progressive disease. Chronic gout can also lead to deposits of hard lumps of uric acid in the tissues, particularly in and around the joints and may cause joint destruction, decreased kidney function, and kidney stones (nephrolithiasis).Gout is characterized by sudden, severe attacks of pain, redness and tenderness in joints, often the joint at the base of the big toe.Gout a complex form of arthritis can affect anyone. Men are more likely to get gout, but women become increasingly susceptible to gout after menopause.An acute attack of gout can wake you up in the middle of the night with the sensation that your big toe is on fire. The affected joint is hot, swollen and so tender that even the weight of the sheet on it may seem intolerable.Fortunately, gout is treatable, and there are ways to reduce the risk that gout will recur. Symptoms :The signs and symptoms of gout are almost always acute, occurring suddenly often at night and without warning. They include: Intense joint pain. Gout usually affects the large joint of your big toe, but it can occur in your feet, ankles, knees, hands and wrists. The pain is likely to be most severe within the first 12 to 24 hours after it begins. Lingering discomfort. After the most severe pain subsides, some joint discomfort may last from a few days to a few weeks. Later attacks are likely to last longer and affect more joints. Inflammation and redness. The affected joint or joints become swollen, tender and red. Physical Examination : Fever may accompany gout attacks. Examine the skin over the painful joint to see whether it is warm, tender, red, or peeling. Check the skin over the affected joint for cuts that may be a source of infection.

Feel the joint to assess pain. Check the range of motion of the affected joint. Examine your hands, elbows, feet, ankles, knees, and earlobes for gritty, chalky clumps of uric acid crystals called tophi. Lab Tests : Joint fluid test. Your doctor may use a needle to draw fluid from your affected joint. When examined under the microscope, your joint fluid may reveal urate crystals. Blood test. Your doctor may recommend a blood test to measure the uric acid level in your blood. Blood test results can be misleading, though. Some people have high uric acid levels, but never experience gout. And some people have signs and symptoms of gout, but don't have unusual levels of uric acid in their blood.The most important differential diagnosis in gout is septic arthritis. This should be considered in those with signs of infection or those who do not improve with treatment. To help with diagnosis, a synovial fluid Gram stain and culture may be performed.Other conditions which present similarly include pseudogout and rheumatoid arthritis. Gouty tophi, in particular when not located in a joint, can be mistaken for basal cell carcinoma, or other neoplasms. Complications :People with gout can develop more-severe conditions, such as: Recurrent gout. Some people may never experience gout signs and symptoms again. But others may experience gout several times each year. Medications may help prevent gout attacks in people with recurrent gout. Advanced gout. Untreated gout may cause deposits of urate crystals to form under the skin in nodules called tophi (TOE-fi). Tophi can develop in several areas such as your fingers, hands, feet, elbows or Achilles tendons along the back of your ankle. Tophi usually aren't painful, but they can become swollen and tender during gout attacks. Kidney stones. Urate crystals may collect in the urinary tract of people with gout, causing kidney stones. Medications can help reduce the risk of kidney stones.

95- Rheumatoid arthritis - etiology, pathogenesis, symptoms, diagnosis;

Rheumatoid arthritis (RA) is a form of arthritis that causes pain, swelling, stiffness and loss of function in your joints. It can affect any joint but is common in the wrist and fingers. More women than men get rheumatoid arthritis. It often starts between ages 25 and 55. You might have the disease for only a short time, or symptoms might come and go. The severe form can last a lifetime.Rheumatoid arthritis is different from osteoarthritis, the common arthritis that often comes with older age. RA can affect body parts besides joints, such as your eyes, mouth and lungs. RA is an autoimmune disease, which means the arthritis results from your immune system attacking your body's own tissues. Symptoms : Tender, warm, swollen joints Morning stiffness that may last for hours Firm bumps of tissue under the skin on your arms (rheumatoid nodules) Fatigue, fever and weight loss. Early rheumatoid arthritis tends to affect your smaller joints first particularly the joints that attach your fingers to your hands and your toes to your feet. As the disease progresses, symptoms often spread to the knees, ankles, elbows, hips and shoulders. In most cases, symptoms occur in the same joints on both sides of your body. Physical Examination : Symmetrical joint swelling is characteristic of rheumatoid arthritis that has been persistent for a period of time. However when only a few joints are affected at the beginning of disease, symmetry may not be seen and should not preclude the diagnosis of RA. Careful palpation of the joints can help to distinguish the swelling of joint inflammation from the bony enlargement seen in osteoarthritis, with the

swelling often described as being doughy or spongy in RA in contrast to firm knobby enlargement in osteoarthritis. Swelling of the PIP and MCP joints of the hands is a common early finding. Lab Tests for Rheumatoid Arthritis if theres inflammation in your body complete blood countthe amount of red blood cells, white blood cells, and platelets in body the amount of rheumatic factor in bloodthats an antibody, and some people with RA have a higher amount of that factor than they should Imaging Tests for RA X-rays can help your doctor get a closer look at your joints to see if you have rheumatoid arthritis and how far progressed it is. On an x-ray, your doctor will look at, among other things: swelling around the joint if you have osteophytes (bone spurs) developing on the joint how aligned your joints are. Taking x-rays is also a good way for your doctor to monitor the progression of your rheumatoid arthritishe or she can take yearly x-rays to better monitor your joints changes. Complications Osteoporosis. Rheumatoid arthritis itself, along with some medications used for rheumatoid arthritis, can increase your risk of osteoporosis a condition that weakens your bones and makes them more prone to fracture. Carpal tunnel syndrome. If rheumatoid arthritis affects your wrists, the inflammation can compress the nerve that serves most of your hand and fingers. Heart problems. Rheumatoid arthritis can increase your risk of hardened and blocked arteries, as well as inflammation of the sac that encloses your heart. Lung disease. People with rheumatoid arthritis have an increased risk of inflammation and scarring of the lung tissues, which can lead to progressive shortness of breath.

96- Ankylosing spondylitis (Bechterews disease) - etiology, pathogenesis, symptoms, diagnosis;

Ankylosing spondylitis is an inflammatory disease that can cause some of the vertebrae in your spine to fuse together. This fusing makes the spine less flexible and can result in a hunched-forward posture. A severe case of ankylosing spondylitis can make it impossible for you to lift your head high enough to see forward.Ankylosing spondylitis affects men more often than women. Signs and symptoms of ankylosing spondylitis typically begin in early adulthood. Inflammation also can occur in other parts of your body such as your eyes and bowels. Symptoms: Early signs and symptoms of ankylosing spondylitis may include pain and stiffness in your lower back and hips, especially in the morning and after periods of inactivity.These symptoms may come on so gradually that you don't notice them at first. Over time, symptoms may worsen, improve or stop completely at irregular intervals. The joint between the base of your spine and your pelvis The vertebrae in your lower back The places where your tendons and ligaments attach to bones, mainly in your spine, but sometimes along the back of your heel The cartilage between your breastbone and ribs Your hip and shoulder joints Physical Examination : Before even touching the patient, notice his posture. If he is in a stooped forwardflexed position, chances are he has AS. As you know, vertebral bodies fuse over

time and limit ROM of the spine. You must test ROM of the axial skeleton and peripheral joints, in addition to, assessing for SI joint tenderness which is common. Patients with AS may also have peripheral enthesitis, which is pain and swelling of tendons and ligamentous insertions. Finally, you MUST screen for the extra-articular manifestations of this disease. Perform an occular exam, listen to the heart and lungs and perform a thorough abdominal exam because Crohns and ulcerative colitis are common in patients with AS. Radiology & Lab Tests: There are two categories of diagnostic tests used to identify ankylosing spondylitis: imaging scans (e.g., x-rays, magnetic resonance images) that capture a picture of the spine and affected joints, and blood tests that identify certain markers of ankylosing spondylitis. Imaging Scans In the early disease process, plain x-rays may be read as normal. To diagnose ankylosing spondylitis, the sacroiliac joints (SI joints) at the back of the pelvis must be affected. X-ray evidence of sacroiliitis is one of the most telling signs of this condition. More accurate and earlier diagnosis can be done using magnetic resonance imaging (MRI scans) and or CAT scans (CT scans). Blood Tests An elevated CRP and/or WESR (sedimentation rate) can be found in any inflammatory state, including ankylosing spondylitis. As mentioned previously in this article, 90% of people with ankylosing spondylitis test positive for the HLA B27 gene. Having this gene, however, does not necessarily mean that ankylosing spondylitis is present or that it will develop. 8% of healthy Caucasians and 2% of health African-Americans carry this gene. In fact, a healthy person who carries this gene and has no relatives with ankylosing spondylitis has only a 2% chance of getting this form of arthritis. Complications : Eye inflammation (uveitis). One of the most common complications of ankylosing spondylitis, uveitis can cause rapid-onset eye pain, sensitivity to light and blurred vision. See your doctor right away if you develop these symptoms. Compression fractures. Some people experience a thinning of their bones during the early stages of ankylosing spondylitis. Weakened vertebrae may crumble, increasing the severity of your stooped posture. Vertebral fractures sometimes can damage the spinal cord and the nerves that pass through the spine. Difficulty breathing. If ankylosing spondylitis affects your ribs, the fused bones can't move when you breathe making it difficult to fully inflate your lungs. Heart problems. Ankylosing spondylitis can cause problems with your aorta, the largest artery in your body. The inflamed aorta can enlarge to the point that it distorts the shape of the aortic valve in the heart, which impairs its function.

97- Degenerative arthropathy - etiology, pathogenesis, symptoms, diagnosis;

Osteoarthritis (OA) also known as degenerative arthritis or degenerative joint disease or osteoarthrosis, is a group of mechanical abnormalities involving degradation of joints,including articular cartilage and subchondral bone. Classification

Primary osteoarthritis - most common in the older age group as the result of wear and tear on articular cartilage over time.

Secondary osteoarthritis - results from a previous process that damaged cartilage such as trauma, or inflammatory arthritis.

Primary osteoarthritis is a chronic degenerative disorder related to but not caused by aging, as there are people well into their nineties who have no clinical or functional signs of the disease. As a person ages, the water content of the cartilage decreases as a result of a reduced proteoglycan content, thus causing the cartilage to be less resilient. Without the protective effects of the proteoglycans, the collagen fibers of the cartilage can become susceptible to degradation and thus exacerbate the degeneration. Inflammation of the surrounding joint capsule can also occur, though often mild (compared to what occurs in rheumatoid arthritis). This can happen as breakdown products from the cartilage are released into the synovial space, and the cells lining the joint attempt to remove them. New bone outgrowths, called "spurs" or osteophytes, can form on the margins of the joints, possibly in an attempt to improve the congruence of the articular cartilage surfaces. Secondary osteoarthritis is conceptually easier to understand. It refers to degenerative disease of the synovial joints that results from some predisposing condition, usually trauma, that has adversely altered the articular cartilage and/or subchondral bone of the affected joints. Secondary osteoarthritis often occurs in relatively young individuals. Symptoms The main symptom is pain, causing loss of ability and often stiffness. "Pain" is generally described as a sharp ache, or a burning sensation in the associate muscles and tendons. OA can cause a crackling noise (called "crepitus") when the affected joint is moved or touched, and patients may experience muscle spasm and contractions in the tendons. Occasionally, the joints may also be filled with fluid. Humid and cold weather increases the pain in many patients. Physical Examination For swelling, warmth, or tenderness. For range of motion. To determine the pattern of affected joints (such as one knee, both knees, knuckles, wrists, or shoulders). Often, the pattern of joints affected can help a doctor tell the difference between osteoarthritis and other types of arthritis such as rheumatoid arthritis. To note any bony knobs (osteophytic changes) on joints (especially the fingers). Any signs of unequal leg lengths, muscle weakness, or muscle wasting. During a physical exam, the doctor also will do an evaluation of the lungs, heart, liver, and kidneys. Laboratory tests : Routine laboratory tests are usually normal so their value is in ruling out other types of arthritis, especially inflammatory types of arthritis, or establishing a baseline for monitoring treatment. Synovial fluid analysis also helps rule out other conditions. Synovial fluid analysis to look for signs of joint infection and to detect monosodium urate (uric acid) crystals (that could indicate gout) or calcium pyrophosphate crystals that may contribute to joint damage in osteoarthritis. Radiological Examination Bones appearing closer to each other: As cartilage wears away, the joint space can narrow. Cysts: As the body responds to cartilage destruction and attempts to stabilize the joint, cysts or fluid-filled cavities can form in the bone. Increased bone density or uneven joints: When bones are no longer

cushioned by cartilage, they can rub against one another, creating friction. The body responds by laying down more bone in response, increasing bone density. Increased bone creates uneven joint surfaces and osteophytes (bone spurs) around the joint margins. MRI is very sensitive to bony and soft tissue changes when dedicated protocols for the musculoskeletal system are used. MRI can demonstrate reactive bone edema or soft tissue swelling as well as small cartilage or bone fragments in the joint. CT (computed tomography) examinations are excellent for demonstrating the degree of osteophyte (bone spur) formation and its relationship to the adjacent soft tissues. Ultrasound is extremely sensitive for identifying synovial cysts that can form in association with osteoarthritis. Complications: Rapid, complete breakdown of cartilage resulting in loose tissue material in the joint (chondrolysis). Bone death (osteonecrosis). Stress fractures (hairline crack in the bone that develops gradually in response to repeated injury or stress). Bleeding inside the joint. Infection in the joint. Deterioration or rupture of the tendons and ligaments around the joint, leading to loss of stability. Pinched nerve (in osteoarthritis of the spine).