Suppurative Lung Diseases PDF

SUPPURATIVE LUNG DISEASES AHMED RASHAD MASHAAL 1. Lung abscess primary and secondary. 2. Bronchiectasis. 3. Mucoviscidosis. Definition: Acute destructive infections of the lungs and/or bronchi accompanied by the elaboration of pus.  DEFINITION LUNG DISEASES...

SUPPURATIVE LUNG DISEASES AHMED RASHAD MASHAAL 1. Lung abscess primary and secondary. 2. Bronchiectasis. 3. Mucoviscidosis. Definition: Acute destructive infections of the lungs and/or bronchi accompanied by the elaboration of pus.  DEFINITION LUNG DISEASES CHARACTERIZED BY COUGH AND EXPECTORATION OF SPUTUM WHICH IS: A. INCREASED AMOUNT (MORE THAN ONE CUP/DAY) B. PURULENT YELLOW OR GREEN IN COLOR C. BAD ODOR D. RELATED TO POSTURE. Suppurative lung syndrome includes: 1. Lung abscess. 2. Bronchiectasis.  I. LUNG ABSCESS Definition: A cavity in the lung filed with pus and rupture into a bronchus. Causes: 1. Foreign body inhalation with infection distal to the obstruction. 2. Pneumonia: if inadequately treated as in staphylococcal type. 3. Obstruction of a bronchus by a tumor with infection distal to the obstruction. 4. Extension from sub diaphragmatic liver abscess 5. Infection of pulmonary infarction 6. Pyemia through blood stream from an abscess in a remote (distant) area  I. LUNG ABSCESS Symptoms: 1- suppurative syndrome with expectoration increases when lying over the healthy side. 2- hemoptysis. 3- fever. 4- clubbing of fingers. 5- rupture of abscess into pleural sac causing empyema (pus in pleural cavity).  II. BRONCHIECTASIS DEFINITION: ABNORMAL PERMANENT DILATATION OF THE DISTAL BRONCHI WITH ACCUMULATION OF PUS. Types: 1-Congenital: (immotile cilia syndrome) 2-Acquired: Secondary to severe recurrent infection leading to destruction of the bronchial muscles & elastic fibers, fibrosis & weakness of the wall and dilatation of lumen. (e.g. chronic bronchitis).  II. BRONCHIECTASIS Clinical picture: Recurrent attacks of cough & expectoration of large amount of purulent feoted sputum related to posture. Chronic toxemia symptoms: recurrent fever, weight loss, pallor, clubbing of fingers. Halitosis. Haemoptysis may occur in 50% of patients.  II. BRONCHIECTASIS INVESTIGATIONS: 1. CHEST X-RAY. 2. CT. CHEST. 3. SPUTUM CULTURE & SENSITIVITY. 4. BRONCHOSCOPY TO: ▪ DIAGNOSE THE UNDERLYING CAUSE. ▪ DRAIN THE PUS. ▪ INJECTING ANTIBIOTICS.  II. BRONCHIECTASIS TREATMENT: 1. POSTURAL DRAINAGE OF THE PUS WITH THE ASSISTANCE OF PHYSIOTHERAPIST. 2. ANTIBIOTICS FOR EXACERBATIONS. 3. MUCOLYTICS + EXPECTORANTS + BRONCHODILATORS. 4. SURGERY IN COMPLICATED CAUSES.  OBSTRUCTIVE LUNG DISEASES 1. Emphysema 2. Chronic bronchitis 3. Chronic obstructive pulmonary disease 4. Bronchial Asthma 5. Cystic fibrosis. Definition: These diseases are a heterogeneous group of pulmonary disorders that share in common obstruction of air flow and deranged gas exchange  BRONCHIAL ASTHMA Chronic inflammatory disease of the lung airways. Characterized by Paroxysmal attacks of dyspnea that resolves spontaneously or with therapy. Cough. Wheezes. Chest tightness due to air way obstruction. The etiology of the disease is incompletely understood.  BRONCHIAL ASTHMA TYPES & PATHOPHYSIOLOGY 1- Extrinsic asthma 2- Intrinsic asthma Known definite external cause No causative agent identified ❑ Occurs in atopic children & young 1. Often starts at middle age. adults. 2. Non-antigenic stimuli include: ❑ Mediated by exposure to allergen in Respiratory tract infections. patients with history of allergy. Emotional stress. ❑ Patients have high levels of IgE and Exercise. eosinophils. Cold weather. ❑ IgE binds to the antigen (allergen) Perfumes. forming antibody → antigen complex Cigarette smoking. which then attaches to mast cells. 3. Mechanism: Mast cells degranulate and release mediators resulting in inflammation, Probably highly sensitive vagal spasm, increased mucous secretion receptors in the bronchial tree →stimulation and the asthma starts. of these receptors → release of mast cells mediators → bronchospasm.  BRONCHIAL ASTHMA TYPES & PATHOPHYSIOLOGY 1. Extrinsic asthma 2. Intrinsic asthma Known definite external cause No causative agent identified  BRONCHIAL ASTHMA Pathology: The previously mentioned stimuli result in the following changes: 1. Bronchospasm (contraction of the small muscles). 2. Edema of bronchial mucosa 3. Excessive mucous blocking the lumen. 4. Cellular infiltration in the submucosa (eosinophils, lymphocytes, mast cells).  BRONCHIAL ASTHMA Clinical picture: Complications: 1. The attack usually occur 1. Pneumothorax. At night During sleep 2. Status asthmaticus: Asthma Early morning. failed to resolve with therapy 2. The attack may last few minutes to within 24 hours. Patient should several hours then resolves spontaneously or with therapy. be hospitalized to receive 3. Patient complains from: intensive therapy. Dyspnea 3. Recurrent bronchial infections Cough (asthmatic bronchitis). Thick mucoid sputum Wheezy tight chest (may be silent in severe attack).  BRONCHIAL ASTHMA INVESTIGATIONS: 1. Pulmonary function tests 2. Chest x-ray: Hyperinflation. Estimate the degee of Pneumothorax. obstruction Emphysema. ↓ FEV1 (forced expiratory value in 1sec) 3. Arterial blood gases analysis (ABG): ↓ FEV1/FVC (forced vital capacity) hypopoxia & hypocarbia (acute ↓ PEF (peak flow meter) severe asthma)→ hypercarbia 4. Skin hypersensitivity test. 5. Sputum & blood esinophilia. 6. Elevated serum IgE levels.  BRONCHIAL ASTHMA TREATMENT 1. Prophylaxis: Avoid exposure to the triggering factors & proper treatment of respiratory infection. 2. Therapeutic: Inhaled agents: - Rapid-Acting B2-agonists (RABA): salbutamol/salmetrol. - Inhaled corticosteroids (ICS). - Long-acting B2-agonist: formoterol - Inhaled anticholinergic drugs: ipratropium. Mast cells stabilizers: ketotifen. Anti-leukotrines: montelukast. Oral steroids. Biologisics: omalizumab Status asthmaticus : IV. Theophylline or IV. Steroids. TUBERCULOSIS  TUBERCULOSIS CAUSATIVE ORGANISM Mycobacterium tuberculosis is acid fast, alcohol fast aerobic bacillus, highly resistant to antibiotics. Mode of transmission: droplet infection from patients with open pulmonary tuberculosis. Mycobacterium tuberculosis two types: 1) human bacillus 98%: inhalation of infected droplets. It affects lungs (pulmonary tuberculosis). Bones, genito urinary and joints are affected by blood spread. 2) bovine bacillus 2%: intake of infected milk causing intestinal tuberculosis. It may affects tonsils and cervical lymph nodes.  TB SPREADS THROUGH THE AIR TB SPREADS FROM PERSON TO PERSON WHEN SOMEONE WITH CONTAGIOUS TB COUGHS, SPEAKS, OR SINGS. 19  TUBERCULOSIS Epidemiology: The disease is prevalent in developing countries with low socioeconomic standards, poor nutrition & bad ventilation. TB is increasing in developed countries as well with increasing number of: AIDS patients. Malignancies. The use of immunosuppressive drugs → which result in depression of the host immune defense mechanisms. Factors that increase the risk of TB: 1. Immunocompromised patients as HIV, malignancy and steroid therapy 2. Diabetes mellitus 3. Chronic renal failure 4. Malnutrition 5. Close contact with a patient who is sputum smear positive  A. PRIMARY TB Pathology: (CHILDHOOD) The first infection with M. Tuberculosis is known as primary T.B. Site: Usually affect the upper to mid zones of the lungs. The classic primary triad of pathology complex is known as Ghon’s focus + lymphangitis + lymphadenitis. Ghon’s focus (disease specific granuloma): central area of necrosis (caseation) surrounded by infected macrophages & foamy giant cells (macrophages engulfing m. Tuberculosis) followed by inflammatory cells (t-lymphocytes), followed by fibrosis. The draining lymph nodes at the hilum are inflamed: regional lymphangitis & lymphadenitis. Fate: 1. 80% heals by fibrosis & calcification (TB Dormant inside). 2. 20% due to depressed host defense mechanisms → clinical progression.  A- PRIMARY TB (CHILDHOOD) Clinical picture TB Pneumonia Primary T.B. Is asymptomatic in the great majority of individuals. In minority of immune suppressed patients, may cause: 1. TB pneumonia. 2. Pleural effusion, pericardial effusion. 3. Blood spread to other organs. 4. Enlarged lymph node may cause compression of bronchus → lung collapse of the affected segment. Left upper lung zone Pleural effusion collapse  B. SECONDARY TB (ADULTHOOD) Pathology: The source of infection is either: 1-Endogenous: reactivation of the dormant primary disease. 2-Exogenous: reinfection from open TB case. Endogenous infection is much more common due to decreased immunity as in: AIDS. Immunosuppressive drugs. Malnutrition. Uncontrolled diabetes mellitus. Secondary TB may present as: 1. Pulmonary TB. 2. Extrapulmonary TB. The lesions of pulmonary TB usually affects the apex or upper zones of the lungs with cavities formation surrounded by fibrosis.  B. SECONDARY TB (ADULTHOOD) Clinical picture: I. Post-primary is characterized by: 1. TB toxemia: night fever, night sweat, loss of appetite & loss of weight. 2. Chronic productive cough: mucoid, mucopurulant or blood-stained sputum (typical feature). 3. Pleural effusion and lung consolidation (TB pneumonia) → in advanced cases. II. Asymptomatic cases are discovered by routine X-ray chest in the form of apical lung cavitation and fibrosis. III. Symptoms of extra-pulmonary tuberculosis (blood spread): 1. Cervical lymphadenopathy with formation of cold abscess and skin sinus. 2. Bone, joint, meninges, intestine, kidneys and/ or pericardium affection.  INVESTIGATIONS TUBERCULIN TEST Chest x-ray: Purified protein derivative (PPD) is Typically shows nodular shadows in injected (0.1ml.) In forearm. Induration the upper zones. (nodule) 10 mm in diameter or more after 72 hours is considered positive. C.T./ MRI chest more sensitive. 1. Tuberculin positive with normal x ray chest is considered immune. Sputum examination for TB Bacilli 2. Tuberculin positive with abnormal x (Repeatedly for 3 successive days) by: ray chest is considered infected. 1. Smear (ZN stain). 3. Tuberculin negative child needs BCG vaccination. 2. Culture (Bactec). 3. PCR.  MANAGEMENT PROPHYLAXIS: TREATMENT: Generally, rest in bed till symptoms disappear, good nutrition. Brief hospitalization is required for highly infectious patients (open TB), patients become non-infectious after Good housing & nutrition. 2 weeks of beginning therapy. BCG vaccination (gives 10 – 15 years Symptomatic therapy eg. Expectorants. protection) of children & young adults. Specific therapy: It is compulsory in egypt during first 3 A- pulmonary TB months after birth. Antibiotic course for 6 months: - Rifampicin 600 mg with isoniazid 300 mg for 6 months Sanitary milk supply. + - Pyrazinamide (for the first 2 months). B- extrapulmonary TB Treatment for longer periods up to 12 – 18 months. - Rifampicin 600 mg with isoniazid 300 mg for 12-18 months + - Pyrazinamide + ethambutol (for the first 3-4 months). Infective Endocarditis DR Dina Attia Professor of Tropical Medicine Faculty of Medicine, Beni-Suef University Faculty of Dentistry, Al Ahram Canadian University 2024 Anatomy of the heart  Infective endocarditis Definition 2. Caused by colonization 1. A serious infection of and invasion to the heart the endocardium valve or mural including heart valves. endocardium by microbe. 4. Leading to formation of 3. The heart valve large friable vegetations, affected is either native which is composed from (normal or diseased) or thrombotic debris (fibrin prosthetic. + Platelets) & the organisms. Often lead to destruction of the affected cardiac tissue. Pathogenethesis  Infective endocarditis Etiology: The combination of two factors bacteremia and underlying cardiac disease 1. Bacteremia Causative organisms: Gram positive cocci; strept. Viridans, strep faecalis Gram negative bacilli; Hemophilus, Klebsiella, pseudomonas, brucella, HACEK Other organisms; Fungi, rickettsiae Routes of infection Dental procedures e.g. Tooth extraction, Surgery, Scaling, Instrumentation beyond the root apex during endodontic treatment, oral or upper respiratory surgeries e.g. strept. Viridans Gastrointestinal and genitourinary procedures e.g. strept. Faecalis. Cardiac surgery and catheterization e.g. Staphaureus 2. Underlying cardiac disease: Valvular lesions e.g mitral incompetence, aortic incompetence, aortic stenosis. Congenital anomalies; VSD, PDA and coarctation of the aorta. Prosthetic valves  Clinical picture: 1.General manifestations: Fever Anorexia, loss of weight and weakness Marked pallor and toxic facies Pulse: tachycardia or absent pulse Eyes: conjunctival petechiae, Roth spots and sudden blindness Hands and lower limbs: Pale clubbing Osler’s nodules Splinter hemorrhage Janeway lesions Pallor, petechiae  Osler nodules Janeway Lesions Roth Spots Retinal hemorrhages with Pale centers Painful erythematous nodules On tips of figers and toes Painless erythematous macules On tips on palms and soles of feet  Alterations of the already present murmurs with development of new murmurs 2. Cardiac manifestations Features of the underlying cause e.g. MI Precipitation of heart failure. Clinical picture 3. Embolization Spleen: enlarged soft and tender Stitching pain with splenic rub Kidneys: acute glomerulonephritis Focal embolic glomerulonephritis Renal infarction CNS: cerebral embolism Subarachnoid hemorrhage Lungs: pulmonary infarction and infections Joints: arthralgia 4. Immune processes 5. Complications: Heart failure Embolization Renal failure Mycotic aneurysms Complications of therapy  Investigations: Blood culture: most important and 80% positive Bone marrow culture Blood picture: normocytic anemia, leucopenia with monocytosis in SBE or PNL in ABE ESR and CRP raised Urine analysis: microscopic or macroscopic hematuria Proteinuria or casts Immunological tests: increased gamma globulins Cardiac investigations: Echocardiography Chest X-ray and ECG  Treatment: I. Prophylactic 1. Antibiotics Dental procedures: Amoxycillin 3gram oral 1hr before the procedure and 1.5 g 6 hrs later Erythromycin (for penicillin allergic patients), 1 gram oral 1 hr before the procedure and 0.5 gram 6 hrs later Gastrointestinal or genitourinary procedure: Ampicillin 2 gram and gentamycin 80 mg IM or IV half an hr before the procedure and repeat it 8 hrs later. Cardiac surgery and catheterization Cefotaxime 2 gram IV 2 hrs before the procedure and 1 gram 6 hrs for 4 doses after 2. Correction of predisposing factors e.g. congenital defects II. Therapeutic 1. Specific treatment Once infective endocarditis is suspected, treatment must be started immediately, with bactericidal drugs, in large doses and given parenterally. Treatment must be continuous 4-6 weeks, some patients require longer periods of treatment Antibiotics include: SBE: (strept. Viridans and fecalis) Crytaline penicillin G: 2-4 million units/ 4 hr IV Or Ampicillin: 2gram /4 hr IV. Plus Streptomycin 0.5 gram /12 hr IM Or Gentamycin 80 gram / 8hrs IV For ABE: (staphaureus and gram -ve bacilli) As with SBE plus cloxacillin 2 gram / 4 hr IV Resistant cases: according the blood cultures Fungal endocarditis is suspected; Amphotericin B is given 2. General care: Complete bed rest Light nutrient diet 3. Symptomatic treatment: antipyretics 4. Treatment of complications: Heart failure Renal failure 5. Surgical treatment: Valve replacement Replacement of infected prosthesis Excision of infected ductus arteriosus or coarctation Hypertension Ahmed Rashad Mashaal Physiology 1  Factors influence blood pressure: Blood pressure = Cardiac output (CO) x systemic vascular resistance (SVR)  N.B. CO = SV X HR  Systolic pressure depends on cardiac output.  Diastolic pressure depends on peripheral resistance. Physiology 2 Definition  Risk factors of Types Primary hypertension Secondary hypertension as a complication of another condition or disease 1- Renal disorders 2- Endocrinal causes 1. Parenchymal diseases as glomerulonephritis. A. Adrenal ( suprarenal) cortex:  Cushing syndrome (increased cortisol) 2. Reno – vascular disease as  Conn's disease (increased aldosterone) renal artery stenosis. Both cause sodium and water retention.  In this case ischemia leads to decrease blood flow to B. Suprarenal medulla: kidney leading to release of  Pheochromocytoma: renin leading to increase in increased adrenaline and nor-adrenaline arterial blood pressure. leading to vasoconstriction. 3- Others: Drugs: Contraceptive pills – Cortisone – NSAIDS - Cocaine. Neurological disorders: Brain tumors – Head injury – Brain oedema. Congenital narrowing of aorta (Coarctation of aorta). Clinical picture 1 Silent Killer disease Symptoms of complications  Usually asymptomatic.  The patient may complain of: 1. headache. 2. Dizziness & Vertigo. 3. Epistaxis. 4. Blurred vision. 5. Nausea, vomiting. 6. Chest tightness.  Clinical picture 2 (complications) 1. Cardiac:  Left ventricular hypertrophy.  Coronary artery disease.  Heart failure.  Peripheral vascular disease. 2. Cerebral:  Cerebrovascular stroke (infarction).  Brain haemorrhage (rupture of aneurysm).  Brain oedema in hypertensive emergency. 3. Renal:  Nephrosclerosis end in renal failure 4. Retinal:  retinopathy (detected by fundus examination). Management Treatment Diagnosis ISCHEMIC HEART DISEASES Ahmed Rashad Mashaal  Introduction Definition: Coronary anatomy  Also known as coronary artery disease.  Myocardial ischemia occurs when there is an imbalance between the blood supply carrying oxygen and nutrients to the heart and the demands of the heart.  Atherosclerosis is by far the main cause of IHD.  Other rare causes: vasculitis- vasospasm.  Overview Etiology Clinical presentation  Coronary atherosclerosis is the main cause of the coronary artery disease.  Patients may manifest  Risk factors of coronary heart clinically as: disease are: 1- Cardiac pain (angina 1. More common in middle age males. 2. Diabetes mellitus pectoris or myocardial 3. Hypertension infarction). 4. Obesity 2- Arrhythmia. 5. Cigarette smoking 3- Heart failure. 6. Hyperlipidemia 4- Sudden death. 7. Lack of exercise (sedentary life style)  Angina Pectoris 1  Transient myocardial ischemia results in chest pain. It is retrosternal pain which is compressing in nature, tends to spread to the shoulders, lower jaw and left arm.  Angina pectoris occurs when the heart is over working as in emotional stress, muscular exercise, heavy meals and excess smoking.  The attack usually lasts few minutes and is relieved by rest and the intake of sublingual nitrates. Angina Pectoris 2 Investigations: Treatment  ECG: Not helpful. a. Physical and mental rest  Stress ECG: high diagnostic b. Sublingual nitrates during the attack yield. ( it dilates coronary arteries)  Echocardiography: highly c. Correction of risk factors as smoking and obesity. suggestive. d. Long acting coronary dilators  Angiography: cardiac e. Beta blockers to decrease heart rate and blood pressure. catheter with contrast f. Aspirin to minimize the risk of injection (diagnostic and myocardial infarction. therapeutic). g. Cardiac catheter with angioplasty (PCI) or CABG.  Myocardial infarction 1 Definition Clinical picture  It is an ischaemic necrosis of a part of the cardiac muscle as a 1- Chest pain similar to that of angina with the following differences: result of sudden & complete a. More severe. cut of blood supply. The cause b. More prolonged. is usually thrombosis on the c. Occurs without precipitating factors top of coronary atheroma. as stress and exercise. d. It is not relieved by rest or sublingual nitrates. 2- It may present as shock and the patient is cold with pale skin. 3- Other complications are heart failure, arrhythmia or sudden death.  Myocardial infarction 2 Investigations: Management  ER admission & Oxygen  Assessment on ER basis. supplementation if hypoxia is present.  a. ECG: suggestive findings.  Sublingual nitrates or even IV  b. Elevation of serum enzymes: nitroglycerin. ❑ lactate dehydrogenase (LDH).  Analgesia: by opiates. ❑ Aspartate aminotransferase (AST).  Thrombolytic agents within 6 hours of starting symptoms (to ❑ Creatinine kinase (CK) or the dissolve the thrombus) and more specific CK-MB. should be followed by ❑ Troponin. anticoagulants.  PCI after thrombolysis.  Treatment of complications. End of cardiology Thank you