Pulmonary Diseases and Thoracic Surgery (M3517) Course Specifications PDF

 Course Specifications A. Basic Information 1-Program Title: Bachelor degree in Physical therapy( Program 2016) 2- Academic year :2024-2025 3-Department Offering the Program (s): All departments. 4-Department Responsible for the course: Department of pulmonology - Faculty of med...

 Course Specifications A. Basic Information 1-Program Title: Bachelor degree in Physical therapy( Program 2016) 2- Academic year :2024-2025 3-Department Offering the Program (s): All departments. 4-Department Responsible for the course: Department of pulmonology - Faculty of medicine Al-Azhar University in collaboration with the department of Physical therapy of internal medicine and elderly 5-Course Title and Code: Pulmonary Diseases and Thoracic Surgery (M3517) 6-Year/ Level: 3rd year/ level 5 7- No. of credit Hours/ Units: 2 H/W Lecture: 2 H/W Practical: 0 H/W Clinical: 0 H/W Contact hours: 2 H/W 8- Teaching staff: Dr.Eman Mostafa 9-Authorization Date of Course Specification: Department:3/9/2024 Faculty council :15/9/2024 B. Professional Information 1. Course Aims: This course provides the student with the fundamental knowledge about the development of pulmonary system, Physiology of the respiratory system , Hypoxia & ABG , Pulmonary function tests. Evaluate patients with chest diseases; identify pathogenesis, signs and symptoms different chest disorders. 2. Intended Learning Outcomes From The Course (ILOs): a. Knowledge and Understanding Upon successful completion of the course the students should be able to: a.1 -Identify anatomical and physiological changes of pulmonary diseases ( A2). a.2 - Describe perfectly the signs and symptoms of chest diseases ( A2). a.3 - list the difference between the pathogenesis of restrictive and obstructive lung diseases ( A2). a.4 - Identify each chest problem according to its characteristics features and know the details of important points related to chest diseases ( A2) a.5 - Outline the medical treatment and assessment for different chest diseases ( A2). b.Intellectual Skills Upon successful completion of the course the students should be able to: b.1 -Discuss basic anatomical and physiological changes of pulmonary dysfunctions ( B1). b.2 - Synthesize proper list for history taken from patients as medical history and surgical history ( B3) b.3 - Differentiate between abnormalities changes between restrictive and obstructive lung diseases ( B1)-(B2). b.4 – Discuss different chest problems ( B1). b.5 - Interpret the medical evaluative and treatment procedures to the chest patients like clinical laboratory studies, imaging test, lung biopsy and other non-invasive diagnostic tests ( B1,B2) b.6 - Discuss mental correlation between academic knowledge and different cases ( B1) c. Professional and Practical skills N.A d.General and Transferable Skills Upon successful completion of the course the students should be able to: d.1- Demonstrate the effective use of English language and medical terminology (D2) 3. Course Content: No. of credit hours ILOS Th Prac clin Tot Knowledge Intellectu Professional General and and al Skills and Practical Transferable Skills No Topics Understan skills ding Theoretical 2 0 0 2 a1 b1 ------- d1 part : 1 Development of pulmonary system.Anatomy of  cardiovascular system. embryology of the lungs. development of the respiratory system 2 Physiology of 2 0 0 2 a1 b1 ------- d1 the respiratory system  Central regulatio n of respirati on.Peripheral regulation of respiration 3 Hypoxia & 2 0 0 2 a4 b2,b3, ------- d1 Arterial blood gases b4.types of respiratory failure.acidosis and alkalosis 4 Pulmonary 2 0 0 2 a5 b5 ------- d1 function tests  Lung volumes  Lung capacitie s Diffusion capacity 5 History and 2 0 0 2 a5 b2,b5 ------- d1 clinical examination   General examinat ion  Localize d examinat ion  Ausculta tion Percussion 6 Mid term 7 COPD 2 0 0 2 a2-a3 b3,b4 ------- d1  Asthma  Chronic bronchiti s Emphysema 8 Bronchial 2 0 0 2 a2-a5 b2-b5 ------- d1 asthma  Patholog y  Signs and sympto ms  Diagnosi s treatment 9 Suppurative 2 0 0 2 a2-a5 b2-b5 ------- d1 lung disease & Pleural disorders  Patholog y  Signs and sympto ms  Diagnosi s  treatment 10 Restrictive 2 0 0 2 a2-a5 b2-b5 ------- d1 lung disease  Patholog y  Signs and sympto ms  Diagnosi s treatment 11 2 0 0 2 a2-a4 b2-b4 ------- d1 Pneumonia  Patholog y  Signs and sympto ms 12 2 0 0 2 a1-a5 b1-b6 ------- d1 Pneumonia  Diagnosi s treatment 13 COVID 19 and 2 0 0 2 a5 b5 ------- d1 vaccine  Patholog y Types of vaccines 14 Revision 15 Final theoretical  exam 4. Teaching and Learning Methods: Teaching and Learning Teaching and ILOS Methods Learning Knowledge Intellectual Profession General Methods in this and Skills al and and Understandi Practical Transferab course ng skills le Skills Interactive lecture √ a1-a5 b1-b6 ------- d1 -- -- -- -- Clinical training -- -- -- -- -- Lab training -- Discussion √ a1-a5 b1-b6 ------- d1 Self –based Learning -- -- -- -- -- )Project( Self –based Learning -- -- -- -- -- )Research( -- -- -- -- Problem solving -- -- -- -- -- Brain storming -- -- -- -- -- Case study -- -- -- -- -- Critical thinking -- -- -- -- -- Cooperative learning -- E- learning √ a1-a5 b1-b6 d1 -- -- -- -- Simulation -- Blended learning √ a1-a5 b1-b6 d1 -- -- -- -- Creative learning -- 5. Student Assessment: Assessment Methods used ILOS No Methods in course Knowledge Intellectual Professiona General and Transferab and Skills l and Skills Understandin Practical g skills 1 Theoretical exam √ a1-a5 b1-b5 ____ d1 2 practical exams ____ ____ ____ ____ ____ 3 clinical exams ____ ____ ____ ____ ____ Crouse work Midterm theoretical √ a1,a4,a5 b1-b2 ____ d1 exam Midterm practical ____ ____ ____ ____ ____ 4 exam Midterm clinical ____ ____ ____ ____ ____ exam Research ____ ____ ____ ____ ____ Presentation ____ ____ ____ ____ ____ Project ____ ____ ____ ____ ____ Quizzes ____ ____ ____ ____ ____ Assignments √ a1-a4 b1-b6 ____-- d1-- Attendance: - Lecture _ ____ ____ ____ ____ - Practical _ ____ ____ ____ ____ - Clinical _ ____ ____ ____ ____ - Lab -- ____ ____ ____ ____ No Assessment method Semester week Weighting (%) 1. Theoretical exam Examination 40%=40 Marks period starting from 15th week 2. Practical and clinical exams ___ ___ 3. Crouse work: During course 60%=60 Marks  midterm theoretical exam Week 6th 40%=40 Marks Mid term practical and clinical ----- ------- exam assignments, During course 20%=20Marks Quiz ----- ------- Total 100% = 100 marks 6. List Of Text Books And References: a- List of Text Books And References:. C Ronald B. George MD (Editor),2022: chest Medicine: Essentials of Pulmonary and C inricritical Care Medicine 5th Edition.. PhilipT.Cagle,2021 Pulmonary pathology,3rd edition. b- Lectures Notes: B basics of pulmonary Dr Eman Mostafa 2024-2025 7. Facilities Required For Teaching And Learning:  Lecture room and white board.  CPU and over-head projector. Course lecturer : Name :Dr / Eman Mostafa Signature : C course coordinator: Name : : Ass.Prof.Dr/ Ahmed Signature : Mokhtar H Head of departments: Name : Ass.Prof.Dr/ Ahmed Signature : Mokhtar  List of content List of content Page number 1) Development of pulmonary system 2) Anatomy of CVS 3) Physiology of respiratory system 4) Hypoxia 5) ABG 6) Pulmonary function tests 7) Diaphragm 8) History and clinical examination 9) COPD 10) Bronchial asthma 11) Restrictive lung diseases 12) Suppurative lung disease 13) Pleural disorders 14) Pneumonia 15) COVID 19 and vaccine 16) Thoracic surgery A.Thoracic incisions B. Intervention pulmonary procedure C. lung surgery  Development of pulmonary system Development of the lower respiratory tract begins on day 22 and continues to form the trachea, lungs, bronchi, and alveoli. The process divides into five stages: embryonic, pseudoglandular, canalicular, saccular, and alveolar stage. Although the process begins early on in fetal development, complete maturation does not take place until the child is approximately 8 years of age. Mechanism of oxygenation during fetal life  During fetal development, the placenta acts as the sole exchange surface  Oxygenated, nutrient-rich blood enters the placenta via the umbilical vein and into the inferior vena cava, bypassing the liver through a shunt known as ductus venosus.  A rudimentary valve at the opening of the inferior vena cava shifts the blood from the right atrium to the left atrium through the foramen ovale and septum secundum, before passing into the aorta to supply the brain.  The deoxygenated blood from the brain returns into the right atrium via the superior vena cava and subsequently gets shifted to the right ventricle.  Typically, the deoxygenated blood would enter the pulmonary circulation via the pulmonary arteries, however as the lungs are not necessary for respiration during gestation, the blood is diverted into the aorta through the ductus arteriosus and returns to the placenta via the umbilical arteries.  SURFACTANT  Surfactant is a surface acting material or agent that is responsible for lowering the surface tension of a fluid.  Pulmonary surfactant is a surface-active complex of phospholipids and proteins formed by type II alveolar cells. The proteins and lipids that make up the surfactant have both hydrophilic and hydrophobic regions. By adsorbing to the air-water interface of alveoli, with hydrophilic head groups in the water and the hydrophobic tails facing towards the air, the main lipid component of surfactant, dipalmitoylphosphatidylcholine (DPPC), reduces surface tension.  As a medication, pulmonary surfactant is on the WHO Model List of Essential Medicines, the most important medications needed in a basic health system  Surfactant that lines the epithelium of the alveoli in lungs is known as pulmonary surfactant and it  decreases the surface tension on the alveolar membrane. Source of secretion of pulmonary surfactant Pulmonary surfactant is secreted by two types of cells: 1. Type II alveolar epithelial cells in the lungs, which are called surfactant secreting alveolar cells or pneumocytes. 2 Clara cells, which are situated in the bronchioles. These cells are also called bronchiolar exocrine cells Functions of surfactant a) Surfactant reduces the surface tension in the alveoli of lungs and prevents collapsing tendency of lungs. b) Surfactant is responsible for stabilization of the alveoli, which is necessary to withstand the collapsing tendency. c) It plays an important role in the inflation of lungs after birth. a. Surfactant play role in defense within the lungs against infection and inflammation Effect of deficiency of surfactant  Infant respiratory distress syndrome (IRDS) is caused by lack of surfactant, commonly seen in premature babies born before 28–32 weeks of gestation.  Congenital surfactant deficiency  Pulmonary alveolar proteinosis  Surfactant metabolism dysfunction  CARDIOVASCULAR SYSTEM ANATOMY The cardiovascular system consists of  The heart,  Blood vessels, and  The approximately 5 liters of blood that the blood vessels transport. The heart consists of four chambers:  Atria: the two upper chambers (they receive blood).  Ventricles: the two lower chambers (they discharge blood). The left atria and left ventricle are separated from the right atria and right ventricle by a wall of muscle called the septum   The wall of the heart consists of three layers of tissue:  Epicardium — protective layer mostly made of connective tissue.  Myocardium — the muscles of the heart.  Endocardium — lines the inside of the heart and protects the valves and chambers.  These layers are covered in a thin protective coating called the pericardium. Heart Valves  The heart is equipped with four valves, which allow blood to flow in only one direction through the heart chambers.  The two atrioventricular (AV) valves, the mitral valve (bicuspid valve), and the tricuspid valve, which are between the upper chambers (atria) and the lower chambers (ventricles).  The aortic valve and the pulmonary valve, are in the arteries leaving the heart.  Great Vessels The great blood vessels provide a pathway for the entire cardiac circulation to proceed.  Aorta  Superior and inferior vena cava.  Pulmonary arteries.  Pulmonary veins.  PHYSIOLOGY OF THE HEART DIVISIONS OF THE CIRCULATORY SYSTEM (1) The systemic (or greater) circulation This circulation starts from the left ventricle →aorta → large arteries → small arteries → arterioles → capillaries → venules → veins → SVC and IVC (superior and inferior venae cavae) → right atrium. (2) The pulmonary (or lesser) circulation This circulation lies in series with the systemic circulation, and it starts from the right ventricle → pulmonary trunk (= pulmonary artery) → lungs → pulmonary capillaries → 4 pulmonary veins → left atrium. (3) The special circulations These include the circulations at specific sites e.g. coronary and cerebral circulations. INTRINSIC CONDUCTION SYSTEM OF THE HEART  The spontaneous contractions of the cardiac muscle cells occurs in a regular and continuous way, giving rhythm to the heart.  The components of the cardiac conduction system are the SA node, AV node, bundle of His, bundle branches, and Purkinje fibers.  Cardiac muscle cells. Cardiac muscle cells can and do contract spontaneously and independently, even if all nervous connections are severed  The electrical impulse travels from the sinus node to the atrio-ventricular node (also called AV node). There, impulses are slowed down for a very short period, then continue down the conduction pathway via the bundle of His into the ventricles The cardiac cycle The stages of the cardiac cycle can be roughly divided into the four stages:  Filling phase – the ventricles fill during diastole and atrial systole  Isovolumetric contraction – the ventricles contract, building up pressure ready to pump blood into the aorta/pulmonary trunk  Outflow phase – the ventricles continue to contract, pushing blood into the aorta and the pulmonary trunk. Also known as systole   Isovolumetric relaxation – the ventricles relax, ready to re-fill with blood in the next filling phase THE CONTROLE OF HEART RATE THE AUTONOMIC NERVOUS SYSTEM  Parasympathetic The parasympathetic input into the heart is via the vagus nerve. When stimulated, acts to decrease in heart rate.  Sympathetic The fibres release noradrenaline, which increase heart rate, as well as increasing the force of contraction.  CHEMICAL REGULATION OF THE HEART RATE  Changes in blood gases  Hormonal control, e.g. adrenaline  Drugs PHYSIOLOGY OF THE RESPIRATORY SYSTEM  Respiratory system is one of the systems of the human body.  Other than its major function, which is supplying the cells with needed oxygen to produce energy and getting rid of carbon dioxide , it also has other functions , such as : 1. Vocalization , or sound production. 2. Participation in acid base balance. 3. Participation in fluid balance by insensible water elimination (vapors ). 4. Facilitating venous return. 5. Participation in blood pressure regulation : Lungs produce Angiotensin converting enzyme ( ACE) 6. Immune function : Lungs produce mucous that trap foreign particles and have cilia that move foreign particles away from the lung. 7. They also produce alpha 1 antitrypsin that protect the lungs themselves from the effect of elastase and other proteolytic enzymes Breathing:  The processes of inspiration and expiration are vital for providing oxygen to tissues and removing carbon dioxide from the body. MECHANICS OF BREATHING: INSPIRATION  Allows air to be moved into the lungs and requires the contraction of various muscles. It is the active part of the breathing process, which is initiated by the respiratory control center in medulla oblongata (Brain stem).  Activation of medulla causes a contraction of the diaphragm and intercostal muscles leading to an expansion of thoracic cavity and a decrease in the pleural space pressure.   In normal quite breathing the diaphragm moves downward about 1 cm but on forced inspiration/expiration total movement could be up to 10 cm.  When it is paralysed it moves to the opposite direction (upwards) with inspiration, paradoxical movement.  The external intercostal muscles connect adjacent ribs. When they contract the ribs are pulled upward and forward causing further increase in the volume of the thoracic cavity. As a result fresh air flows along the branching airways into the alveoli until the alveolar pressure equals to the pressure at the airway opening. The diaphragm is the most important muscle of inspiration. EXPIRATION:  Expiration is a passive event due to elastic recoil of the lungs. However, when a great deal of air has to be removed quickly, as in exercise, or when the airways narrow excessively during expiration, as in asthma, the internal intercostal muscles and the anterior abdominal muscles contract and accelerate expiration by raising pleural pressure.  The diaphragm and external intercostal muscles relax and return to their resting position  The elastic recoil of the stretched lungs causes them to recoil back to their original volume rather than due to an active movement  When the pressure within the lungs is greater than the outside, air rushes out of the lungs as gas molecules move from an area of high pressure to low pressure FORCED BREATHING Forced inspiration  This is similar to normal inspiration (diaphragm and external intercostals) but requires effort from the inspiratory accessory muscles such as  scalenes,  sternocleidomastoid,  pectoralis major and minor,  serratus anterior and  latissimus dorsi. Forced expiration  Unlike normal expiration, this is an active process. It involves contraction of the abdominal muscles which forces the diaphragm upwards reducing the volume of the thoracic cavity.  It also requires contraction of the  internal intercostal muscles and  innermost intercostal muscles which pull the ribs downwards.  Both these actions lead to a decreased thoracic volume and increase pressure so the air move out quicker than in normal expiration.  Control Of Respiration Breathing is an automatic and rhythmic act produced by networks of neurons in the hindbrain (the pons and medulla). The neural networks direct muscles that form the walls of the thorax and abdomen and produce pressure gradients that move air into and out of the lungs. The respiratory rhythm and the length of each phase of respiration are set by reciprocal stimulatory and inhibitory interconnection of these brain-stem neurons. An important characteristic of the human respiratory system is its ability to adjust breathing patterns to changes in both the internal milieu and the external environment. Ventilation increases and decreases in proportion to swings in carbon dioxide production and oxygen consumption caused by changes in metabolic rate. The respiratory system is also able to compensate for disturbances that affect the mechanics of breathing, such as the airway narrowing that occurs in an asthmatic attack. Breathing also undergoes appropriate adjustments when the mechanical advantage of the respiratory muscles is altered by postural changes or by movement. This flexibility in breathing patterns in large part arises from sensors distributed throughout the body that send signals to the respiratory neuronal networks in the brain. Chemoreceptors detect changes in blood oxygen levels and change the acidity of the blood and brain. Mechanoreceptors monitor the expansion of the lung, the size of the airway, the force of respiratory muscle contraction, and the extent of muscle shortening 1. Neural mechanism Respiratory Center In Medulla  Inspiratory center  Expiratory center In Pons  Pneumotaxic center. acts on inspiratory center to stop inspiration therefore regulates inspiration and expiration.  Apneustic center. causes Apneusis [deep inspiration] when Pneumotaxic center is damaged 2. Chemical mechanism  Chemical factors which affect the ventilation are:-  PO2  PCO2  H+ ion  Their effect is mediated via respiratory chemoreceptor. There are two types of Chemoreceptors 1. Peripheral Chemoreceptors are Carotid bodies & Aortic bodies. 2. Central Chemoreceptors They are located in the medulla near the respiratory center. Effect of PO2, PCO2 , and H+ ion On Peripheral & Central Chemoreceptors  Decreased PO2, increased PCO2, increased H+ ion concentration in arterial blood stimulates Peripheral Chemoreceptors.  Most important stimulating factor is decreased PO2 on peripheral chemoreceptors.  Increased PCO2 in the arterial blood and increased H+ ion in the brain extracellular fluid (ECF) strongly stimulates the central chemoreceptors and dominant control of ventilation. 3. Baroreceptors 4. Stretch receptors FUNCTION OF THE RESPIRATORY SYSTEM  Gas exchange is the process by which oxygen and carbon dioxide move between the bloodstream and the lungs.  This is the primary function of the respiratory system and is essential for ensuring a constant supply of oxygen to tissues.  Respiration has two forms : 1. External respiration , which is the function of respiratory system , through which the body gains the oxygen and get rid of carbon dioxide. 2. Internal respiration , which occurs inside the cell , where the oxygen burns glucose to produce energy , CO2 , and synthetic water.  Respiration occurs in three steps : 1- Ventilation: The movement of air between the atmosphere and alveoli 2- Perfusion The movement of blood through the pulmonary capillaries 3- Diffusion (Gas transfer):  Movement of gases between the alveoli, plasma, and red blood cells  The diffusion barrier in the lungs is roughly 0.6 µm.  HYPOXEMIA  Although the terms hypoxia and hypoxemia are often used interchangeably, they are not the same.  Hypoxemia is defined as a condition where arterial oxygen tension (Pao2) is below normal (normal Pao2 = 80– 100mmHg).  Hypoxia is defined as the failure of oxygenation at the tissue level. It is not measured directly by a laboratory value (though an increased arterial lactate level usually accompanies tissue hypoxia).  Arterial blood gases For optimal functioning of cells…Acids and bases in the body must be in balance The Body and pH Homeostasis of pH is tightly controlled as pH has an effects on: – Protein function – Enzyme function – Hormones – Electrolyte Balance (Na+, K+, Cl-) pH is determined by CO2 tension and HCO3 Interpretation of ABGs NORMAL VALUES pH = 7.35 - 7.45 ( 7.4 ) pCO2 = 33 - 45 ( 40 ) mEq/L HCO3 = 22 - 28 ( 24 ) mEq/L pO2 = 80 - 100 mmHg 1) Respiratory failure  Type 1; pO2 low  Type 2; pO2 low, pCO2 high 2) Acid base disorder  RESPIRATORY ALKALOSIS pH~ PATHOGENESIS:  Elimination of CO2 RESPIRATORY ACIDOSIS pH~ PATHOGENESIS:  CO2 retension METABOLIC ACIDOSIS pH  ~ PATHOGENESIS Addition of an acid ( increased anion gap )  Loss of HCO3 or inability to synthesize HCO3( normal anion gap ) METABOLIC ALKALOSIS pH ~ PATHOGENESIS  Loss of hydrogen ion  Gain of HCO3 Steps for interpretation of ABG 1) Look at pO2 For diagnosis of respiratory faliur if low with normal co2 it consider type 1 while if high co2 it consider type 2 2) Look for pH pH low acidosis pH high alkalosis 3) Look for pCO2 pCO2 high acidosis pCO2 low alkalosis 4) Look for HCO3 HCO3 low acidosis HCO3 high alkalosis  LUNG VOLUMES AND CAPACITIES Volumes  Tidal volume. Normal quiet breathing moves approximately 500 ml of air into and out of the lungs with each breath.  Inspiratory reserve volume. The amount of air that can be taken in forcibly over the tidal volume which is normally between 2100 ml to 3200 ml.  Expiratory reserve volume. The amount of air that can be forcibly exhaled after a tidal expiration, is approximately 1200 ml.  Residual volume. is the amount of air that remains in a person's lungs after fully exhaling., about 1200 ml of air still remains in the lungs and it cannot be voluntarily expelled; this is called residual volume, and it is important because it allows gas exchange to go on continuously even between breaths and helps to keep the alveoli inflated.  Dead space volume. Much of the air that enters the respiratory tract remains in the conducting zone passage, it amounts to about 150 ml.  Capacities  Vital capacity (VC). The maximum volume of air that can be expired after taking the deepest possible inspiration. It is the sum of the tidal volume, inspiratory reserve volume, and the expiratory reserve volume (VC = TV + IRV + ERV). Is around 4800 ml in healthy young men,  Functional residual capacity (FRC). Is the volume of air present in the lungs at the end of passive expiration, is about 2400 ml.  Total lung capacity (TLC), about 6,000 mL, is the maximum volume of air that can fill the lungs (TLC = TV + IRV + ERV + RV). Inspiratory capacity (IC), about 3,600 mL, is the maximum volume of air that can be inspired after normal expiration (IC = TV + IRV).  PULMONARY FUNCTION TESTS INDICATION OF PULMONARY FUNCTION: 1) Investigation of patients with symptoms/signs/ investigations that suggest pulmonary disease e.g. Cough Wheeze Breathlessness Crackles Abnormal chest x-ray 2) Monitoring patients with known pulmonary disease for progression and response to treatment e.g. Interstitial fibrosis COPD Asthma Pulmonary vascular disease 3) Investigation of patients with disease that may have a respiratory complications e.g. Connective tissue disorders Neuromuscular diseases 4) Preoperative evaluation prior to e.g. Lung resection Abdominal surgery Cardiothoracic surgery 5) Evaluation patients a risk of lung diseases e.g.  Exposure to pulmonary toxins such a radiation, medication, or environmental or occupational exposure RELATIVE CONTRAINDICATIONS ARE: 1. Haemoptysis of unknown origin (forced expiratory maneuver may aggravate the underlying condition); 2. Unstable cardiovascular status (forced expiratory maneuver may worsen angina or cause changes in blood pressure) or ‘recent’ myocardial infarction within the last month or pulmonary embolus; 3. Thoracic, abdominal or cerebral aneurysms (danger of rupture due to increased thoracic pressure); 4. ‘Recent’ eye surgery (e.g, cataract); 5. Presence of an acute illness or symptom that might interfere with test performance (e.g, nausea, vomiting); 6. Recent thoracic or abdominal surgery; 7. Pneumothorax. Subject preparation Record the type and dosage of any (inhaled or oral) medication that may alter lung function and when the drugs were last administered. Activities that should preferably be avoided prior to lung function testing Smoking within at least 1 h of testing Consuming alcohol within 4 h of testing Performing vigorous exercise within 30 min of testing  Wearing clothing that substantially restricts full chest and abdominal expansion Eating a large meal within 2 h of testing Lung volume and capacities Tidal volume. Normal quiet breathing moves approximately 500 ml of air into and out of the lungs with each breath. Amount of air moved in or out of lungs during single respiratory cycle at rest Inspiratory reserve volume. The amount of air that can be taken in forcibly over the tidal volume which is normally between 2100 ml to 3200 ml. Expiratory reserve volume. The amount of air that can be forcibly exhaled after a tidal expiration, is approximately 1200 ml. Residual volume. is the amount of air that remains in a person's lungs after fully exhaling., about 1200 ml of air still remains in the lungs and it cannot be voluntarily expelled; this is called residual volume, and it is important because it allows gas exchange to go on continuously even between breaths and helps to keep the alveoli inflated. Dead space volume. The air that enters the respiratory tract remains in the conducting zone passage, it amounts to about 150 ml. Inspiratory capacity (IC), about 3,600 mL, is the maximum volume of air that can be inspired after normal expiration (IC = TV + IRV).  Vital capacity (VC). The maximum volume of air that can be expired after taking the deepest possible inspiration. It is the sum of the tidal volume, inspiratory reserve volume, and the expiratory reserve volume (VC = TV + IRV + ERV). Is around 4800 ml in healthy young men, Functional residual capacity (FRC). Is the volume of air present in the lungs at the end of normal expiration, is about 2400 ml. Total lung capacity (TLC), about 6,000 mL, is the maximum volume of air that can fill the lungs (TLC = TV + IRV + ERV + RV).  SPIROMETRY and FLOW VOLUME LOOPS Data obtained from spirometry 1. Forced vital capacity (FVC), 2. Forced expiratory volume in one second (FEV1), 3. The ratio of the two (FEV1/FVC), which should be about 80% in normal patients (An FEV1/FVC 50% of peripheral blood haematocrit. Turbid or milky: empyema, chylothorax, pseudochylothorax (clear supernatant after centrifuging favours empyema; cloudy after centrifuging suggests chylothorax or pseudochylothorax. Viscous: mesothelioma Food particles: Oesophageal rupture Bile-stained: Chylothorax (biliary fistula) Black: aspergillus infection Brown: ‘anchovy sauce’amoebic liver abscess draining into pleural space Urine odour: Urinothorax Putrid odour:anaerobic empyema Biochemistry for measurement of glucose, protein, and lactate dehydrogenase (LDH) - Is the pleural effusion a transudate or an exudate? Helpful in narrowing the differential diagnosis. In patients with a normal serum protein, pleural fluid protein 30g/L = exudate. In borderline cases (protein 25–35g/L) or in patients with abnormal serum protein, apply Light’s criteria (table 4). Table (4): Light criteria for distinguish of transudative and exudative pleural effusion 3. Cytology for examination for malignant cells (yield 76% in malignancy) and differential leucocytic count (table 5). Table (5): Relevance of pleural fluid differential cell count Neutrophilic predominant: Parapneumonic, Pulmonary embolism Mononuclear cells predominant: any chronic effusion, e.g. malignancy, TB Lymphocytic predominant: TB, especially if >80%; other causes include cardiac failure, malignancy, sarcoidosis, lymphoma, rheumatoid pleurisy, post-CABG, chylothorax eosinophils air or blood in pleural space (hemothorax, pulmonary infarct, pneumothorax, previous tap), malignancy, infection (Parapneumonic, TB, fungal, parasitic), drug- and asbestos-induced effusions, Churg–Strauss syndrome, or idiopathic Mesothelial cells predominate: in transudates; variable numbers in exudates, typically suppressed in inflammatory conditions, e.g. TB Lupus erythematosus cells: diagnostic of SLE Microbiology for Gram stain and microscopy, culture. For suspected pleural infection, also send pleural fluid in blood culture bottles. Low threshold for acid fast bacilli (AFB) stain and tuberculosis culture 5. pH measured using a heparinized syringe in a blood gas analyz Further investigations if the diagnosis remains unclear: 1. CT chest with pleural phase contrast (ideally scan prior to complete fluid drainage to improve images of pleural surfaces; useful in distinguishing benign and malignant pleural disease. 2. Further pleural fluid analysis e.g. cholesterol, triglyceride, chylomicrons, haematocrit, adenosine Deaminase, amylase, fungal stains. Pleural fluid triglyceride and cholesterol measure in turbid or milky effusions or where chylothorax is suspected. o Chylothorax occurs following disruption of the thoracic duct, and pleural fluid may appear turbid, milky, serous, or bloodstained. Causes of chylothorax: 1. Trauma or following thoracotomy. 2. Malignancy (particularly lymphoma). 3. Pulmonary lymphangioleiomatosis. 4. TB. o Pseudochylothorax occurs due to cholesterol crystal deposition in chronic effusions, most commonly due to rheumatoid pleurisy or TB, and may cause a milky effusion; raised pleural fluid cholesterol and cholesterol crystals at microscopy distinguish it from chylothorax. Pleural fluid amylase abnormal if pleural fluid amylase > upper normal limit for serum amylase. Causes include: o Pleural malignancy and esophageal rupture (both associated with raised salivary amylase) o Pancreatic disease (acute and chronic pancreatitis, pancreatic pseudocyst; associated with raised pancreatic amylase). Note: may be normal early in the course of acute pancreatitis or esophageal rupture. 3. Pleural tissue biopsy: - For histology and TB culture using image-guided or thoracoscopic biopsies. These techniques are superior to Abrams’ closed pleural biopsy for malignant disease and TB. Medical thoracoscopy with the patient under conscious sedation and local anesthesia has emerged as a diagnostic tool to directly visualize and take a biopsy specimen from the parietal pleura in cases of undiagnosed exudative effusions. Closed-needle pleural biopsy is a blind technique that can be performed at the patient's bedside. 4. Bronchoscopy: undiagnosed effusions, unless the patient has Hemoptysis or a CXR/CT pulmonary abnormality. and limit bronchoscopic views, and so, if bronchoscopy is indicated, it is best performed following drainage of the effusion. Apply diagnostic approach to patients with pleural effusion: Treatment of pleural effusion: Etiology unknown in 10–15%: monitoring alone may be appropriate underlying medical disorder. However, regardless of whether transudative or exudative, large, refractory pleural effusions causing severe respiratory symptoms can be drained to provide symptomatic relief. the underlying etiology of the effusion. Pneumonia, malignancy, and TB cause most exudative pleural effusions, with the remainder typically deemed idiopathic. icated parapneumonic effusions and empyema should be drained to prevent development of fibrosing pleuritis. Malignant effusions are usually drained to palliate symptoms and may require pleurodesis to prevent recurrence. oportion of all pleural effusions and are associated with exudative pleural effusions. However, early recognition of this iatrogenic cause of pleural effusion avoids unnecessary additional diagnostic procedures and leads to definitive therapy, which is discontinuation of the medication. Criteria for referral to cardiothoracic surgery: 1. Parapneumonic effusions that cannot be drained adequately by needle or small-bore catheters. 2. Establish a diagnosis and for pleural sclerosis therapy of exudative effusions. 3. Pleurodesis by insufflating talc directly onto the pleural surface using video-assisted thoracoscopy is an alternative to using talc slurries. 4. Decortication is usually required for trapped lungs to remove the thick, inelastic pleural peel that restricts ventilation and produces progressive or refractory dyspnea. 5. In patients with chronic, organizing parapneumonic pleural effusions, technically demanding operations may be required to drain loculated pleural fluid and to obliterate the pleural space. 6. Surgically implanted pleuroperitoneal shunts are another treatment option for recurrent, symptomatic effusions, most often in the setting of malignancy, but they are also used for management of chylous effusions. 7. In unusual cases, surgery might be required to close diaphragmatic defects (thereby preventing recurrent accumulation of pleural effusions in patients with ascites) and to ligate the thoracic duct to prevent reaccumulation of chylous effusions.  2-Pneumothorax (PNX)  Definition of pneumothorax: Pneumothorax is air in the pleural space. May occur with apparently normal lungs (1° pneumothorax) or in the presence of underlying lung disease (2° pneumothorax). May occur spontaneously or following trauma.  Classification and risk factors of pneumothorax: 1°primary Pathogenesis is poorly understood; pneumothoraxes are presumed to occur following an air leak from apical sub pleural blebs and bullae, although small airway inflammation is often also present and may contribute by increasing airways resistance, causing ‘emphysema-like changes’ (ELC). 2°secoundry Underlying diseases include: COPD (60% of cases), asthma, ILD, necrotizing pneumonia, TB, PCP, CF, LCH, LAM, Marfan’s syndrome, oesophageal rupture, lung cancer, catamenial pneumothorax, and pulmonary infarction P neumothorax may be the first presentation of the underlying disease.  Different types of pneumothorax with special concern to the emergency :  Different management plans for pneumothorax   Indications of referral of patients with pneumothorax to cardiothoracic surgeon: Indications for cardiothoracic surgical referral 1) Second ipsilateral pneumothorax 2) First contralateral pneumothorax 3) Bilateral spontaneous pneumothorax 4) Persistent air leak or failure of lung to re-expand (3–5 days of drainage) 5) Professions at risk (e.g. pilots, divers) after first pneumothorax.  Pneumonia Pneumonia is an infection in one or both lungs. Bacteria, viruses, and fungi cause it. The infection causes inflammation in the air sacs of the lungs, which are called alveoli. The alveoli fill with fluid or pus, making it difficult to breathe. Pneumonia risk factors Anyone can get pneumonia, but certain groups do have a higher risk. These groups include:  infants from birth to 2 years old  people ages 65 years and older  people with weakened immune systems because of disease or use of medications, such as steroids or certain cancer drugs  people with certain chronic medical conditions, such as asthma, cystic fibrosis, diabetes, or heart failure  people who’ve recently had a respiratory infection, such as a cold or the flu  people who’ve been recently or are currently hospitalized, particularly if they were or are on a ventilator  people who’ve had a stroke, have problems swallowing, or have a condition that causes immobility  people who smoke, use certain types of drugs, or drink excessive amounts of alcohol  people who’ve been exposed to lung irritants, such as pollution, fumes, and certain chemicals Clinical picture Pneumonia symptoms can be mild to life-threatening. They can include:  coughing that may produce phlegm (mucus)  fever  sweating or chills  shortness of breath that happens while doing normal activities or even while resting  chest pain that’s worse when you breathe or cough  feelings of tiredness or fatigue  loss of appetite  nausea or vomiting  headaches Other symptoms can vary according to your age and general health:  Children under 5 years old may have fast breathing or wheezing.  Infants may appear to have no symptoms, but sometimes they may vomit, lack energy, or have trouble drinking or eating.  Older people may have milder symptoms. They can also exhibit confusion or a lower than normal body temperature.       Pneumonia complications Pneumonia may cause complications, especially in people with weakened immune systems or chronic conditions, such as diabetes.  Worsened chronic conditions  Bacteremia  Lung abscesses  Impaired breathing  Acute respiratory distress syndrome  Pleural effusion  Death Pneumonia stages Pneumonia may be classified based off the area of the lungs it’s affecting: 1. Bronchopneumonia 2. Lobar pneumonia Lobar pneumonia can be further divided into four stages based off how it’s progressed: 1. Congestion. Lung tissue appears heavy and congested. Fluid filled with infectious organisms has accumulated in the air sacs. 2. Red hepatization. Red bloods cells and immune cells have entered into the fluid. This makes the lungs appear red and solid in appearance. 3. Gray hepatization. The red blood cells have begun to break down while immune cells remain. The breakdown of red blood cells causes a change in color, from red to gray.  4. Resolution. Immune cells have begun to clear the infection. A productive cough helps eject remaining fluid from the lung Causes of pneumonia There are several types of infectious agents that can cause pneumonia. Bacterial pneumonia The most common cause of bacterial pneumonia is Streptococcus pneumoniae. Other causes include:  Mycoplasma pneumoniae  Haemophilus influenzae  Legionella pneumophila Viral pneumonia Respiratory viruses are often the cause of pneumonia. Some examples include:  influenza (flu)  respiratory syncytial virus (RSV)  rhinoviruses (common cold) Viral pneumonia is usually milder and can improve in one to three weeks without treatment. Fungal pneumonia Fungi from soil or bird droppings can cause pneumonia. They most often cause pneumonia in people with weakened immune systems. Examples of fungi that can cause pneumonia include:  Pneumocystis jirovecii  Cryptococcus species  Histoplasmosis species Types of pneumonia Pneumonia can also be classified according to where or how it was acquired. Hospital-acquired pneumonia (HAP) This type of bacterial pneumonia is acquired during a hospital stay. It can be more serious than other types, as the bacteria involved may be more resistant to antibiotics. Community-acquired pneumonia (CAP) Community-acquired pneumonia (CAP) refers to pneumonia that’s acquired outside of a medical or institutional setting. Ventilator-associated pneumonia (VAP) When people who are using a ventilator get pneumonia, it’s called VAP. Aspiration pneumonia Aspiration pneumonia happens when you inhale bacteria into your lungs from food, drink, or saliva. This type is more likely to occur if you have a swallowing problem or if you’re too sedate from the use of medications, alcohol, or other drugs. Pneumonia diagnosis By history of previouse symptoms with risk factor and by examination such as crackling. Pneumonia treatment. Oral antibiotics can treat most cases of bacterial pneumonia. Antibiotic medications don’t work on viruses. In some cases, your doctor may prescribe an antiviral. However, many cases of viral pneumonia clear on their own with at-home care. Antifungal medications are used to fight fungal pneumonia. You may have to take this medication for several weeks to clear the infection. At the hospital, doctors can keep track of patients heart rate, temperature, and breathing. Hospital treatment may include:  intravenous antibiotics injected into a vein  respiratory therapy, which involves delivering specific medications directly into the lungs or teaching patients to perform breathing exercises to maximize patients oxygenation  oxygen therapy to maintain oxygen levels in patients bloodstream (received through a nasal tube, face mask, or ventilator, depending on severity) Duration of Therapy The recommended duration of antibiotic therapy has not changed from previously published guidelines. Patients with CAP should be treated for a minimum of 5 days, with antibiotic therapy continued until the patient achieves clinical stability. Validated measures of clinical stability include resolution of vital sign abnormalities (heart rate, respiratory rate, blood pressure, oxygen saturation, and temperature); ability to eat; and normal mental status. Given that most patients achieve clinical stability within 48 to 72 hours after therapy initiation, a 5-day course typically is sufficient. Because of its long half-life and high concentrations in lung tissue, some clinicians administer azithromycin for 3 days (a total of 1.5 g) in patients without pneumonia caused by Legionella. CAP due to suspected or proven MRSA or P aeruginosa should be treated for 7 days. In CAP patients whose symptoms resolve within 7 days, routine follow-up chest imaging is not recommended. Pneumonia prevention Vaccination The first line of defense against pneumonia is to get vaccinated. There are several vaccines that can help prevent pneumonia. Other prevention tips  stop smoking  Regularly wash hands with soap and water.  Cover your coughs and sneezes. Promptly dispose used tissues.  Maintain a healthy lifestyle to strengthen immune system. Get enough rest, eat a healthy diet, and get regular exercise.  Thoracic incisions Thoracic incisions are performed in patients undergoing surgeries for the following conditions:  Lung cancer  Noncancerous lung masses  Disorders of the heart  Aortic aneurysm (ballooning or bulging of the aorta at certain weak areas in its wall)  Aortic dissection/transection (tears in or rupture of the aorta)  Tumors in the spine  Tumors in the esophagus  Chest injuries The various types of thoracic incisions are as follows:  Sternotomy: It is made over the breastbone (sternum) .  Different types of sternotomy incisions are: o Median sternotomy: This incision is made in the midline along the length of the sternum. It is the incision of choice for most surgical procedures on the heart. It gives excellent exposure of the heart, covering of the heart (pericardium), great vessels, thymus, and lower part of the windpipe (trachea). This incision is quick to perform and less painful compared with a thoracotomy incision. o Reoperative or repeat sternotomy o Partial sternotomy  Thoracotomy: It is the most widely used for thoracic   procedures. It is of four major types: o In posterolateral thoracotomies, the incision runs toward the back and side of the chest. o In anterolateral (anterior) thoracotomies, the incision runs toward the front and/or side of the chest.  o In axillary thoracotomies, the incision is made on the armpit (axilla). o In muscle-sparing thoracotomies, incisions are spared or avoided on a muscle or muscle group in the chest. Its advantages are reduced postoperative pain, decreased narcotic usage and improved shoulder- girdle muscle strength.  Anterior mediastinoscopy: This incision is done to stage and diagnose advanced upper-lobe lung cancers   Transverse thoracosternotomy: It involves a long horizontal incision made on the chest. This incision provides excellent wide exposure to both the lungs and great vessels, but it causes increased postoperative pain, frequently requires the patient to be on postoperative ventilatory support and carries a serious risk of breastbone malunion (improper joining of the surgically cut breastbone) and chest wall dysfunction.   Thoracoabdominal incision: It provides wide exposure of the lower chest and upper abdomen and is suitable for surgeries on the esophagus, abdominal part of the aorta and spine.  Video-assisted thoracoscopic surgery (VATS): It is a procedure in which thoracoscope (a small tube) is inserted through a small incision between the ribs. A small camera is attached at the end of the tube which lets the surgeon observe the entire chest cavity without having to open the chest or spread the ribs. Complication of thoracic incision: The complications of thoracic incisions vary with the type of incision made. Generally, the complications include  Pain  Scarring  Nonunion or malunion of the sternum  Bleeding  Infections  Injury to muscles, nerves or blood vessels  Interventional Pulmonology Procedures Procedures for interventional pulmonology include: 1. Flexible bronchoscopy. For visualization, airway management , or even for treatment or taken biopsy The bronchoscope has a channel at its tip, through which a doctor can pass small tools. Using these tools, the doctor can perform several other interventional pulmonology procedures.  Bronchoalveolar lavage. Bronchoalveolar lavage is performed during bronchoscopy. Sterile water is injected through the bronchoscope into a segment of the lung. The fluid is then suctioned back and sent for tests. Bronchoalveolar lavage can help diagnose infection, cancer, bleeding, and other conditions.  Biopsy of lung or lymph node. During bronchoscopy, a doctor may collect a small piece of tissue from either the lung or a nearby lymph node.  The interventional pulmonologist can use a needle or forceps advanced through the bronchoscope to get a sample of tissue. Biopsies can detect cancer, infection, sarcoidosis, and other conditions.  For people with lung cancer or other cancers, interventional pulmonology biopsies can often accurately identify spread  of cancer into lymph nodes. This can prevent unnecessary surgery or help determine the best choice for treatment.  Airway stent (bronchial stent).   Advanced cancer or certain other conditions can constrict or compress an airway tube (bronchus). If the bronchus becomes blocked, difficulty breathing, cough, and pneumonia can result.  Using a bronchoscope, a doctor can advance a wire mesh stent into a narrowed airway. Expanding the stent can open a bronchus and relieve symptoms caused by the constriction.  Balloon bronchoplasty. A doctor advances a deflated balloon into a section of abnormally narrowed airway. By inflating the balloon with water, the airway is expanded, potentially relieving symptoms. Balloon bronchoplasty may be performed prior to airway stent placement to help expand a bronchus. 2. Rigid bronchoscopy.  In rigid bronchoscopy, a long metal tube (rigid bronchoscope) is advanced into a person’s windpipe and main airways. The rigid bronchoscope’s large diameter allows the doctor to use more sophisticated surgical tools and techniques.  Rigid bronchoscopy requires general anesthesia (unconsciousness with assisted breathing), similar to a surgical procedure.  Foreign body removal. Bronchoscopy is the preferred interventional pulmonology procedure to remove inhaled foreign objects that are lodged in an airway. A doctor may be able to remove the object using flexible bronchoscopy, or rigid bronchoscopy may be required.  3. Pleuroscopy. A doctor cuts small incisions in the chest wall and advances a pleuroscope (a type of endoscope) into the chest cavity. The pleuroscope is advanced around the chest wall and lung on one side. Pleuroscopy can diagnose some conditions of the pleura (lining of the lung). Pleuroscopy also allows a view of the outside edges of the lung, which bronchoscopy cannot provide. 4. Thoracentesis. To drain fluid from around the lungs (pleural effusion), a doctor inserts a needle into the chest wall. A plastic catheter is advanced over the needle, which is then removed. The excess pleural fluid is suctioned out of the chest and the catheter is removed and discarded. 5. Pleurodesis. Pleurodesis is an interventional pulmonology procedure performed for people with recurring pleural effusions (fluid around the lungs). In pleurodesis, a doctor makes an incision in the chest wall. A plastic tube is inserted into the chest cavity, and an irritating chemical is sprayed around the lung. Over time, the inflamed lung lining (pleura) adheres tightly to the chest wall. This prevents fluid from reaccumulating around the lung. 6. Indwelling pleural catheter. A pleural catheter is an alternative to pleurodesis for treatment of a recurrent pleural effusion. Through minor surgery, a plastic catheter is tunneled beneath the skin, with its tip placed inside the chest cavity. As pleural fluid accumulates around the lung, a person can drain the indwelling pleural catheter at home, using special sterile supplies. 7. Bronchoscopic thermoplasty. Thermoplasty is an interventional pulmonology procedure for certain people with severe asthma that can’t be controlled  with medications. During bronchoscopy, a doctor applies a heat probe to the walls of the airways. The heat destroys the smooth muscle layers whose constriction contributes to asthma symptoms Interventional Pulmonary Diagnostics Interventional pulmonology procedures offer the potential advantage of avoiding more invasive surgery. For example, before interventional pulmonology, biopsy of lymph nodes in the chest required chest wall surgery. Two recent advances in technology are extending the reach of interventional pulmonology procedures:  Endobronchial ultrasound system (EBUS): An ultrasound probe on the tip of a bronchoscope allows a doctor to biopsy lymph nodes with more precision. In experienced hands, EBUS increases the likelihood of a correct diagnosis significantly.  Electromagnetic navigation bronchoscopy (superDimension): An advanced system that guides the bronchoscope farther than traditional bronchoscopy allows. This system permits biopsy of hard-to-reach abnormal areas of the lung, which would otherwise require more invasive testing. Interventional Pulmonology Risks and Limitations Although interventional pulmonology procedures carry low risks, they are not risk-free. Uncommon complications of interventional pulmonology procedures include:  Pneumothorax (collapsed lung)  Bleeding  Oversedation, leading to pneumonia or the need for temporary life support  Lung surgery Lung surgery is surgery done to repair or remove lung tissue. There are many common lung surgeries, including: 1. Biopsy of an unknown growth 2. Lobectomy, to remove one or more lobes of a lung 3. Lung transplant 4. Pneumonectomy, to remove a lung 5. Surgery to prevent the buildup or return of fluid to the chest (pleurodesis) 6. Surgery to remove an infection in the chest cavity (empyema) 7. Surgery to remove blood in the chest cavity, particularly after trauma 8. Surgery to remove small balloon-like tissues (blebs) that cause lung collapse (pneumothorax) 9. Wedge resection, to remove part of a lobe in a lung 10. A thoracotomy is a surgical cut that a surgeon makes to open the chest wall.  There are two common ways to do surgery on lungs which are thoracotomy and video-assisted thoracoscopic surgery (VATS). Robotic surgery may also be used.  Lung surgery using a thoracotomy is called open surgery.  Thoracotomy or video-assisted thoracoscopic surgery may be done to:  1. Remove cancer (such as lung cancer) or biopsy an unknown growth 2. Treat injuries that cause lung tissue to collapse (pneumothorax or hemothorax) 3. Treat permanently collapsed lung tissue (atelectasis) 4. Remove lung tissue that is diseased or damaged from emphysema or bronchiectasis 5. Remove blood or blood clots (hemothorax) 6. Remove tumors, such as solitary pulmonary nodule 7. Inflate lung tissue that has collapsed (This may be due to disease such as chronic obstructive pulmonary disease, or an injury.) 8. Remove infection in the chest cavity (empyema) 9. Stop fluid buildup in the chest cavity (pleurodesis) 10. Remove a blood clot from the pulmonary artery (pulmonary embolism) 11. Treat complications of tuberculosis Video-assisted thoracoscopic surgery can be used to treat many of these conditions. In some cases, video surgery may not be possible, and the surgeon may have to switch to an open surgery. Complication of lung sugery includes 1. Failure of the lung to expand 2. Injury to the lungs or blood vessels 3. Need for a chest tube after surgery 4. Pain 5. Prolonged air leak 6. Repeated fluid buildup in the chest cavity 7. Bleeding 8. Infection 9. Heart rhythm disturbances 10. Damage to the diaphragm, esophagus, or trachea  Refrances 1. Alfille PH, Wiener-Kronish JP, Bagchi A. Preoperative evaluation. In: Broaddus VC, Mason RJ, Ernst JD, et al, eds. Murray and Nadel's Textbook of Respiratory Medicine. 6th ed. Philadelphia, PA: Elsevier Saunders; 2016:chap 27. 2. Feller-Kopman DJ, Decamp MM. Interventional and surgical approaches to lung disease. In: Goldman L, Schafer AI, eds. Goldman-Cecil Medicine. 26th ed. Philadelphia, PA: Elsevier; 2020:chap 93. 3. Lumb A, Thomas C. Pulmonary surgery. In: Lumb A, Thomas C, eds. Nunn and Lumb's Applied Respiratory Physiology. 9th ed. Philadelphia, PA: Elsevier; 2021:chap 33. 4. Putnam JB. Lung, chest wall, pleura, and mediastinum. In: Townsend CM Jr, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 20th ed. Philadelphia, PA: Elsevier Saunders; 2017:chap 57. 5. https://emcrit.org/ibcc/COVID19/ 6. UpToDate on Coronaviruses, SARS, MERS, COVID-19 7. CDC: https://www.cdc.gov/coronavirus/2019- ncov/index.html 8. WHO: https://www.who.int/health-topics/coronavirus 9. Online courses at: https://openwho.org/ 10. https://www.worldometers.info/coronavirus/ 11. https://coronavirus.1point3acres.com/en?fbclid=IwAR 3A3clE1Ztxi- fNBgTWtVOobWuUBGFJ1S3NBPFlAaYVruBcAtzeOcq pIjQ 12. Dr James Lawler Presentation at American Hospital Association/ National Ebola Training and Education Center 13. Oxford Handbook of Respiratory Medicine (3 edn) 2018 Stephen Chapman, Grace Robinson, John Stradling, Sophie West, and John Wrightson 14. Davidson's Principles and Practice of Medicine (2016) 23rd Edition: Stuart Ralston Ian Penman Mark Strachan Richard Hobson 15. Harrison's Principles of Internal Medicine, 20e (2021) J. Larry Jameson, Anthony S. Fauci, Dennis L. Kasper, Stephen L. Hauser, Dan L. Longo, Joseph Loscalzo 16. Crofton and Douglas's Respiratory Diseases (Fifth Edition) 2018 17. Fishman's Pulmonary Diseases and Disorders, 5e (2020) Michael A. Grippi, Jack A. Elias, Jay A. Fishman, Robert M. Kotloff, Allan I. Pack, Robert M. Senior, Mark D. Siegel  Sheet for students Case number (1) A 42-year-old man works as a gardener ،married but has no children. He came to the outpatient clinic complaining of dyspnea, which has been worsened last 2 weeks ,associated with productive cough of large amount of yellowish sputum , increased while leaning forward, sometimes tinged with blood and sometimes progress to frank hemoptysis. He smoked one pack of cigarette daily for 25 years. He has had a long history of upper and lower respiratory problems starting in early childhood for which he was told that he had asthma and previously treated by inhaler but stopped it because of being ineffective. He had recurrent chest infection during his childhood. The patient is unaware of any other significant symptoms during infancy and early childhood. On general examination: He was conscious, oriented, dyspneic and afebrile. No pallor, cyanosis, clubbing or jaundice, but he has bilateral lower limb edema. His weight is 51 kg with BMI 16.6kg\m2 (norm= 18- 25kg\m2), pulse: 90/min, regular, normal volume, no special characters, RR: 22/min (norm= 12-20), JVP: not raised and temp: 37 (norm= 36.8-37.2). While local examination :by inspection there were diminished chest movements bilateral and increase in anteroposterior diameter of the chest, by palpation there were decrease in chest expansion and movement over left infra-mammary and subscapular areas, palpable rhonchi, impaired (heterogeneous) tactail vocal fremitus (TVF )over inframammary and subscapular areas bilaterally, by percussion there were resonance bare area(norm=dull), liver is low presented at 6th and 7th intercostal spaces midclavicular and mid-axillary lines (norm=5th and 6th ) Auscultation: Vesicular breathing with prolonged expiration with sonorous rhonchi all over the chest and coarse crepitations over inframammary and subscapular areas bilaterally. Laboratory tests were done and showed: Hb 9.6 gm (norm=14-16gm), TLC 13: 600 cells/cu.mm (norm= 4- 11), CRP= 6 (norm= up to5), total protein: 5.4 gm (Norm = 6-8.3 gm/dl), Albumin: 3 gm/dl (Norm= 3.5-5 mg/dl). Normal liver enzymes and renal function tests. Chest X-ray: hyperinflation, increased broncho- vascular marking with multiple cystic changes (honeycombing) scattered bilaterally, and decreased cardiothoracic ratio (ribbon shaped heart)  High resolution CT chest (HRCT) showed bilateral extensive cystic (red circle) and varicose (blue arrow), tram-line (green arrow) bronchiectasis. Sputum gram stain: gram negative and gram positive cocci. Sputum culture: pseudomonas acrogenous and Methicillin-Resistant Staphylococcus aureus (MRSA). Antibiotic sensitivity: pseudomonas aeruginosa sensitive was to colistin sulphate and meronamin, while Methicillin-Resistant Staphylococcus aureus was sensitive to Vancomycin and linezolid. The patient was treated by meronamin 1gm every 8 hours, Vancomycin 1 gm every 12 hours. He also received expectorant syrup, Salbutamol and Atrovent nebulization, good hydration and nutrition, with chest physiotherapy for 10 days. All patient symptoms were improved apart from hemoptysis which still recur every now and then sometime became frank hemoptysis of about 100-200 cc daily. 1. List the differential diagnosis for this patients? 2. What is the most probable diagnosis of this patient? Give reason for your diagnosis. 3. Identify the most probable disease etiology in this patient? 4. Recognize the most confirmatory diagnostic test for this disease? 5. Recognize the causes of decreased serum protein and albumin in this patient? 6. What are other tests required to this case? 7. Construct a treatment plan for this patient? 8. Identify the non-pharmacological management for this disease? 9. List the complications of this disease? 10. What are the criteria of referral to cardiothoracic surgery in similar condition?  Case number (2) History A 66 years old mechanic with a history of smoking , the patient smoked one pack of cigarettes per day for forty year and quit smoking one year ago due to dyspnea..he is complaining of dyspnea on moderate exertion over the past five years that accelerates over the last year to dyspnea on mild exertion the condition was associated with several episodes of productive cough over the past two years. The sputum is usually scant and clear. However, recently it has become yellow and continues all day not associated with chest wheeze or chest pain , No haemoptysis He is now dyspneic at rest. And also he is complaining of morning headaches and very mild lower limb oedema which is disappear when the patient raising his leg no history for ascites. His past medical history was significant for smoking, depression, hypertension and hyperlipidemia. The patient reported that his father had chronic obstructive pulmonary disease there was no other family history for any disease Physical Examination He was alert and oriented Obvious respiratory distress with prominent use of accessory muscles. Temperature 37.5; Blood pressure 140/90; pulse 95 b/m; respiratory rate 28. Head/neck reveal distended neck veins throughout expiration. Chest reveals increased A-P diameter; reduced chest wall excursion; lungs hyperresonant to percussion; auscultation reveals a prolonged expiratory phase with diminished breath sounds and generalized rhonchi. Heart reveal; distant heart sound with regular rhythm and no murmurs. Extremities reveal trace pitting edema of the lower extremities. Investigation: 1)EKG reveals low voltage; right axis; peaked P waves 2)Laboratory reveals a-WBC 8,500 with normal differential and Hgb 16.7 gm. b-ESR 45 c- serum albumin 3.2 gm/dl Chest x- ray reveals hyperinflation of lungs with an increase in the retrosternal space, low flattened diaphragm; hyperlucent lung field with prominent hila and narrow heart silhouette Axial CT image obtained in a 66- year-old man with COPD and severe airflow obstruction shows mild emphysema (relative low-attenuation area with attenuation of −950 HU or lower, 5.8%). Low-attenuation areas representing emphysematous change (“holes”) are indicated by arrowheads. -Pulmonary function test revealed FEV1 = 40.8 -Arterial blood gases pao2 49 , paco2 59 and o2 sat. 90 on room air Answer the following questions 1-Identify the diagnosis of this patient? 2-Recognize the risk factor for this disease in this patient? 3-List other risk factors for this disease? 4-Recognize the clinical data for this disease in this patient? 5-List other clinical manifestation of this disease? 6-Describe the stages of this disease ? 7-Recognise the finding of x-ray in this patient? 8- Identify the treatment options for this patient? 9- What are the spirometric classification of COPD severity based on past-bronchodilator FEV1? 10-Identify long term oxygen therapy in COPD? 11-What are the surgical treatment and when the patient need it ?