3 - Summary and MCQs Year 4 Internal Medicine Notes

Year 4 Internal Medicine study notes: 3 - Summary and MCQs. Full notes on OmpathStudy. Free notes for medical students worldwide.

3 - Summary and MCQs Year 4 · Internal Medicine Collection: 4TH YEAR ALL NOTES / IMED / I MED BEAUTIFUL NOTES -- 1 \n\nRestrictive Pulmonary Diseases: A group of disorders characterized by ​reduced expansion of the lung, ​reduction in total lung capacity​, ​increased work of breathing​ and ​inadequate ventilation and/or oxygenation​ (decreased lung compliance).\n\n The hallmark feature of these disorders is ​reduced compliance ​(i.e., more pressure is required to expand the lungs\nbecause they are stiff), which in turn causes difficulty in breathing (dyspnea). Divided into: \n1. Intrinsic lung diseases/ diseases of the lung parenchyma/primary interstitial lung disease \n2. Extrinsic disorders or extraparenchymal diseases: \nThe chest wall, pleura, and respiratory muscles are the components of the respiratory pump, and they need to \nfunction normally for effective ventilation. Pulmonary interstitium: It is the area of the lung between the alveolar epithelial and capillary endothelial basement membranes (fused in the thinnest portions) It is composed of:\n­ Elastic tissue. ­ Fibroblasts.\n­ A few mast cells. ­ Occasional mononuclear cells.\n\n 2 \n\nWhat are the changes that occur? \n❏ Hypoxia. \n❏ Diffuse infiltration by small nodules, irregular lines, or “ground­glass shadows.” With progression, patients can\ndevelop ​respiratory failure​, often in association with pulmonary hypertension and ​cor pulmonale. \n❏ “Honeycomb” lung​. Major Categories of Chronic Interstitial Lung Disease: \n1. Occupational:\nPneumoconiosis:\n­ Anthracosis and coal worker's pneumoconiosis.\n­ Silicosis.\n­ Asbestosis.\n2. Fibrosing: ​ (occupational diseases are also fibrosing diseases)\nUsual interstitial pneumonia (idiopathic pulmonary\nfibrosis).\n3. Immune diseases:\n­ Sarcoidosis.\n­ Goodpasture syndrome.\n­ Hypersensitibity pneumonitis(extrinsic allergic\nalveolitis).\n­ Systemic lupus erythematosus.\n­ ​Systemic sclerosis (scleroderma).\n­ Wegener granulomatosis.\n4. Drugs:​ ​Chemotherapy, methotrexate, bleomyxin toxicity. \n5. Radiation Reactions. \n6. Smoking related: \n­ ​Eosinophilic granuloma.\n­ ​ esquamative interstitial pneumonia.\nD\n­ Respiratory bronchiolitis­associated interstitial lung disease. Pathogenesis: \n● ​Influx​ of inflammatory cells into the alveoli and alveolar walls.\n● ​ istortion ​of the normal structure of alveoli.\nD\n● Release of ​chemical mediators.\n● Promotion of ​fibrosis.\n\n 3 \n\n EXTRA\n\nThe summarized pathogenesis of Restrictive Lung Diseases\n\n 4 \n\nSUMMARY\n\n ­ Diffuse interstitial fibrosis of the lung gives rise to restrictive lung diseases characterized by r​educed lung \ncompliance​ and ​reduced​ forced vital capacity (FVC). The ratio of FEV to FVC is normal. \n­ The diseases that cause ​diffuse interstitial fibrosis are heterogeneous. The unifying pathogenetic factor is injury to \nthe alveoli with activation of macrophages and release of ​fibrogenic cytokines such as TGF­β. \n­ Idiopathic pulmonary fibrosis is prototypic of restrictive lung diseases. It is characterized by patchy interstitial \nfibrosis, fibroblastic foci, and formation of cystic spaces (honeycomb lung). This histologic pattern is known as \nusual interstitial pneumonia (UIP).\n\n 5 \n\nAcute Respiratory Distress Syndrome (ARDS):​ ​(Affects both adults and neonatal) Adult respiratory distress syndrome: ARDS is a severe form of acute lung injury with diffuse alveolar injury. Produced by diffuse alveolar damage with resultant increase in alveolar capillary permeability, causing leakage of protein­rich fluid into alveoli. It is also known as shock lung/ diffuse alveolar damage/ adult respiratory failure/acute alveolar injury/ traumatic wet lung. Characteristics include the formation of an i​ ntra­alveolar hyaline membrane​ composed of fibrin and cellular debris.\n\n ➔ ARDS can be a manifestation of the ​severe acute respiratory syndrome (SARS)​. \n➔ ARDS is initiated by ​damage to alveolar capillary endothelium​ and ​alveolar epithelium​. ​It is:\n● Rapid acute onset progressive severe life threatening respiratory insufficiency, cyanosis, severe arterial hypoxia.\n● Decreased arterial oxygen pressure.\n● Refractory to oxygen therapy and that may progress to multiorgan failure.\n● Bilateral pulmonary infiltrates (edema).\n● Absence of evidence of left sided heart failure.\n● It is the most common cause of non­ cardiogenic pulmonary edema\n\n 6 \n\nClinical features characterized by:\n­ Cyanosis. ­ May progress to multisystem organ failure.\n\n Dr. Rikabbi’s Note: \nUsually caused by:\n­ Major trauma ­ Aspiration of gastric juice ­ Septicaemia ­ Severe infections ­ Shocks.\nThere are two types of ARDS:\n­ Direct:\nIf the injury is in the interstitial area.. like the damage of the lining cells.\n­ Indirect:\nWhen there is a septicaemia which can cause some problems to the alveolar capillaries and then the alveoli.\n\n 7 \n\nPathogenesis: Diffuse alveolar damage which leads to → increase in alveolar capillary perm
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