Respiratory Tract and Lung Diseases PDF 10/21/2020

10/21/2020 Major Functions of Respiratory Tract I ► Gas Exchange site Respiratory Tract and...

10/21/2020 Major Functions of Respiratory Tract I ► Gas Exchange site Respiratory Tract and  Oxygen in Lung Diseases  Carbon Dioxide out Z ► Secondary maintenance of normal pH 1 2 Components Of Respiratory Tract ► Lungs  Primary gas exchange organ ► Muscles of Respiration  Diaphragm  Internal and external intercostals muscles  abdominal muscles ► Pleural spaces small - spaces around lungs filled wiflvid to reduce friction ► Upper respiratory tract ► Nasopharynx throat ► Trachea ► Bronchi ► Larynx 3 4 Categories of Atelectasis yoa Lung Diseases  Compression Atelectasis something buildsup around ► Due to compression of lungs by materials in pleural ► Atelectasis space  Collapse of the lung ► Air – pneumothorax pushes againthragm ► Fluid – pleural effusion or ascites in belly  Loss of lung volume due to inadequate in pleural space as fluid expansion of airspaces in lungs  Resorption Atelectasis ► Obstruction prevents air from reaching air  Gives rise to hypoxia exchange surface stops/blocks air from getting through of breath ↳ shortness ► Most common due to obstruction of bronchus by mucous or muco-purulent plug -> mucus buildup  Asthma swollen a narrow airways excess mulous of airways > -  Chronic Bronchitis long term inflammation production  Tumors of airway epithelium growths block air  Enlarged lymph nodes due to Tuberculosis 5 6 1  10/21/2020 ► Microatelectasis  Loss of lung expansion due to loss of open surfactant > slippery substance that keeps airways of  Neonatal lung longs may not have enough surfactant causing parts long to collapse  Adults due to disease affecting surfactant production ► Contraction Atelectasis Stiff tissue  Due to fibrotic changes in lung or pleura which will interfere with expansion and cause increased elastic recoil b membrane & causes long more easily around long to revoilo 7 8 9 10 Obstructive Lung Diseases  A limitation of airflow to gas exchange surfaces = Asthma airways tighten resulting from an increase in resistance due to a ► Episodic and reversible bronchiospasms overreaction of airways partial or complete obstruction resulting from an exaggerated broncho-  Types: restrictor response to various causes:  Asthma  Increased sensitivity to broncho-constrictive sensitivityUses  Emphysema   Chronic Bronchitis Cystic Fibrosis-genetic condition causing thickmusengs agents such as histamine and methacholine allergic rxn testairway  Bronchioectasis air passages become wider + inflamed be of repeated  Various etiology many of which are unknown infection  Bronchiolitis inflammation of smaller airways ► Common in the general population  Characteristics in of Obstructive Disease  5% of adults are affected air lungs  Total Lung capacity is generally normal  Forced Vital Capacity is normal how much air can be forcefully exhaled  8-9% of children are affected  Expiratory flow rate is decreased -air moves out of longs more lowly 11 12 2  10/21/2020 Extrinsic Asthma ► usually initiated by a Type I hypersensitivity reaction after exposure to allergen ► Most common form is Atopic Asthma - ► Most commonly occurs early in life > allergicresora family 13 14 Intrinsic Asthma Manifestations of Asthma Lairways) ► Occlusion of bronchi and bronchioles by ► Notas well understood as extrinsic form. thick mucous plugs dead ► Causes: ► mucous contains sloughed epithelial cells  viral infections and inflammatory cells such as eosinophils Swell  inhaled pollutants such as sulfur-dioxide and ► Edema and hyperemia of walls of R redness increased blood flow narrows ozone bronchioles airways - ► All of the above will affect “normal” non- ► Eosinophils, mast cells, macrophages and asthmatics but asthmatics will have extreme lymphocytes are found in mucosal tissue reaction in mucosal lining of airways causing more inflammation 15 16 Manifestations of Asthma ► Increased thickness of basement membrane Becomes larger more cells ► Hypertrophy and hyperplasia of smooth muscle produces excess mucous ► increased size of submucosal mucous glands ► increased number of goblet cells cells produce mucony 17 18 3  10/21/2020 19 20 permanent Chronic Obstructive Pulmonary Clinical Signs of Asthma Disease COPD ► dyspnea shortness of breath ► Airflow obstruction resulting in increased ► Wheezing difficulty in expiration exhaling difficult ► Expiration difficulty can't breath out ► Etiology: common causes ► Hypercapnea PCO-inblood  Chronic Bronchitis persistent inflammation of airway mucous production ► Acidosis excess CO: can cause , , acidity difficultynarrowing of bron as  Emphysema damage to air sacs Calveoli) loss of ► Can last for a variable period of time , elasticity a ► Can subside spontaneously  The two commonly coexist ► Can be severe enough to cause life threatening hypoxia and anoxia lacka W Oxygen 21 22 & Emphysema away ► Destruction of the walls of airspaces distal to the terminal bronchioles ► A common disease – most found with it are asymptomatic ► Commonly associated with smoking ► Types:  Centriacinar Emphysema  Panacinar Emphysema 23 24 4  10/21/2020 Emphysema Types: ► Centriacinar Emphysema closer to center  The central or proximal parts of the acini formed by respiratory bronchioles are affected and the distal alveoli are spared.  More common in upper lung lobes ► Panacinar Emphysema whole air say  The acini are uniformly enlarged from the level of the respiratory bronchioles to the terminal blind alveoli  More common in lower lung lobes 25 26 Pathogenesis of Emphysema ► Not well understood enzymes break down proteins ► Most likely caused by excess protease or elastase activity unopposed by appropriate antiprotease regulation i ► Primary source of cellular elastase are neutrophils and macrophages ► Inflammation will cause increased movement of neutrophils and macrophages to lung tissue causing increased release of elastase and increased elastolytic activity ► Smoking will cause increase in accumulation of neutrophils and macrophages and release of elastases ► smoking will inhibit alpha 1 antitrypsin which is an antielastase elastops regulates eastase so w toeast PLUS if · alpha / is inhibited then it 27 Can't stop elastase - > Which is enzymes 28 that break down proteins like elastin keepslungsa Clinical signs Of Emphysema ► Dyspnea ► Cough and wheezing associated with chronic bronchitis ► Weight loss ► Prolonged expiration ► Changes in posture – sitting forward, hunched over to help squeeze air out of lungs ► hypoxia – cyanosis low oxygen-blue ► increased CO2 will decrease pH ► Right side heart failure due to increased resistance to blood flow through lung tissue (pulmonary hypertension) - ↓ 29 vesteanower blood 30 5  10/21/2020  = Chronic Bronchitis commonly associated with emphysema  common in smokers and urban dwellers Apollution  Also a common condition  Manifestations of Chronic Bronchitis ► Associated with a persistent cough for at least 3 months in at least 2 consecutive years ► Associated with inflammation, fibrosis and narrowing of bronchioles thickening ► Eventual damage to bronchiolar wall and onset of emphysema  Forms of Chronic Bronchitis ► Simple Chronic Bronchitis mildest ► Chronic Mucopurulent bronchitis mucus contains bus thick ► Chronic Asthmatic Bronchitis features of asthma ↓ chronic bronchitis 31 32 Pathogenesis of Chronic Bronchitis ►A - Bronchiectasis permanent dilation of the bronchi and Irritation due to smoke, air pollution ► bronchioles due to destruction of muscle - these Mininga (sulfurdioxide) and elastic supporting connective tissue ► Hypersecretion of mucous that starts in large ► Usually associated with chronic necrotizing airways in response to irritation body produces excess mucous ► Hypertrophy of mucous glands in submucosa infections long term chronic infections that cause necrosis (tissue & Become larger normal selly produces the MoCUs ► Metaplastic formation of mucin secreting goblet ► Often associated with: death) cells on surface of epithelium  Pneumonia go tells swelling ► Edema of bronchiolar wall  whooping cough causes fibrosis ► Fibrosis in bronchiolar wall continued inflammation which stiffens walls  foreign body ► Smooth muscle hyperplasia increase in #  influenza virus Which thickens ↳ away 33 34 Group of disorders - lungsmoras Pathogenesis Of Bronchiectasis Restrictive Lung Disease ►also called interstitial lung disease  Most often associated with obstruction of airway and ►Characterized by reduced compliance - chronic persistent infection  Normal clearance mechanisms are hampered by ►More pressure is required to expand lungs obstruction causing the build up of secretions ►Usually associated with damage to and changes in ToWag  leads to more microorganism growth – infections the interstitial space  Usually affects the dependent parts of the lung – the ►Interstitial fluid or fibrosis results in “stiffening” of inferior aspect lungs e  Necrosis of lung tissue can form lung abscesses ►Also associated with damage to alveolar epithelium  Hypoxia less oxygen  Hypercapnia build-up of CO2 in pockets of pis blood and interstitial vasculature ►Manifestations of Restrictive Lung Disease axus  Minor to severe hypoxia  Pulmonary Hypertension increased pressure  respiratory failure  Right Heart Failure  Pulmonary Hypertension narrow stiff vessels  Right Heart Failure 35 36 6  10/21/2020 Acute Restrictive Lung Disease ARDS ► Acute onset develops quickly ► Causing diffuse alveolar damagewidespread damage to alveoli ► Poor to grim prognosis significant mortality ► Pathogenesis Of ARDS  In all cases macrophages and neutrophils are involved in mediating the injury to the epithelium and endothelium of the lung tissue  Multiple causes ► Infection ► Physical Injury ► InhaledIrritants ► Chemical Injury ► Uremia Kidney failure-waste products build in blood up 37 38 Manifestations Of ARDS ► Capillary Congestion ► Interstitial and intra-alveolar edema and hemorrhage flvid builds up within spaces between cells (interstitial) a leaks into alveoli ► Necrosis of alveolar epithelial cells ► Neutrophils collect in capillaries leading to swelling of ↓ bleeding lungs ► Fibrin thrombi in capillaries tiny blood clots ► Hyaline (Gr. hyalos = glass) membranes line the alveoli ► Hyaline is a protein-rich edema fluid with necrotic epithelial tissue cells ► Eventual interstitial fibrosis 39 40 Chronic Restrictive Lung causes Etiology of Chronic Restrictive Lung Disease Disease ► Many known and many unknown causes ► Idiopathic Pulmonary Fibrosis ► Associated with reduced Forced Vital  An immune response of unknown origin Capacity A in amt of air a person can forcibly exhale ► Sarcoidosis (Gr. sarkos = flesh) ► Disease evolves over time from low grade  A multi-system disease of unknown origin inflammation that may resemble a more causing non-caseating small clumps granulomas in many of limited form of ARDS tissues and organs inflammatory cells  Lesions are associated with a cell-mediated ► Leads to damage to epithelial tissue and immune response to an unidentified antigen increased fibroblast activity Tellattackingforeignsubsa se is Unidentified 41 42 7  10/21/2020 Hypersensitivity Pneumonitis ► Also called Allergic Alveolitis ► Immunologically mediated inflammatory lung disease immune rxn triggered by inhaled dust/allenges ► An occupational disease farming , mold exposure more dust or allergens ► Damage in this disease occurs at the alveoli - > site for gas (unlike bronchial asthma which occurs in the exchange bronchi) airways ► Manifestations  Mononuclear cell infiltrates in alveoli and alveolar walls  Cough  Dyspnea  Weight Loss  Respiratory failure and death in severe cases 43 44 affect blood flow in &Vascular longs Lung Diseases ► Pulmonary Thromboembolism ► A major clinical problem ► Very common in hospitalized patients ► Majority of emboli are venous and circulate through as right-sided cardiac thrombi ► Most arise from the veins of the lower extremities ► Most will arise from between the Popliteal veins superior to the iliac 45 46 T veins behind the 5 veins knew wn that behind the knee Up to the superiorly iliac veis in the pelvis  Major factors that predispose persons to venous thrombi in the lower extremities: ► Prolonged bed rest, with leg immobilization ► Surgical procedures of the legs especially the ankle and knee ► Trauma such a fracture and burns ► Congestive Heart Failure CHF ► Disseminated Cancer spread from original lication ► IV catheters 47 48 8  10/21/2020 Pneumonia air sals functional tissue (alveoli) ► Inflammation of the parenchymal structures of the lungs ► The leading cause of death in debilitated weakened Pulmonary Infections patients ► Most likely due to microorganisms but could be due to chemical agents ► Classification Schemes of Pneumonia 49 50 Classification by type of microbe Classification by type of microbe ► Bacterial  Strep. pneumoniae most common ► Viral  Staph aureus  Strep. pyogenes  Respiratory syncytial virus RSV  Gram negative bacilli –  Cyclomegalovirus umv ► Escherichia coli  Influenza Avian form bird flu ► Klebsiella phuemoniae  Corona virus - SARS severe acute respiratory syndrome ► Fungal Disease ► Protozoan  Hantavirus spread by rodents ► Mycobacterial  Mycoplasma pneumoniae walking preumonia ► Chlamydia psittaci bird exposure ► Richettsial insects 51 52 53 54 9  10/21/2020 ► Classification by Location Lobular/Lobar Pneumonia Bronchopneumonia ► Lobular – Part of One lobe  Refers to a patchy distribution of inflammation ► Lobar – entire lobe involving more than one lobe -  95% are caused by Streptococcus pneumoniae  generally associated with bacterial infections ► Manifestations/clinical signs  The airspaces are homogeneously filled with an  Initially will affect the bronchi first and then the main airways exudate fluid cell debris , , bronchioles and alveoli smaller airways air sacs  Can be seen on radiograph as areas of consolidationfilled/dense opaque  Caused by a variety of organisms 6  Sudden onset of symptoms 5  May bebacteria in body bacteria outside body endogenous, exogenous or nosocomial hospital stay infection Hyperthermia – up to 106 degrees F  Chills and involuntary shaking  Manifestations of Bronchopneumonia  Malaise fatigue ►Acute but can be insidious -> develop more gradually  Productive Cough – sputum often containing blood and ►There is a high grade fever pus ►cough that is usually productive - > pus or blood  reduction in lung sounds over affected area  Neutrophilia –With a “left shift” Pin immature neutrophils ►Crackles and wheezes on exhalation breathing  Pain associated with inspiration and expiration due to inflammation of pleural lining – pleuritis – pleurisy lung lining 55 56 Interstitial Pneumonia Named based on Type of Occurrence also referred to a pneumonitis ► between alveoli ► Primary Pneumonia ► Primarily involves the alveoli and interstitial tissue  Associated with direct inhalation of the pathogen ► The organisms involved are primarily viruses and other  Typical pneumonias include lobar/lobular, intracellular pathogens such as Mycobacterium and Mycoplasma species bronchopneumonia and interstitial pneumonia ► Pneumonitis associated with viruses are especially more  The manifestations of these have been explained common common in children earlier cause)  Respiratory Syncytial Virus  Primary atypical pneumonia falls-under this heading ► When occurring in adults most likely associated with - influenza virus ► doesn't cause consolidation Most commonly associated with Mycoplasma pneumoniae exudate in or ► Immunosuppressed persons may show pneumonitis induced by cytomegalovirus  There is little exudates and no consolidation of lung tissue Gungs ► Manifestations > not - noticeable symptoms  The Leukocyte count is generally only slightly elevated  May be severe or subclinical  afebrile not always having a fever  fatigue ► Slight increase or decreased (viral) leukocytes 57 58 Secondary Pneumonia Pneumoconiosis  Most often occurs after lungs have been ►a non-neoplastic condition associated with damaged reaction to the inhalation of inorganic dust  organisms may spread from other areas of the ► Includes: body infection from other body area  Most likely seen in immune suppressed  Coal dust individuals people wl bad immone systems  Silica  Aspiration Pneumonia  Beryllium inhalation ►Associated with aspiration of foreign matter food liquid  Asbestos  gastric secretions - > vomiting X can ► Most likely an occupational hazard or a get in  meconium - home-based hazard > first stool of newborn lugs ►Will also give rise to secondary infections 59 60 10  10/21/2020 Coal Dust ► Also called Black Lung Disease or Anthracosis ► Associated with exposure in coal mines or from home exposure ► Induction of inflammatory response and the physical obstruction of the gas exchange surfaces 61 62 Silica (silicon dioxide) ► Causing Silicosis ► The crystalline forms are most reactive – quartz ► Non-crystalline forms are least reactive – Talc, mica, vermiculite ► Occurs in association with any process that exposes one to fine silica dust that can be inhaled  sandblasting  quarrying ► Manifestations associated with and intense inflammatory response and progressive fibrosis ► Effects of fibrosis may not show up for years after exposure 63 64 Beryllium can cause& Asbestos is this (natural ) this ► Asbestosis inhalation of dus ► Causing Berylliosis ► Fibrous crystalline structure ► Exposure from dusts or fumes of metallic ► Occupational hazard beryllium or its oxides, alloys and salts ► Mining, Insulation ► An occupational hazard – nuclear and ► Manifestations: aerospace industry exposure * Parenchymal Interstitial Fibrosis – the classical form of long tissue asbestosis scaring of ► Causing granulomatous disease in lungs  pleural effusions accumulation of fluid in pleural clusters of immune  Bronchiogenic carcinoma long cancer carity cellscausing inflammation rscarring  Malignant mesotheliomas rare but aggressive cancer affects pleura or peritoneum  laryngeal carcinoma cancer of larynx  Extrapulmonary neoplasms including colon carcinoma cancer outside lungs 65 66 11  10/21/2020 development of tumors /cancer Lung Neoplasia ► Bronchial Carcinoma most common long cancer 6)  The major pulmonary neoplasia associated with smoking and asbestosis  Four Subtypes:  Pulmonary Adenocarcinoma  Squamous Cell Carcinoma  Large cell Undifferentiated Carcinoma  Small cell Carcinoma ► Males 2x more at risk ► Account for >100,000 deaths per year in the USA ► Malignant Mesothelioma of abdomen  Rare in the general population slining  involves the pleural and peritoneal membranes  Associated with exposure to asbestos  Long Latent period – 25-40years how long it takes for symptoms to appear 67 68 69 70 12