Lung Anatomy and Physiology Pre-Lecture Notes PDF

Lung Anatomy and Physiology Pre-Lecture Notes: Thoracic cage ○ All the ribs, the sternum itself ○ All play a part in working together with other parts of the respiratory system ○ Provides protection Intercostal muscles ○ Helps us breathe...

Lung Anatomy and Physiology Pre-Lecture Notes: Thoracic cage ○ All the ribs, the sternum itself ○ All play a part in working together with other parts of the respiratory system ○ Provides protection Intercostal muscles ○ Helps us breathe ○ Control contraction and relaxation of chest and diaphragm ○ Allows us to cough if we have changes from centers in the throat and upper airways that signal to the brain ○ Helps when we are sick by clearing mucus and other debris from upper airways Not as efficient as cleaning lower airways Pleural sac (outside of lungs) ○ Just like the heart having seripericardium, it is a fluid-filled sac that the lungs can expand and contract inside of with zero friction. Possible for infection in this lining Also possible to have a decrease in secrecy/lubricating fluid = painful inflammation as you breathe Diaphragm ○ Sits as high up as fifth rib ○ mainl y controlled by phrenic nerve innervation Allows us to breathe involuntary and voluntary change our breathing pattern As you take a deep breath ○ Diaphragm goes down, space where lungs are increaches for more oxygen exchange ○ As it goes up, lung is relaxed in chest cavity Right lung (3 sections) ○ Superior lobe Has sections via lobe but you don’t need to know ○ Middle lobe ○ Inferior lobe Very large lobe ○ Sectioned off by specific type of fissures Horizontal fissure = separates superior and middle lobe Oblique fissure = separates middle and inferior lobe ○ Lung is bigger than left because heart takes up space of left (heart ges towards left hip in oblique manner) Heart wont interact with lung itself Left lung (2 sections) ○ Superior lobe ○ Inferior lobe ○ Oblique fissure = separates superior and inferior lobe of left lung  Lungs are quite tough but also soft, easily damaged and structures inside as well So many structures that even if some are damaged you can still live normally Lungs have a unique combo of airway and blood vessels for exchange of gases efficently involuntary ○ Regulated in the brain as brain understands blood oxygen levels and can control speed of oxygenation and heart rate Voluntary thus we have control of the lungs Lungs have lobes which are sectioned it makes it easier for a lung to be removed ○ Unique abilitt Airways of the lungs ○ 1st part: Trachea aka the long tube from top part of pharnyx (the back of your mouth, orophirocavity oropharnyx) Cartilaginous rings: strong rings and kep and maintain the pipe shape without actually bending too much or breaking apart Injuries to trachea are dangerous as if airway collpases it’s your main airway and how you breathe ○ 2nd part: Bronchus Each side of trachea will have branches of bronchi that go off into lung itself called primary bronchus Primary bronchus as they branch off will be intermediate bronchus or secondary As you go further down it changes from bronchus to bronchioles into the site of gas exchange (the aleveoli or aleveolus singular) ○ Trachea → primary bronchus → intermediate or secondary bronchus → tertiary/segmental → alveoli Alveoli ○ Bronchial or smooth muscles ○ Where gas exchange occurs Oxygenation of blood and ability to exchange O2 with CO2 Red refers to oxygenated In the lungs Arteries carry deoxygenated blood which is opposite from your body, in the systemic blood flow arteries usually carry oxygenated blood In the lungs because you come back to heart the deoxygenated blood is in pulmonary artery and oxygenated blood is in pulmonary vein In aleveoli blood will come in deoxygenated and leave oxygenated Type 1 alveolar cells allow for diffusion ○ Occurs in fluid which is surfactant and exchange will occur by a certain set of processes ○ Alveoli have their own macrophages Colour of blood changes = dalton’s law Alveoli has own macrophages so they have their own defense mechanisms  ○ Some interplay between macrophases ○ Type 1 cells are responsible for people getting very sick when they get COVID Lung holds its shape and how structures get in and out is through a specific shape is because of hylum ○ Hylum enables things like bronchus and blood vessels to pass into lungs while it holds structure, and helps hold lungs ○ Hylum is very soft tissue, moves a lot because it moves with you ○ Hylum allows for major structures to pass into lung and blood vessels in general All together gas exchange will occur with help from blood vessels Why a shorter distance to left lung than from right? ○ In the heart right atrium blood comes back from body through right ventricle and blood ejected through conus arteriosus (a funnel) towards pulmonary valve ○ Goes off to lungs through pulmonary trunk and branches off Pulmonary arteries ○ Arties in lungs = deoxygenated blood ○ You get blood flow of low oxygen to pulmonary arteries which work in tandem with bronchi all of them at levl of alveoli ○ This will oxygenate blood and returend to heart via pulmonary veins ○ Right ventricle → pulmonary trunk in pulmonary arteries → sites of oxygen and carbon dioxide tranfer → blood returned to heart via pulmonary vein from both lungs Left atrium is fed by pulmonary veins which carry oxygenated blood Return of blood to heart (before it goes to body) ○ Oxygenated blood returns to heart into left atrium ○ Pushed by left ventricle ○ Ejected through aortic valve into aorta and out into the body Vasculature is not needed to know Everything works in tandem Brain signals to heart and to lungs and to intercostal muscles and other things to keep us alive Pulmonary ventilation or breathed is induced by changes in volume of lungs + air pressure During normal inhalation, diaphragm and external intercostal muscles contract and rib cage elevates As volume of lungs increase, air pressure drops below atm pressure and air rushes in During normal exhalation, muscles relax, lungs become smaller and pressure inside rises and air expelled Boyles law explains between volume and air pressure ○ Volume increase = lower pressure ○ Lower volume = higher pressure Bodies demand for more oxygen changes normal to forced breathing ○ Additonla muscles indcrease changes in volume of thoracic cavity so more air can pass rapidly through  ○ Gas exchange occurs in lungs as oxygen diffuses rom alevoli into bloodstream and carbon diffuses from bloodstream ○ Dalton’s law = in gs mixture, pressure exerted by each gass is independent The gas mixture in alveolus has high oxygen partial pressure while partial pressure of oxygen in surrounding pulmonary capillaries is low, so oxygen diffuses from alveolus into pulmonary capillary and co2 diffuses out of capillary and into alveoli Class Lecture Notes Gas Exchange Two functions of respiration Ventilation Gas exchange Pheumothorax Escape of air into pleural space due to lung injury or disease (i.e. gunshot) Manifestations ○ Chest pain ○ Shortness of breath ○ Reduced breath sounds on affected side ○ Diagnostic: Lung collapse and air in pleural cavity Types: ○ Closed pneumothorax  No outer wounds going into the chest cavity., everything is inside Lung has failed so its developed a hole, leaking an air Pleural cavity pressure is < the atmospheric pressure When the air is equalizing with lung = bad ○ Open pneumothorax Gun shots, any holes from the outside Pleural cavity pressure is = atmospheric pressure The lung will be able to inflate Sucking chest wound ○ Tension pneumothorax Often seen in accidents (severe) like metal penetrates a wound in the cavity, so severe it pushes the heart more to the left, Doesnt damage heart but its compressing the lung and making tension to collapse the lung so this is extremely dangerous, most pressing out of all types Pleural cavity pressure is > the atm pressure Atelecstasis Collapse of lung Obstructure atelectasis ○ Mucus secretions, tumour, foreign object ○ Obstructed bronchus ○ Reduced volume ○ Mediastinal structure shift ○ Diaphragm elevation When one of lungs collapses diaphragm will shift and uneven, makes it spasm and tightens up so people are struggling to breathe since it won’t contract properly Pneumonia Inflammation of the lung Typically it affects one lobe at a time, starts at upper bronchi then to base of lungs? Then you’re in trouble Progression can vary Exudate spreads through lung → exudate fills alveoli → affected lung portion becomes relatively solid → Exudate may reach pleural surface ○ Difficult to treat because you can’t clear the lungs, the mucus is a good thing tho because it helps get rid of pathogens Etiology: Most important, serves as a guide for treatment ○ Corticosteroids to suppress inflammatory or to thin out mucus ○ Pulmonary levage = wash out the lungs, brutal and last case scenario ○ Surgery may require lobe to be removed because it could lead to necrosis? Locaiton: What part of the lung is impacted? Predisposing factors? ○ Post-op pneumonia  Opportunistic since with a operation in the cavity your body may be weak ○ Aspiration pneumonia Vomit Children inhale something weird ○ Obstructive pneumonia Foreign objects Cases involving tumours which cause opportunistic infection Pneumocystic Pneumonia Cause: pneumocytis carinii, a protozoan parasite of low pathogenicity Affects mainly immunocompromised persons (i.e. premmature infants), rare in general but more common in these types of people Forms cysts inside the lungs and does life cycle of a guinea worm releases eggs in lungs to create more cysts Organisms attack and injure alveolar lining Cough, dyspnea, pulmonary consolidation as these cysts become bigger Diagnosis made by lung biopsy, bronchoscopy, or from bronchial secretions Introduction to SARS-CoV-1 Official name: Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV-1) First Identified: November 2002 in Guangdong, China Family: Coronaviridae Genome: Single-stranded RNA Transmission: Human-to-human transmission primarily through respiratory droplets Disease: Causes SARS Impact of SARS-CoV-1 Outbreak: The 2002-2003 SARS outbreak Global Spread: Spread to more than 24 countries across North America, South America, Europe, and Asia Health Impact: Over 8,000 confirmed cases and 774 deaths globally Symptoms: Fever, cough, difficulty breathing, pneumonia Containment: Effective public health measures led to containment by July 2003 Rapid response and global cooperation were key in controlling the SARS-CoV-1 outbreak. SARS-CoV-2 Official Name: Severe Acute Respiratory Syndrome  Coronavirus 2 (SARS-CoV-2) First Identified: December 2019 in Wuhan, China Family: Coronaviridae Genome: Single-stranded RNA Transmission: Primarily through respiratory droplets Disease: Causes Coronavirus Disease 2019 (COVID-19 Impact of SARS-CoV-2 Global Pandemic: Declared a pandemic by the World Health Organization in March 2020 Health Impact: Millions of confirmed cases and deaths worldwide Symptoms: Range from mild (fever, cough) to severe (pneumonia, organ failure) Vaccination: Development and global distribution of vaccines Social Changes: Adoption of new norms like social distancing, remote work, and increased focus on hygiene Tuberculosis Infection from acid-fast bacterium, Mycobacterium tuberculosis Organisms resistant to destruction ○ Capsule is full of waxes and fatty substances so its hard Transmission: Airborne droplets Granuloma: Giant cell with central necrosis (uncontrolled tissue death) inside, indicates development of cell-mediated immunity (T cells summoned to fight infection, but causes inflammation or necrosis in parts of lung) Multinucleated giant cells: Bacteria plus fused monocytes and periphery of lymphocytes and plasma Cells Hyperinflammation, tissue breaking out/down? Mycobacterium lodge within pulmonary alveoli Granulomas are formed Spreads into kidneys, bones, uterus, fallopian tubes, Others if not stopped If infection is arrested, granulomas heal with scarring (you dont want scars on chest because you won’t have oxygen exchange and no healing of the scars itself) When granulomas formed, they still contain organisms and can cause reactivation TB Infection may be asymptomatic, detected only by chest X-ray and/or Mantoux test Secondary focus of infection may progress, even if  pulmonary infection has healed Diagnosis ○ Skin test (Mantoux test): identifies different types of cell which will migrate? ○ Chest X-ray ○ Sputum culture Sample of sputum (thick mucus in lungs) help diagnose Reactive Tuberculosis Reactivated tuberculosis: Active tuberculosis in adults from reactivation of an old infection; healed focus of tuberculosis flares up with lowered immune resistance Tissue itself and granulomas not only stored active infection and it can reinfect and flares up typically when immune resistance is low Miliary tuberculosis Multiple foci (small, white nodules, 1-2 mm in diameter) of disseminated tuberculosis, resembling millet seeds, usually affects ill people Nodules errode aka burst and leak infection, typically in lungs is hardening or solidification of lobe(s); aids patients or high immunosuppressiont people high risk because opportunistic infection Drug Resistant TB Resistant strains of organisms emerge with failure to complete treatment or premature cessation of treatment or overuse of antibioticis, very small so hard to see in x-ray Multidrug-resistant tuberculosis (MDR TB): one drug is ineffective to treating, or multiple ○ Caused by organisms resistant to at least two of the available anti-TB drugs ○ Treatment course is prolonged and outcome isn’t satisfactory to what ur looking for Extensively drug-resistant tuberculosis (XDR TB): nothing is working T_T ○ Caused by organisms that’re no longer controlled by many anti TB drugs, found mainly in europe africa and asia ‘ ○ Treating everything as it occurs and patient is hydrated and function to some degree Bronchitis Inflammation of the tracheobronchial mucosa ○ As trachea split into bronchi on both sides, the large catilagous structures lead to acute or chronic bronchitis Acute bronchitis ○ Infection that’s common, from bacterial or typically viral like cold and flu ○ Week or two its gone ○ Let it do its thing and youre fine Chronic bronchitis ○ Chronic irritation ○ Lasts for a long time ○ Typically in people with lung pathologies (atm pollution, smokers, etc)  Bronchiectasis ○ Wall of bronchi weakens through inflammation and inflammatory processes, becoming more sac-life rather than keeping structure ○ Typically bronchi are stiff, but after this they lose their rigidity which is bad because they’re large and a structural aspect holding up lower airways, trouble breathing as they also retain secretion which makes u develop chronic cough to get the mucus out, followed by infections of pulmonary system Not more structurally sound causes fluid build up in the lungs Diagnosis made by bronchogram via chest x-ray ○ Air bronchogram, air trapped inside lungs due to failure of bronchi COPD Chronic obstructive pulmonary disease (COPD) ○ Combo of of emphysema and chronic bronchitis aka where the gas exchange occurs In pulmonary emphysema, Destruction of fine alveolar structure of lungs with formation of large cystic spaces ○ Starts in upper lobes and as it goes deeper into lungs it gets worse because that’s where gas exchange occurs/alveoli are there You see a lot of coughing, often chronic bronchitis involved since there is the chronic inflammation of the terminal bronchioles Three main anatomic derangements in COPD ○ Inflammation and narrowing of terminal bronchioles because it is the component similar to bronchitis Leads to bronchioles muchosa swelling Reduced caliber for bronchioles, they lose their structure and thus lose function because of increased bronchial secretions to fight off insection and increased resistance to air flow Air enters lungs more readily than it can be expelled leading to air being trapped ○ Dilatation and coalescence of pulmonary airspace (things are changing shape + sagging) Diffusion of gases is less efficient from large cystic spaces, air becomes trapped in lungs Coalesance refers to grouping of the pulmonary air space which is bad because they should be separate so if damaged only one of them is, but together you can lose function in lungs ○ Loss of lung elasticity, can’t take deep breaths and air jammed into lungs Lungs dont recoil normally following exspiration, lungs become consolidated and air is trapped in lungs Chronic irritation: Smoking and inhalation of injurious agents Pathogenesis Inflammatory swelling of mucosa  Narrows bronchioles; increased resistance to expiration ○ Lower oxygen saturation in blood, exchange becomes inefficent Leukocytes accumulate in bronchioles and alveoli Coughing and increased intrabronchial pressure Retention of secretions predisposes to pulmonary infection Lungs damaged by emphysema cannot be restored to Normal (once scarred, its done for like you need transplant or leads to fatal) Oxygen and helium as a treatment because helium can blow up lungs back to original lung Emphysema Chronic lung condition Part of Chronic Obstructure Pulmonary Disease (COPD) Inflammation of alveoli, making it malformed and stretched out so blood vessels in this for site of exchange don’t work efficently Leads to shortness of breath Causes and risk factors: ○ Long-term exposure to irritants (e.g., tobacco smoke) ○ Genetic factors (e.g., Alpha-1 antitrypsin deficiency) ○ Age and history of smoking Can be at any age Alpha-1 antitrypsin deficiency This deficiency leads to emphysema Low antitrypsin level correlates with lung disease (lower antitrypsin, higher lung disease) because it protects lungs from proteolytic enzymes Inhibits neutrophils ○ Antitrypsin normally inactivates enzymes that can injure alveolar basically, thus needed and protects the lungs from such enzymes ○ Regulated by genetics (both parents need defect) Released from leukocytes in lung ○ Specific antitrypsin molecular enzyme (alpha-1-globulin) prevents lung damage from lysosomes and lysosomal enzymes are released from leukocytes Deficiency permits enzymes that normally occur and remain active to damage lung tissue ○ Typical enzymes will damage lung if uncontrolled ○ So enzymes released, damages lung Severe antitrypsin deficiency ○ Low levels of antitrypsyn and correlates with lung disease because it protects lungs Digestion of connective tissues of alveolar septa, terminal air passages  Deficiency leads to connective tissues in alveolus digested by enzymes and enzyme is running amok so concentration is not being moderated Alveoli tissue eaten?, affects main site of gas exchange Develops progressive pulmonary emphysema ○ Tends to manifest in young ages so basically its emphysema for young people ○ Tends to affect lower lobes first (very large, high concentration site of gas exchange) so if lower lobes affected first, not a lot of symptoms like chronic bronchitis because upper airways are initially affected in that case, with this deficiency there’s an absent cough and no associated bronchitis and excessive mucus production Moderate antitrypsin deficiency Does not develop into severe emphysema at early age ○ Typically because it is caught + treatable Susceptible to lung damage from smoking, atmospheric pollution, and respiratory infections Scar tissue for sure but it will heal in months like a 60 day pack of smoker quitting Not associaed with bronchitis Can lead to risk of pneumonia but very severy ill at a young age can cause this Asthma Spasmodic contraction of smooth wall muscles of bronchi and bronchioles Dyspnea and wheezing on expiration Greater impact on expiration than on inspiration ○ Airways are constricted so what happens in inspiration so they’re taking short hyperventialling breaths which interrupts normal breathing pattern so as upper airways spasm they close (cant get air out as efficiently) Attacks are precipitated by allergens: Inhalation of dust, pollens, animal dander, other allergens Inhaler causes immediate relaxation of the lung to resume breathing from contractions ○ In severe attacks you need epinephrine that’ll block mass cells to slow down immune system It can be dangerous when it fully closes the lungs, but that’s very rare ARDS Acute respiratory distress syndrome (ARDS) ○ Came from after getting COVID as people treated covid as just respiratory and not this and inflammation disease ○ Comes from severe infection or severe injury (traumatic shock, gastric vomit and passed out so hci from stomach goes into lungs for example, toxic gases, etc), can be fatal Severe injury Systemic infection (septic shock)  ○ Ends up with things like shock (systemic blood pressure), blood is prioritized to major organs ○ Septic shock occurs and as BP falls, you become unstable Aspiration of acid gastric contents Inhalation of irritant or toxic gases Damage caused by SARS Damaged alveolar capillaries (brings oxygenated blood back to heart/body) leak fluid and protein Impaired surfactant production from damaged alveolar lining cells Lubrication fails Not getting oxygenated blood Formation of intra-alveolar hyaline membrane You’ll see fallen blood pressure Pulmonary Fibrosis Fibrous thickening of alveolar septa from irritant gases, organic and inorganic particles Walls of alveoli gets scarring within it and as alveoli thickens, gas exchange becomes inefficent It makes lungs rigid, restricting normal respiratory excursions Diffusion of gases is hampered due to increased alveolar thickness Causes progressive respiratory disability similar to emphysema Collagen diseases ○ Aqquaint them more to emphysema ○ Tissues in lung cause lungs to scar Pneumoconiosis Lung Cancer Usually smoking-related neoplasm Common malignant tumor in both men and women Arises from mucosa of bronchi and bronchioles ○ Larger parts of the lungs as there is a rich vascular network at these points bronchogenic carcinoma Classification ○ Squamous cell carcinoma Very common Long term smoking Most common tumour diagnosed ○ Adenocarcinoma Very common but slightly less than squamous cell carcinoma ○ Large cell carcinoma Large cell carcinomas, large epithelial cells ○ Small cell carcinoma Small irregular cells with reduced cytoplasm They look like lymphocytes (something that’s normal), thus easily missed ○ Depending on subtypes and the history it can change outcome of treatment, and lung cancer can spread to other parts of the body