Chapter 22: Respiratory System Dr Renata Uribe Shenzhou University November 2015 Func?onal Anatomy of the Respiratory System FUNCTIONAL ANATOMY •  Respiratory zone – site of gas exchange –  Respiratory bronchioles, alveolar ducts, alveoli •  Conduc2ng zone – set of passageways from the outside environment to the respiratory zone: cleanse, moisten and warm the air –  Nose, nasal cavity, paranasal sinuses, pharynx, larynx, trachea, bronchi and lungs FUNCTIONS •  Respiratory system func?ons to supply the body with O2 and remove CO2 •  Respira?on involves 4 processes: –  Pulmonary ven2la2on – moving air IN (INSPIRATION) and OUT (EXPIRATION) of the lungs –  ** External respira2on – O2 moved from lungs to blood and CO2 moved from blood to lungs –  Transports of gases – transport of O2 from lungs and CO2 from cells (cardiovascular system) –  Internal respira2on – O2 moved from blood to cells and CO2 moved from cells to blood •  What is cellular respira?on? Produc?on of ATP in the cell – uses O2 and releases CO2 THE NOSE AND PARANASAL SINUSES THE NOSE AND PARANASAL SINUSES •
•
•
•
•
•
Provides airway Moistens air Warms air Filters air Resona?ng chamber for speech Houses olfactory receptors HOMEOSTATIC IMBALANCE •  Rhini?s: –  Inflamma?on of the nasal mucosa with excessive mucus produc?on, nasal conges?on and postnasal drip. •  Sinusi?ts: inflamed sinuses –  Spread of rhini?s to the sinuses, when when passageways are blocked with mucus/infec?ous material, the air in the cavi?es is absorbed: vacuum sinus headache PHARYNX (throat) Pharynx (Throat) •  Connects nasal cavity and mouth to larynx and esophagus •  Nasopharynx –  Only an air passageway –  Con?nuous with nasal cavity –  Closed off by the uvula, preven?ng food from entering the nasal cavity •  Oropharynx –  Both swallowed food and air can pass through –  Stra?fied squamous epithelium, more protec?ve Pharynx (Throat) •  Laryngopharynx –  Passageway for food and air –  Stra?fied squamous epithelium –  Posterior to epiglo`s and extends to larynx LARYNX Larynx •  3 func?ons –  Provide an open airway –  Switching mechanism between air and food channels –  Voice produc?on (vocal folds) •  Framework of nine car?lages –  Thyroid car?lage with a prominence (Adam’s apple) –  Cricoid car?lage (Below to tracheostomy) –  Arytenoid, cuneiform, corniculate car?lages (lateral and posterior walls) –  Epiglo`s: elas?c car?lage with mucosa covering Epiglo`s •  Flap of elas?c car?lage covered with a mucous membrane •  During swallowing, the larynx is pulled superiorly •  Epiglo`s tups to cover laryngeal inlet •  If anything other than air enters the trachea, a cough reflex will expell it –  This reflex is absent in unconsciousness Voice Voice •  Vocal ligaments (from arytenoid to thyroid car?lage) form the core of the vocal folds •  Vocal folds vibrate, producing sound as air passes through the glo`s –  Closing of the glo`s can also serve to increase abdominal pressure (defeca?on) •  Ves?bular folds (false vocal cords) have a func?on in swallowing •  Laryngeal muscles change length and tension of vocal folds Voice •  Intermident release of expired air and opening and closing of the glo`s causes sound waves •  The force of air rush determines the loudness •  The tension of the vocal folds determines the pitch •  Sound is determined by resonance in pharynx, oral, nasal and sinus cavi?es •  Enuncia?on depends on shaping of sound by muscles in pharynx, tongue, soe palate and lips –  Puberty: vocal folds become longer and thicker, slowing the vibra?on TRACHEA Trachea •  Mucosa –  Pseudostra?fied epithelium with goblet cells and cilia, propelling mucus upward –  Smoking destroys cilia: cough •  Lamina propria –  With elas?c fibers •  Submucosa –  With seromucous glands •  Adven??a –  16-­‐20 C-­‐shaped rings of hyaline car?lage that prevent collapse when pressure is nega?ve Trachea •  Not protected by bone – car?lage protects it •  Concentric rings of car?lage •  Inside layer mucosa – Respiratory System made of pseudoestra?fied ciliated columnar epithelium – GIANT LONG CILIA are constantly wiggling producing Mucus – SMOKERS – paralyze cilia in your trachea BRONCHI AND SUBDIVISIONS •  Order of branching: –  Primary –  Secondary (lobar) –  Ter?ary (segmental) –  Bronchioles •  Smallest bronchioles have special name –  Terminal – Thinnest –  Respiratory – connect to alveolar ducts •  As branches decrease in diameter –  Car?lage rings disappear –  Mucosa changes from pseudostra?fied columnar to columnar, then cuboidal epithelium –  Amount of smooth muscle increases due to lack of car?lage BRONCHI AND SUBDIVISIONS Respiratory zone – respiratory bronchioles, alveolar ducts, and alveoli •  Respiratory membrane –  Wall of alveolus (simple squamous epithelium+basement membrane) –  Wall of capillary (simple squamous epithelium+ basement membrane) Conduc?ng Zone •  Trachea bifurca?on: right and lee primary bronchi –  Right is wider, shorter and more ver?cal: common site for inhaled foreign objects •  Subdivides into lobar bronchi – segmental bronchi – bronchioles (<1mm) – terminal bronchioles •  Along this way –  Less and less car?lage support –  Pseudostra?fied columnar – columnar – cuboidal epithelium without cilia –  Rela?vely more smooth muscle Alveoli •  Surrounded by elas?c fibers •  Alveolar pores connect alveoli equalizing air pressure and providing alternate routes of air flow •  Alveolar macrophages (dust cells) keep the alveoli sterile Respiratory Membrane (RM) •  Func?onal structure – it is where they meet – alveolus meets up with capillaries to have gas exchange •  RM is where lungs are making contact with your blood •  RM composed of epithelial wall of the alveolus (basement membrane is part of the epithelium) and the capillaries wall •  This is the point where the body decides: what to get in from the air we breath. •  Heart àpulmonary àartery branched smaller and smaller àarterioles into lungs became à capillaries àwrapped around the alveoli à venules •  Pulmonary vein – takes the O2 out to the heart and distribute to the body Respiratory Zone •  The place of gas exchange •  (terminal bronchioles) – respiratory bronchioles – alveolar ducts – alveolar sacs – alveoli (300 million) •  The respiratory membrane/ the alveolar wall/ air-­‐blood barrier –  Squamous epithelial ‘type I pneumocyte cells’: O2 and CO2 diffuse across the membrane –  Cuboidal ‘type II pneumocyte cells’: secrete surfactant, lowering the surface tension of water, preven?ng alveolar collapse (it is like a “soap”) Lungs and Pleurae •  Lungs: –  Costal surface, apex, base –  Hilum: entrance of vessels, bronchi and nerves –  Right lung: superior and inferior lobe (oblique fissure) –  Lee lung: superior, middle, inferior lobe (oblique and horizontal fissure) –  Lobes consist of bronchopulmonary segments separated by connec?ve ?ssue septa (each with its own artery, vein and segmentary bronchus) –  Lobules: smallest unit, served by a large bronchiole –  Mostly air – in elas?c connec?ve ?ssue (stroma) Lungs & Pleura •  Outer Structure of the lungs – Right lung looks different then lee lung – hear •  Right lung is bigger 3 lobes •  Lee lung is smaller 2 lobes •  Both lungs have oblique fissure •  Right lung you also have horizontal fissure •  Bodom of the lungs are boundary muscle diaphragm •  Rib cage anterior boundaries •  MUSCLES – INTERCOSTAL MUSCLES -­‐ breath Blood Supply and Innerva?on •  Two circula?ons –  Pulmonary: arteries deliver deoxygenated blood, capillary network around alveoli, pulmonary veins bring freshly oxygenated blood to the heart –  Bronchial: (systemic) oxygenated arterial blood to lung ?ssue •  Pulmonary (nerve) plexus –  Parasympathe?c motor fibers (bronchoconstric?on), sympathe?c motor fibers (bronchodila?on) and visceral sensory fibers. veins The Pleurae •  Thin double layered serosa –  Parietal pleura: covers thoracic wall and superior face of the diaphragm –  Visceral pleura: covers external lung surface, lining the fissures –  Pleural cavity is filled with pleural fluid: surface tension of the fluid keeps the two layers together so the lungs don’t collapse when the pressure becomes nega?ve. Review: •  Nasal cavity -­‐ air gets warmed, moistened, cleaned •  Concha – air flows larger surface area to get cleaned and moistened •  Leaves nasal cavity enters pharynx •  Leaves pharynx – epiglo`s is up •  Larynx – irregular shaped pieces of car?lage – 2 important things: helps make sure that air travels one way &food another. Voice produc?on. •  Trachea – perfect concentric rings of car?lages – ensures airway – cillias -­‐ smokers Review •  Trachea in chest cavity àbranches and 2 por?ons called bronchia •  Lung is the house that alouds to have pressure – it is like a big balloon around the bronchial tree •  Branchingàbranchingà network bronchioles – end of bronchiole terminal & respiratory bronchiole – hundreds of ALVEOLI à where gas exchanges – across RESPIRATORY MEMBRANE – O2 TO THE BLOOD AND CO2 LEAVES THE BLOOD CROSSING RESPIRATORY MEMBRANE TO THE LUNG AND OUTà Physiology of the Respiratory System Pressure Rela?onships in the Thoracic Cavity •  Pressures are always rela?ve to atmospheric pressure (760mmHg) –  Nega?ve pressures are below 760mmHg, and posi?ve pressures above 760mmHg •  Intrapulmonary pressure is the pressure in the alveoli (760mmHg) •  Intrapleural pressure is always lower than intrapulmonary pressure (756mmHg) •  Transpulmonary pressure = Intrapulmonary – Intrapleural pressure (4mmHg) Pressure Rela?onships in the Thoracic Cavity PRESSURE RELATIONSHIPS: •  ATMOSPHERIC PRESSURE – P atm –
–
–
–
Pressure exerted by gases surrounding the body At sea level around our body -­‐ 760mmHg = 1 atm Nega?ve respiratory pressure – anything below atmospheric pressure Posi?ve respiratory pressure – anything above atmospheric pressure •  INTRAPULMONARY PRESSURE – P pul –  Pressure in the alveoli –  Rises and falls with breathing but always equalizes with atmospheric pressure –  Pressure in the lungs – in the alveoli – this is the one that changes as we breathe in and out (pulling more air in and out) –  Lungs are always trying to equalize with the P atm PRESSURE RELATIONSHIPS: •  INTRAPLEURAL PRESSURE P ip –  Pressure in the pleural cavity –  Always a nega?ve pressure (<Patm and <Ppul) –  Fluctuates with breathing –  Should always stay nega?ve – •  Nega?ve P ip is caused by opposing forces –  2 inward forces promote lung collapse •
•
•
•
Elas?c recoil of lungs decreases lung size Surface tension of alveolar fluid reduces alveolar size One outward force tends to enlarge lungs Elas?city of the chest wall pull the thorax outward Intrapleural Pressure •  Lung-­‐collapsing forces –  The elas?c lungs have a tendens to recoil –  Surface tension of alveolar fluid draw alveoli to the smallest possible dimension •  Natural elas?city of chest wall tends to pull the thorax outward and to enlarge the lungs •  Because of the nega?ve intrapleural pressure, neither of the opposing forces is dominant. –  The amount of fluid is minimal, because otherwise the pressure would become posi?ve Laws of Pulmonary ven?la?on •
BOYLE´S LAW: –  Pressure and volume of a gas are inversely propor2onal at constant temperature –  Increase V= Decrease P –  Important note: gas always flows from higher pressure to lower pressure •
INSPIRATION: –
–
–
–
•
•
External intercostal & diaphragm contrac?ons Volume of the thoracic cavity increases resul?ng in a decrease in the pressure Ppul<Patm Air rushes into the lungs Inspira?on ends when Ppul=Patm Expira2on –  Muscle relax –  Volume of the thoracic cavity decreases resul?ng in an increase in the pressure Ppul>Patm –  Air flows out the lungs QUITE BREATHING VS FORCE BREATHING –  (try to get more O2 or trying to get rid of CO2) Pulmonary Ven?la?on •  Volume changes lead to pressure changes •  Pressure changes leads to flow –  Boyle’s Law: •  Inspira?on and expira?on •  Mechanical processes that depend on volume changes in the thoracic cavity •  Volume changes à pressure changes •  Pressure changes à gases flow to equalize pressure Boyle´s Law •  The rela?onship between the pressure and volume of gas •  Pressure (P) varies inversely with volume (V): p1V1= P2V2 •  An increase in volume = decrease in pressure •  A decrease in volume = increase in pressure Boyle´s Law This rela?onship is given by Boyle’s Law •  At constant temperature the pressure of a gas varies inversely with its volume Boyle´s Law Boyle’ s Law Background: •  Pulmonary ven?la?on = Mechanical process that depends on volume changes in the thoracic cavity Volume changes lead to pressure changes Pressure changes lead to the flow of gases to equalize pressures Boyle´s Law At constant temperature the pressure of a gas varies inversely with its volume P x V = C P=pressure V=volume C=constant Surface: 1atm x 10l = 10bar/l (constant) 10mtr depth 2atm x? = 10bar/l size 1/2 20mtr depth 3atm x? = 10bar/l size 1/3 30mtr depth 4atm x? = 10bar/l size 1/4 Inspira?on •  An ac?ve process –  Inspiratory muscles contract –  Thoracic volumes increases –  Lungs are stretched and intrapulmonary volume increases –  Intrapulmonary pressure drops (to -­‐1mmHg) –  Air flows into the lungs, down its pressure gradient, un?l Ppul=Patm Expira?on •  Quiet expira?on is normally a passive process –
–
–
–
–
Inspiratory muscles relax Thoracic cavity volume decreases Elas?c lungs recoil and intrapulmonary volume decreases Ppul rises (to+1mmHg) Air flows out the lungs down its pressure gradient un?l Ppul=0 •  Note: forced expira?on is an ac?ve process: it uses abdominal and internal intercostal muscles Basic proper?es of gases: Daltons-­‐s Law of Par?al Pressures •  Total pressure exerted by a mixture of gases is the sum of the pressure exerted by each gas •  The par?al pressure of each gas is directly propor?onal to its % in the mixture How do we know which gas that is brought into our lungs should go to our blood? •  Alveoli – running next to the alveoli – capillaries – blood •  Deep breath IN – O2, CO2, Hydrogen, Argo, sulfured gas and others •  We only need the O2 – the rest we breathe it all out •  Dalton´s says that •  The pressure of an en2re mixture is the sum of the pressure of each gas – directly propor2onal to the % in the mixture –  “The P is related to how much you have – If you have more of it you have a higher pressure” Dalton´s •  More O2 in the lungs •  High concentra?on of CO2 in the blood •  Dalton´s says: If you have a high concentra?on you have a high pressure of CO2 in the blood •  “If I have a lot of CO2 In my blood that means I have a high pressure of CO2 in my blood” then I do in my alveoli – So in my alveoli I have a low concentra?on of CO2 which means I have a low pressure of CO2 •  GAS GO FROM HIGHER PRESSURE TO LOW PRESSURE – •  The pressure is higher in the blood & that´s why CO2 goes to alveoli which has the less pressure (out by breathing) Daltons •  Low concentra?on of O2 in the blood – the pressure is going to be LOW •  In the lungs if “I have a higher concentra?on of O2 – the pressure is higher “ •  And gas (O2) goes from high pressure of O2 to low pressure of O2 – from the lung to the blood Basic Proper?es of Gases: Henry´s Law •  When a mixture of gases is in contact with a liquid , each gas will dissolve in the liquid in propor?on to its par?al pressure •  At equilibrium, the par?al pressures in the 2 phases will be equal •  The amount of gas that will dissolve in a liquid also depends upon its solubility –  CO2 is 20 ?mes more soluble in water than O2 –  Very lidle N2 dissolves in water Henry´s law •  Henry’s Law Water takes up, of gas condensed by one, two, or more addi:onal atmospheres, a quan:ty which, ordinarily compressed, would be equal to twice, thrice, the volume absorbed under the common pressure of the atmosphere." •  In other words, the amount of dissolved gas is propor?onal to its par?al pressure in the gas phase. •  The propor?onality factor is called the Henry's law constant. Henry´s law •
•
•
•
•
•
•
•
•
•
•
Where do I have more of which gas? High concentra2on of O2 in the blood – high pressure of O2 Low concentra2on of O2 in the cell – low pressure of O2 O2 flows from a high pressure to a low pressure – so it will go to the cell Where do I have more of which gas? Where do I have more CO2? Cell has high concentra?on of CO2 with high pressure of CO2 in the cell Low concentra?on of CO2 and low pressure of CO2 in the blood CO2 goes from the cell to the blood (from high pressure to low pressure) And now we have > CO2 in our blood going back to the lungs and more CO2 in our blood means more pressure co2 Relax muscles decrease our volume increase our pressure in our lungs and CO2 leaves. Inspira?on Expira?on NEUROCHEMICAL CONTROL NEUROCHEMICAL CONTROL •  Respiratory center if the the CNS is located in the lateral medulla oblongata of the brainstem; •  Impulses travel down down the phrenic nerves to the intercostal nerves to the intercostal muscled between the ribs. Neurons •  The respiratory center consist of different groups of neurons •  Dorsal respiratory group, determines autonomic rhythm of respira?on •  Ventral respiratory group, is inac?ve during normal respira?on but becomes ac?ve when increased ven?lator effort is needed Factors of influence •  Chemoreceptors respond to the hydrogen ion concentra?on (pH) of arterial blood, the par?al pressure of the arterial carbon dioxide (PACO2) •  Central chemoreceptors respond indirectly to arterial blood by sensing changes in the pH of cerebrospinal fluid (CSF) •  Paco2 also helps regulate ven?la?on. •  If Paco2 is high the respiratory rate increases •  If Paco2 is low the respiratory rate decreases Factors Influencing Ven?la?on •  Airway Resistance –  Fric?on in the respiratory passageways –  2mmHg or less moves 500ml air in and out of the lungs –  Insignificant because •  Airway diameter is huge rela?ve to the viscosity of air •  The cross-­‐sec?onal diameter only increases as the bronchi branch •  Alveolar Surface Tension –  Draws liquid molecules closer together and resists any force that tends to increase the liquid’s surface area –  Without surfactant the alveoli would collapse and the more energy would be required energy to open them. Factors Influencing Ven?la?on •  Lung Compliance –  A measure of the change of lung volume that occurs with a given change in the transpulmonary pressure •  Higher compliance: easier to expand the lungs –  Depends on ?ssue distensibility and alveolar surface tension –  A decrease in surfactant or fibrosis due to inflamma?on decrease lung compliance Respiratory Volumes •  Different respiratory volumes or capaci?es can be measured to gain informa?on about a person’s respiratory status Func?on Tests •  Spirometry –  Can dis?nguish between obstruc?ve (increased resistance) and restric?ve (reduc?on in lung capacity) pulmonary disease. Func?on Tests •  Forced Vital Capacity (FVC) –  Amount of air which can be forcefully exhaled aeer taking the deepest breath possible •  Forced Expiratory Volume (FEV) –  Determines the amount of air expired during specific ?me intervals of the FVC test (normally 80% in 1s) •  Alveolar Ven?la?on Rate –  Index of effec?ve ven?la?on, because it takes dead space into account Gas Exchange •  Dalton’s Law –  Total pressure of a mixture of gases is the sum of pressures of the individual gases in the mixture –  The pressure exerted by each gas (par?al pressure) is directly propor?onal to the percentage of that gas in the mixture •  Henry’s Law –  When gas is in contact with liquid the gas will dissolve in the liquid in propor?on to its par?al pressure –  Equilibrium: the gas par?al pressures in the two phases are the same –  Dependent on: par?al pressure, temperature (less solubility at warmer temperatures), solubility (Oxygen is 1/20 as soluble as CO2) Alveolar Gas •  Atmospheric air is almost en?rely O2 and N2 •  Alveoli more CO2 and water vapor, less O2 –  Gases are exchanged with pulmonary blood –  Air humidifica?on by conduc?ng passages –  Mixing of alveolar gas with each breath (newly inspired – remaining gas) External Respira?on •  Movement of O2 and CO2 across the respiratory membrane is dependent on –  Par?al pressure gradients and gas solubili?es –  Matching of alveolar ven?la?on and blood perfusion –  Structural characteris?cs of the respiratory membrane Internal Respira?on •  Gas exchange in ?ssue follows the same physical laws as gas exchange in the lungs •  Diffusion gradients are reversed –  PO2 is 40mmHg in ?ssue and 100mmHg in arterial blood –  PCO2 is 45mmHg in ?ssue and 40mmHg in arterial blood Homeosta?c Imbalances •
•
•
•
COPD Asthma Tuberculosis Lung cancer COPD •  Chronic Obstruc?ve Pulmonary Disease –  Lung emphysema –  Chronic bronchi?s •  Key features –  80% of pa?ents have a history of smoking –  Dyspnea (shortness of breath) –  Coughing and frequent pulmonary infec?ons –  Hypoven?la?on: respiratory acidosis and hypoxemia COPD Chronic obstruc-ve pulmonary disease refers to lung pulmonary disorders characterized by air flow resistance Chronic bronchi-s is a form of COPD (Chronic Obstruc:ve Pulmonary Disease) an inflamma:on of the bronchi caused by irritants or infec:on Lung Emphysema •  Enlargement of alveoli by destruc?on of alveolar walls –  Breathing requires more energy –  Bronchioles collapse during expira?on, trapping huge volumes of air –  Damaged capillaries cause pulmonary hypertension, increasing the requirements of the right ventricle Chronic Bronchi?s •  Chronic excessive mucus produc?on in the lower airways with inflamma?on and fibrosis of the mucosa •  Obstructs the airways, impairing ven?la?on and gas exchange •  Frequent infec?ons Clinic of COPD •  Pink puffers: lose weight, but normal blood gases •  Blue bloaters: cyanosis with pulmonary hypertension and right-­‐sided heart failure •  Therapy –  Cor?costeroid inhalers and bronchodilators –  Lung volume reduc?on surgery –  Oxygen administra?on, but with care: •  Drives CO2 off Hb, increasing blood acidity •  Oxygen dilates pulmonary arteries, worsening the ven?la?on-­‐perfusion mismatch Cor Pulmonale Cor Pulmonale hypertrophy and dila:on of the right ventricle develop secondary to a disease affec:ng the structure or func:on if the lungs or associated structures •  This condi?on occurs at the end stage of various chronic disorders of the lungs, pulmonary vessels, chest wall and respiratory control center. Cor Pulmonale –  Causes 25% of all types of heart failure –  Strong rela?on between COPD and Cor Pulmonale –  About 85% of pa?ents with Cor Pulmonale also has COPD –  25% of pa?ents with bronchial COPD eventually develop Cor Pulmonale –  Most common in smokers, middle age, elderly men Asthma •  Episodes of coughing, dyspnea, wheezing, and chest ?ghtness –  Reversible obstruc?on: adacks are acute and followed by symptom free periods •  Ac?ve (allergic) inflamma?on thickens the airway walls and bronchospasms then reduce airflow Asthma •  Asthma: a chronic reac:ve airway disorder that can present as a brute aMack •  During an asthma adack , muscles surrounding the tubes ?ghten (bronchospasm) narrowing the air passage and interrup?ng the normal airflow of air into and out of the longs •  Airflow is interrupted by an increase mucus secre?on, forming mucus plugs, and the swelling of the bronchial tubes •  Causes episodic airway obstruc?on •  Mucosal edema •  Long term pulmonary disease characterized by airflow resistance •  Strikes early, twice as many boys than girls are affected Asthma –  One third of pa?ents develop between 10 and 30 –  One third share the disease with another immediate family member •  Signs and symptoms are: –  Cough –  Dyspnea –  Wheezing •  Over reac?ons can be adributed to: –
–
–
–
–
External allergens Pollen Animal dander House dust or mold Food addi?ves •  Gene?cally induced asthma begins in childhood and is commonly by other hereditary allergies, such as eczema and allergic rhini?s Asthma Mild asthma: •  Pa?ents have adequate air exchange and are asymptoma?c between the adacks •  Oeen described as mild intermitend / persistant asthma •  Pa?ent experiences symptoms of cough, wheezing, chest ?ghtness or difficult breathing less than twice a week •  Flare ups are breath but may vary in intensity •  Nigh`me symptoms occur less than twice per month Asthma Moderate asthma •  Nigh`me symptoms occur five or more ?mes per month •  Have normal or below normal air exchange Severe persistant asthma •  Below normal air exchange •  Experience con?nual symptons of cough, wheezing, chest ?ghtness, and difficulty breathing •  Ac?vity level is greatly affected •  Nigh`me symptoms occur frequently Tuberculosis •  Mycobacterium Tuberculosis, spread by coughing –  Replicate within macrophages, adrac?ng lymphocytes forming granulomas •  Fever, night sweats, weight loss, coughing (blood) •  One third of the world popula?on is infected –  Stays latent in 90%, immunodeficiency might lead to symptoma?c disease Lung Cancer Lung Cancer •  90% result of smoking •  Overall five year survival 17% •  The protec?on of nasal hairs, s?cky mucus and cilia is lost by smoking – free radicals and carcinogens in cigaredes cause cancer –  Squamous Cell Carcinoma –  Adenocarcinoma –  Small Cell Carcinoma (most aggressive) •  Therapeu?c developments: an?bodies against growth factors, cancer vaccines and gene therapy Respiratory Disorders Acute respiratory distress Syndrome (ARDS) form of pulmonary edema that can quickly lead to ARF May follow direct or indirect lung injury Difficult to diagnose If not properly diagnosed can prove fatal within 48 hours Shock, sepsis and trauma most common causes •  Trauma related factors may increase likelihood that mirco emboli will develop Acute respiratory failure (ARF) result when lungs can’t adequate maintain oxygena:on or eliminate CO2 •  Results from impaired gas exchange •  Affects the respiratory systems •  CNS •  Cardiovascular system •  Leads to hypxia •  150.000 cases in US •  Mortality rates 50%-­‐70% The End Thank You!