Chap 15- The Lungs Flashcards
divisions of the respiratory system
- air conducting
- gas exchange
air conducting system
- delivers air
- nose
- mouth
- trachea
- bronchi
- bronchioles
gas exchange
- swaps gases between air and blood
- alveoli and capillaries
what protects the respiratory system from harmful inhaled particles?
- mucus
- cilia
- immune cells in lungs- especially macrophages
- capillaries in nose warms and humidify air
what is the V/Q ratio?
- ventilation/ perfusion ratio
- normal ventilation= 4L per min
- normal perfusion = 5L per min
- normal V/Q ratio =0.8
- depends on alveolar and capillary surface area and thickness
gas transportation
- carried by Hb
- once at target, Hb releases gases
- affected by pH and temperature
what does Hb increased affinity for oxygen mean?
- does not release oxygen
- O2 partial pressure curve moves to the left
what does Hb decreased affinity for oxygen mean?
- does not bind oxygen
- O2 partial pressure curve moves to the right
what is surfactant?
- lipoprotein
- coats wall of alveoli
- prevents them from collapsing (reduces surface tension)
lung compliance is due to
- elasticity
- recoil
- surfactant
- negative pressure system
how is breathing controlled?
- by the medulla oblongata
- have chemoreceptors and stretch receptors
obstructive lung disease
- FEV1/FVC <0.7
- partial or complete obstruction of airway
- increases resistance to airflow
restrictive lung disease
- FEV1/FVC is normal or >0.7
- lungs cannot expand to full capacity
what is FEV1
forced expiratory volume in 1 second of FVC
what is FVC
- forced vital capacity
- how much air you can expire after maximum inspiration
what does the FEV1/FVC ratio tell us?
- how much air you can expire within one second
- differentiates between obstructive vs. restrictive lung diseases
what two diseases make up COPD
chronic bronchitis and emphysema
emphysema
- irreversible enlargement of airspace distal to terminal bronchiole
- have destruction of alveolar walls
- small airway fibrosis -> airflow obstruction
what makes up the acinus?
respiratory bronchiole, alveolar duct, alveolus
how do you classify emphysema?
- centriacinar
- panacinar
- distal acinar
- irregular
centriacinar
proximal part of acinus affected
panacinar
entire acinus affected
distal acinar
distal portion of acinus affected
pathogenesis of emphysema
- inflammatory mediators and leukocytes induce structural changes
- proteases are released from inflammatory and epithelial cells-> CT break down, these pts dont have antiproteases
- ROS causes alveolar damage and inflammation
- infection can worsen sx
clinical features of emphysema
- asymptomatic until 1/3 of lung parenchyma is damaged
- dyspnea, cough, wheezing
- weight loss
- “pink puffers”
- hyperinflated lungs
- heart is covered by hyperinflated lungs
chronic bronchitis
- persistent cough with sputum production for at least 3 months in at least 2 consecutive years
- common in smokers and people exposed to air pollution
clinical features of bronchitis
- persistent cough producing sputum
- asymptomatic for many years
- dyspnea on exertion
- hypercappnia
- hypoxemia
- mild cyanosis -> “blue bloaters”
pathogenesis of chronic bronchitis
- smoking destroys cilia in lungs
- excessive mucus not propelled out of lungs
- muscle layer of bronchus undergoes hypertrophy
- excess mucus and hypertrophy cause obstruction
asthma
- chronic disorder of conducting airways
- caused by hypersensitivity especially of bronchus
- divided into early phase and late phase
clinical features of asthma
- recurrent episodes of bronchospasm
- wheezing, breathlessness
- chest tightness
- cough
types of asthma
- atopic asthma- allergic asthma
- non-atopic asthma
- drug induced i.e. aspirin
- occupational
what does the airway in asthmatic pts look like?
- increased number of glands
- hypertrophy of SMC
- a lot of immune cells especially macrophages and eosinophils
- thickening of basement membrane
- mucus secretion
early phase asthma pathogenesis
- allergen processed by T helper 2 cells
- causes stimulation of mucus secretiong glands
- stimulates antibody producing B cells to produce IgE
- eosinophils are recruited
- IgE binds to mast cells
late phase asthma pathogenesis
- next exposure to antigen, IgE antibodies bind to antigen
- causes degranulation of mast cells
- mast cells release histamines and cytokines
- causes sx of asthma
- mucus production, vasodilation, stimulation of vagal receptors -> bronchoconstriction
- eosinophils are recruited which recruit other immune cells
status asthmaticus
- life threatening asthma attack that isn’t responsive to treatment
- can cause respiratory alkalosis and respiratory failure
diagnosis of status asthmaticus
- increased airflow obstruction
- difficulty with exhalation
- peripheral blood eosinophilia
- sputum with eosinophils, curschmann spirals, and charcot-leyden cristals
what are curschmann spirals?
- dead and desquammated epithelial cells
- found in status asthmaticus
what are charcot-leyden crystals?
- dead eosinophils release contents- lysophospholipase
- appears as crystals
- seen in status asthmaticus
bronchiectasis
- destruction of SMC and elastic tissue in bronchus
- uncommon due to antibiotics
clinical course of bronchiectasis
- severe persistent cough
- foul smelling sometimes bloody sputum
- dyspnea and orthopnea
- massive hemoptysis
- cyanosis
complications of bronchiectasis
- cor pulmonlae
- brain abscess
- amyloidosis
what is amyloidosis?
- cytokines stimulate liver to secrete a lot of abnormal proteins
- depsitited into multiple tissues
pneumoconiosis
- non-neoplastic lung restriction due to inhalation of mineral dusts
- usually from work exposure
- small particles and soluble in blood are most dangerous
what does pneumoconiosis development depend on?
- amount of dust retained
- size, shape, buoyancy of particles
- particle solubility and phsyiochemical reactivity
- other irritant exposure i.e. smoking
pathogenesis of pneumoconiosis
- inhaled particles gather in lungs
- engulfed by macrophages
- macrophages release toxic factors -> lung injury and fibrogenic factors
- fibroblasts recruited -> fibrosis
- neutrophils recruited -> inflammation
clinical symptoms of pneumconiosis
- course takes 20-30 years
- cough
- dyspnea
- respiratory failure
- cor pulmonale
- pleural plaques
sarcoidosis
- granulomatous disease, unclear origin
- dx of exclusion
- usually affects bilateral hiler lymphadenopathy or lungs, then eyes and skin
- sx are vague and nonspecific
pathogenesis of sarcoidosis
- inappropriate expansion of CD4+ cells
- release of IL-2 and INF-gamma which causes macrophage activation
- TNF release
- more T cells and macrophages recruited -> granuloma
pulmonary embolism
- important cause of morbidity and mortality in bedridden patients
- occurs in pts with hyper coagulable conditions
pathogenesis of pulmonary embolism
- have respiratory compromise: blood doesnt get past where clot is so alveoli get filled up with blood -> infarction
- have hemodynamic compromise: blood backs up from clot -> RHF
clinical symptoms of pulmonary embolism
- very similar to MI
- chest pain, dyspnea, tachypnea
- fever
- cough
- hemoptysis
- fibrinous pleuritis -> pleural friction rub
pulmonary hypertension
- mean PAP > 25 mmHg at rest
- happen in conditions that increase pulmonary HF, pulmonary vascular resistance, or left heart resistance
- see an increase in endothelin and decrease in NO
secondary causes of pulmonary HTN
- chronic obstructive/ interstitial lung disease
- congenital or acquired heart disease
- recurrent thromboemboli
- autoimmune diseases
- obstructive sleep apnea
pulmonary edema
- leakage of excess interstitial fluid which accumulates in alveolar spaces
- pulmonary edema -> heavy wet lungs
what are the sx of pulmonary edema
- difficulty breathing** (orthopnea, paroxysmal nocturnal dyspnea)
- coughing up blood
- sweating
- anxiety
- pale skin
what are the reasons for fluid to accumulate in the lungs?
- increased hydrostatic pressure (cardiogenic)
- increased capillary permeability (non-cardiogenic)
what is the most common cause of pulmonary edema?
left sided heart failure
atelectasis
- incomplete expansion of the lung or collapse of inflated lung
- insufficient functioning of lung in either case
what is the mediastinum
- area between the two lungs
- occupied by heart, blood vessels, trachea, and esophagus
resorptive atelectasis
- excessive secretion -> obstruction of airway
- air is resorbed from dependent alveoli which collapse
- mediastinum shifts towards affected lung
- i.e. asthma, chronic bronchitis, foreign bodies
compression atelectasis
- something compressing the lungs
- accumulation of significant volumes of fluid, tumor, or air within pleural cavity
- medinastium shifts away from affected lung
contraction atelectasis
- extensive fibrosis prevents lung expansion
- is irreversible
- can happen in pneumoconiosis
acute lung injury
- abrupt onset of significant hypoxemia and bilateral pulmonary infiltrates
- non-cardiogenic
- inflammation causes increased vascular permeability, edema, and epithelial cell death
- diffuse alveolar damage
acute respiratory distress syndrome
severe acute lung injury
clinical features of ARDS
- dyspnea
- tachypnea
- cyanosis
- hypoxemia
- respiratory failure
- ventilation/perfusion mismatch -> respiratory acidosis
- less surfactant -> stuff lungs
pleural effusion
- movement of fluid into the layers of pleura
- common manifestation in both primary and secondary pleural diseases
accumulation of fluid in pleural effusion is due to the following reasons
- increased hydrostatic pressure
- increased vascular permeability
- increased intrapleural negative pressure
- decreased osmotic pressure
- decreased lymphatic drainage
empyema
pleural fluid becomes infected
intrinsic causes of pleural effusion
- malignancy
- infection
- autoimmune
- causes increased permeability and protein rich fluid
extrinsic causes of pleural effision
- heart failure
- kidney failure
- liver failure
- see transudate effusion
pneumonia
- any infection of lung parenchyma
factors that impair defense mechanisms of the lungs and cause pneumonia
- loss/suppression of cough reflex
- injury to cilia
- accumulation of secretions
- immunodeficiency
- pulmonary congestion and edeam
what is the most common type of pneumonia and its cause
- community acquired pneumonia
- due to streptococcus pneumoniae aka pneumococcus
stages of pneumonia
- infection
- edema
- red hepatization
- gray hepatization
- resolution
what is red hepatization?
- congestion in lungs causes leakage of blood cells into alveoli
- appears red and firm
- happens 2-3 days after edema
what is gray hepatization?
- RBC break open and lyse
- other inflammatory infiltrate accumulates
- lungs are gray and firm
- happens 2-3 days after red hepatization
what are the clinical sx of pneumonia?
- fever, shaking, chills
- cough with sputum
- pleuritis
- good prognosis generally
- death can occur if infection spreads to other organs
influenza virus
- type A is most problematic
- affects humans, pigs, horses, and birds
- two different antigens- hemagglutin and neuramidase
hemagglutin
- attach virus to target
- H1-3
neuraminidase
- releases newly formed virions budding from infected cells
- N1 an N2
antigenic shift
- causes pandemics
- antigens on virus replaced through recombination with animal viruses
antigenic drift
- causes epidemics of flu
- spontaneous mutation that alter epitopes on virus
- still resemble other flu viruses so have partial immunity
pathogenesis of influenza
- pneumocytes infected and inhibit Na channels
- causes electrolyte imabalce and water shift
- alveolar edema
- virus hijacks cells -> cell death
- before cells die they recruit other inflammatory cells -> inflammation
lung cancer
- most frequently diagnosed cancer in the world
- most common cause of cancer mortality
- largely due to cardiogenic effects of cigarettes
- most are due to metastasis of other cancers
small cell carcinoma
- exclusively found in smokers
- very aggressive
squamous cell carinoma
- happens close to hilum
- central location in lungs
adenocarcinoma
happens in periphery of lungs
causes of lung cancer
- tobacco smoke
- industrial hazards
- air pollution
- molecular genetics
main symptoms of lung cancer
- persistent dry cough that doesn’t go away in four weeks
- hemoptysis
