Respiratory System Histology Flashcards
what are the two respiratory segments?
types of bronchioles and alveolus
cellular components of respiratory system
-type I pneumocyte
-type II pneumocyte
-surfactant
-alveolar macrophages
what are the two alveolar structures?
interalveolar septa and blood-brain barrier
bronchioles
-first structure in respiratory portion —> directs air movement into alveoli
-clara cells
-smooth muscle cells and elastic fibers- contract and dilate to control airflow
-no cartilage and glands present
what shape are clara cells?
ciliated and non-ciliated columnar and cuboidal
what do clara cells do?
-block and clear debris
-secrete proteins to protect epithelium
-degrade airborne toxins
-regenerate the epithelium
what are the types of bronchioles?
terminal, respiratory, and branching
terminal bronchioles
-most distal conducting airways
-each branches giving rise to two to five respiratory bronchioles
respiratory bronchioles
-initial airways into where gas exchange happens
-presence of alveoli
branching function
-gas exchange
-air velocity
alveoli
-thin-walled sac with type I and type II pneumocytes
-site of gas exchange
-contains elastic and reticular fibers, which provide structural support and allow for expansion/contraction
-opening is sphincter of smooth muscle
-pores of kohn promote collateral circulation and are a route for alveolar macrophages
type I pneumocyte
-facilitates gas exchange between alveoli and capillaries
-thin, squamous cell shape
-covers 97% of lung surfaces, yet only encompasses 10% of total lung cells
type I pneumocyte structural relevance
-type I basal laminae are fused with the laminae of pulmonary capillaries in interalveolar septa
-type I cells join with other cells via tight junctions
-these tight junctions prevent leakage of fluid into alveolar space
type II pneumocyte
-secretes surfactant, a mixture of proteins, phospholipids, and glycosaminoglycans
-also functions as stem cell that differentiates into both type I and II pneumocytes
type II pneumocyte structural relevance
-features numerous membrane-bound multi-lamellar bodies in cytoplasm (responsible making for surfactant)
-found at sites where alveoli walls join
-joined to type I cells by tight junctions and desmosomes
surfactant
-covers the alveolar epithelium
-reduces surface tension in alveoli
-facilitates alveoli expansion during inspiration
-prevents alveolar collapse during expiration
alveolar macrophages
-derived from monocytes of blood
-most numerous cells in lung
-“patrol” air spaces to phagocytose debris and bacteria
-found in the interalveolar septa and on the surface of alveolar lumen
interalveolar septum
-alveolar wall shared by adjacent alveoli
-contains a dense capillary network (pulmonary capillaries)
-perforated by pores of Kohn
what are the 3 components of the interalveolar septum?
epithelium (of adjacent alveoli), interstitium (collagen and elastic fibers), and capillary endothelium
what does the interalveolar septum do?
provides structural basis for gas exchange in the lung
blood-air barrier
-barrier between capillary blood and alveolar air
-specialized region of alveolar wall across which gas exchange occurs —> O2 enters the blood and CO2 enters the alveoli
what is the structure of the blood-air barrier?
trilayered structure:
1. alveolar epithelium (type I pneumocytes) which is a thin layer of surfactant that cover these cells
2. capillary endothelium (endothelial cells)
3. fused basal laminae of these two cells
what do type I pneumocytes do for the blood-air barrier?
form a simple squamous epithelium lining the majority surface area of the alveoli
what do the capillaries provide for the blood-air barrier?
single-layer endothelium
makeup of the blood-air barrier
-cytoplasms of both the type I pneumocytes and endothelial cells are highly attenuated
-the two cell types share a fused basement membrane
-minimize the barrier to increase gas exchange efficiency
air flow in the blood-air barrier
O2 into the alveoli —> cytoplasm of type I pneumocyte —> basement membrane —> cytoplasm of endothelial cells —> reach the blood
CO2 goes the opposite way
functions of the respiratory system
-gas exchange
-regulates blood pH
-sense of smell
-phonation
-air filtration
-excretes water and heat
respiratory and cardiovascular systems
respiratory is involved in gas exchange and cardiovascular is distribution
structural division of the respiratory system
-upper respiratory: nasal cavity, oral cavity, pharynx, epiglottis
-lower respiratory: larynx, esophagus, trachea, primary bronchi, right and left lung
functional division of the respiratory system
-conducting zone: the upper and lower respiratory systems
-respiratory zone: alevolar ducts, alveolar sacs, respiratory bronchiole, atrium, capillary beds, alveoli
visceral pleura
-layer intimately covers the lungs, wrapping every nook and cranny of the lung space
-layers include:
1. mesothelial
2. sub mesothelial
3. external elastic
4. interstitial
5. internal elastic
-secretes pleural fluid
parietal pleura
-layer lines the chest wall and covers the diaphragm and mediastinum
-layers include:
1. mesothelial
2. sub mesothelial
3. fibroadipose
4. interstitial
5. internal elastic
-protective and very fibrous —> provides structure to the lung structure
lung lobule
-fundamental respiratory unit of the lungs
-made up of 10 to 30 acini
-composed of:
1. alveolar ducts
2. alveolar sacs
3. alveoli
-gas exchange
relationship between lung lobule and pleura
-each lobule lies beneath the visceral pleura
-the pleural fluid in the cavity between the visceral and parietal pleura ensures that as each lobule expands and contracts without friction or resistance
layers of trachea and bronchi
-mucosa: innermost layer lined with epithelia cells and contains goblet and basal cells
-submucosa: connective tissue supporting the mucosa
-cartilaginous layer: cartilaginous rings and intervening smooth muscle for structural support
-adventitia: most external fibroelastic layer of connective tissue
what composes the mucosa?
respiratory epithelium and contains goblet cells which produce mucus to keep the airway moist and trap impurities
what does the bronchi have that the trachea does not?
-within the mucosa, the bronchi have the muscularis mucosae that the trachea does not have
-the muscularis mucosae is made up of muscle cells that help expel mucus secretions and facilitates the movement of the mucosa
-helps the bronchi contract and dilate when breathing whereas the trachea needs structural integrity
what does the submucosa do?
-provides hydration
-facilitates nutrient exchange
-allows for elasticity and expansion during breathing
what does the cartilaginous layer do?
made of cartilage rings that provide structural support, ensuring the airways remain open during breathing
what does the adventitia do?
made of connective tissue that anchors the trachea to surrounding structures
epithelia of the trachea
-lined with ciliated pseudostratified epithelial cells
-cilia move in unison to help support mucosal transport towards the pharynx where it can be swallowed and expelled —> necessary mechanism to trap and get rid of dust, microbes, and other particles inhaled with the air
-epithelium also contain goblet and basal cells
what is the primary function of goblet cells?
secrete mucin which form a protective mucus layer lining the epithelium but they are also thought to be involved with immunoregulation
what do basal cells do?
-smaller cells below the layer of pseudostratified epithelial cells —> stem cells that can divide and differentiate into specialized cells
-anchor the basement membrane and replenish the epithelial tissue
epithelia of the bronchi
composed of ciliated pseudostratified epithelial cells, goblet, and basal cells
submucosal glands and ducts (SMG)
-secretory structures found in the submucosa that line cartilaginous airways
-located in the larynx, trachea, and primary bronchi
-tubuloacinar secretory regions joined by ducts
-defend against inhaled and exhaled pathogens
what does the SMG secrete?
a mixture of water, ions, mucus, and antimicrobial proteins that make up the airway surface liquid —> defends against infections and pathogens by physically moving these pathogens out of the lung
what do abnormal SMGS cause?
cystic fibrosis
how do secretions move through the submucosal glands and ducts?
secretions are produced in the secretory region —> move through mucous tubules and accumulate in the non-ciliated collecting ducts —> ciliated ducts connect the SMG to the airway lumen and expel the secretions onto the epithelial surface
cartilage rings
-C shaped rings composed of hyaline cartilage
-located in the trachea
-16-20 C shaped rings that line the entire length of the trachea
-support the trachea and allow it to move and flex without collapsing while breathing
what is at the posterior end of the cartilage rings?
posterior ends of the cartilage rings are connected by smooth muscles —> this is where the esophagus connects
what does the smooth muscle allow the esophagus and trachea to do?
the trachea needs to not collapse and the esophagus need to contract to transport food down —> smooth muscle ensures that both the trachea and esophagus can do their jobs
cartilage plates
-hyaline cartilage structures that are within bronchial walls
-located in the bronchi
-crescent shaped plates or islands
-keep the airway open and the bronchi from collapsing during inhalation and exhalation
segments of bronchi and their cartilage rings
-main primary bronchi is enclosed by cartilage rings
-secondary and segmental bronchi have irregularly arranged crescent-shaped cartilage plates —> numbers will also decrease as e move towards the bronchioles, which lack cartilages and are enclosed by smooth muscles
adventitia
-most superficial layer of the trachea and bronchi
-composed of loose connective tissue
-anchors the trachea and bronchi to adjacent tissues
-provide elasticity, strength, and support
mesothelioma
-simple epithelial cells derived from the mesoderm:
1. serous membranes aka serosa
2. pericardium (heart)
3. pleura (lungs)
4. peritoneum (GI systems)
5. tunica vaginalis (testicles)
malignant mesothelioma
cancerous growth of the mesothelium and 80% of cases is due to asbestos exposure
symptoms and prevalence of malignant mesothelioma
-~4,000 cases/year in the US
-majority of cases are men in their 50-70s
-aggressive cancer, almost always fatal
-even with treatment, the survival is less than 10%
-symptoms are difficulty breathing, painful cough, unintended weight loss
how do the asbestos fibers reach the pleura?
-dominant path is unknown
-inflammation with negative pressure gradient
-macrophage mediated
why does malignant mesothelioma target the parietal pleura?
-pleural fluid is predominantly drained via the lymphatic ducts called stroma on the parietal surface
-stroma are a few microns to 10 microns in diameter
-fibers can become trapped in the stroma
-macrophages can become frustrated and cannot effectively degrade the fibers
overview of malignant mesothelioma
-asbestos fibers are trafficked to pleura (through inflammation + negative pressure gradient or macrophage-mediated)
-asbestos fibers cause frustrated phagocytosis
-mutagenic environment on the parietal mesothelium results in cancerous transformation
chronic bronchitis
-severe, long-term inflammation of the bronchi
-chronic cough for at least three month for two years
-form of COPD
-caused by cigarette smoking or noxious pollutants
symptoms of chronic bronchitis
-coughing and wheezing
-cyanosis (blue color)
-shortness of breath
-lungs appear hyperinflated
how is CB diagnosed?
-in obstructive lung diseases, airflow is limited —> FEV1 falls proportionately faster than FVC so the FEV1/FVC ratio is reduced (less air will get out of your lungs)
-in restrictive lung diseases, FEV1 and FVC are reduced proportionately —> ratio remains normal (less air will get into your lungs)
how do COPD lungs usually appear?
-hyperinflated compared to healthy lungs —> lung tissue is expanded and the lungs appear larger than normal
-this is due to air trapping because the narrowed airways and difficulty exhaling fully
CB pathophysiology
-goblet cell hyperplasia —> excess mucus production —> luminal occlusion
-squamous metaplasia
-cilia are damaged, so the mucus is able to accumulate
-immunosuppression of alveolar macrophages by tobacco smoke (predisposition to lower respiratory tract infection)
squamous metaplasia
-change from pseudostratified ciliated columnar epithelium —> stratified squamous epithelium
-limited window where if the irritants are addressed, the process can be reversed but the cells would go to an intermediate shape and not fully back to the columnar shape
-if not addressed, could lead to a larger neoplastic transformation
goblet cell hyperplasia
-proliferation of goblet cells
-leads to increased production of mucus, which can narrow the airways
treatment for CB
-damage is irreversible —> treatment goals are to stop progression and manage symptoms
-stop smoking
-bronchodilators to relax the muscles in the airways and allow air to flow
-inhaled steriods that can be taken with bronchodilators to reduce inflammation
-supplemental O2 if the O2 levels are consistently low
respiratory distress syndrome (RDS)
-caused by lack of surfactant in premature infant lungs —> leads to alveoli collapse
-also called hyaline membrane disease since the cell debris accumulates in the airways
-60-80% of infants born before 28 weeks have this but 90% survive and the prevalence decreases with gestational age
RDS symptoms
-difficulty breathing
-cyanosis
-rib muscles pulling inwards on inhale
-CO2 —> acidosis —> organ disfunction
RDS physiology
-type II pneumocytes secrete surfactant starting around 28 weeks
-premature infants born before type II pneumocytes are fully develops lack surfactant and have difficulty breathing
-surfactants are amphiphilic so they have both hydrophilic and hydrophobic parts —> when they come into contact with a liquid, the hydrophilic part attaches to the water molecules while the hydrophobic part attaches to the air or oil
RDS treatment
-continuous positive airway pressure (CPAP), which pushes air into the lungs to inflate the alveoli
-surfactant replacement through an endotracheal tube
-mechanical ventilation but only in severe cases and can cause airway/lung injury
-glucocortcoids can be given to women before premature delivery to speed up the development of the lungs and surfactant production
acute respiratory distress syndrome (ARDS)
-inflammation in the lungs due to COVID-19, sepsis, flu
-pneumocytes are the inflammatory cytokines and neutrophils are the proteases, reactive oxygen species
-injury to alveolar-capillary membrane, which makes it more permeable —> leading to pulmonary edema which washes away surfactant and leads to alveoli collapse
