Chapter 13: the lung
Normal anatomy/physiology:
Due to diffusion, O2 and CO2 are exchanged. Right lung has 3 lobes, left lung 2 lobes. Multiple types
of examination. Around the trachea there is cartilages. In the connective tissue are glands to
produce mucous. The epithelium contains cilia, make tapis roulant movement towards the mouth
and nose. Cilia not working well: in Kartagener syndrome (do not function), smoking (damage the
cilia, prevent good movement).
Type II pneumocytes and Clara cells produce surfactant to prevent collapse of the alveoli.
Atelectasis = collapse of lung, which afterwards is filled with fluid.
Diffuse alveolar damage (DAD) = respiratory distress syndrome. Can result in hypoxemia, become
blue (cyanosis), pulmonary oedema (too much fluid), rapid multi organ failure.
Obstructive lung disease:
Chronic injury (smoking for example). Small airway diseases are emphysema, chronic bronchitis.
Hyperresponsiveness is asthma.
Emphysema = damage to alveoli, surface to exchange gasses is smaller. Septum is gone.
Restrictive lung disease:
Interstitial lung disease = can be dust induced (asbestosis). Can result in silicones (no more fluffiness
of the lung). Septum of the alveoli are fibrosing.
Vascular disease:
Saddle pulmonary embolism = truncus pulmonarias. If circulation stops > death.
Thromboembolism = take the form of the vein because it forms there.
Lung infections:
Caused by the airways. Lobar pneumonia (one lobe inflamed). Treated by antibiotics. Alveoli evoke
inflammatory response. There are 4 stages. COVID-19 autopsy shows severe damage when it
resulted in rapid death.
Tuberculosis = infection by mycobacteria. Result in granuloma (a lot of macrophages) which
necrotize.
Lung tumors:
Smoking is the biggest reason for lung cancer. Adenocarcinoma and squamous most frequent.
Adenocarcinoma; 5 types. Lepidic, papilla, acinar, micropapillary and solid.
Squamous cell carcinoma = strong associated with smoking. Mostly in the middle part of the lung.
Small cell cancer develops from neuro-endocrine cells. High associated with smoking. SCLC is
resistant over time to chemotherapy.
Immunotherapy:
Mutation in EGFR gene in tumors, which correlate with the clinical responsiveness to the tyrosine
kinase inhibitor. These mutations lead to increased growth factor signalling. Screening for this
mutation will lead to patients that response to gefitinib.
Mutational load = lung cancer and skin cancer have high mutational load because of UV light and
cigarette smoke.
Checkpoint inhibitor: PDL1 expression on tumor cells is used by tumor cells to inhibit T-cell
activation. Make antibody on PDL receptor, so that PDL1 cannot bind and T cell can be activated.
Normal anatomy/physiology:
Due to diffusion, O2 and CO2 are exchanged. Right lung has 3 lobes, left lung 2 lobes. Multiple types
of examination. Around the trachea there is cartilages. In the connective tissue are glands to
produce mucous. The epithelium contains cilia, make tapis roulant movement towards the mouth
and nose. Cilia not working well: in Kartagener syndrome (do not function), smoking (damage the
cilia, prevent good movement).
Type II pneumocytes and Clara cells produce surfactant to prevent collapse of the alveoli.
Atelectasis = collapse of lung, which afterwards is filled with fluid.
Diffuse alveolar damage (DAD) = respiratory distress syndrome. Can result in hypoxemia, become
blue (cyanosis), pulmonary oedema (too much fluid), rapid multi organ failure.
Obstructive lung disease:
Chronic injury (smoking for example). Small airway diseases are emphysema, chronic bronchitis.
Hyperresponsiveness is asthma.
Emphysema = damage to alveoli, surface to exchange gasses is smaller. Septum is gone.
Restrictive lung disease:
Interstitial lung disease = can be dust induced (asbestosis). Can result in silicones (no more fluffiness
of the lung). Septum of the alveoli are fibrosing.
Vascular disease:
Saddle pulmonary embolism = truncus pulmonarias. If circulation stops > death.
Thromboembolism = take the form of the vein because it forms there.
Lung infections:
Caused by the airways. Lobar pneumonia (one lobe inflamed). Treated by antibiotics. Alveoli evoke
inflammatory response. There are 4 stages. COVID-19 autopsy shows severe damage when it
resulted in rapid death.
Tuberculosis = infection by mycobacteria. Result in granuloma (a lot of macrophages) which
necrotize.
Lung tumors:
Smoking is the biggest reason for lung cancer. Adenocarcinoma and squamous most frequent.
Adenocarcinoma; 5 types. Lepidic, papilla, acinar, micropapillary and solid.
Squamous cell carcinoma = strong associated with smoking. Mostly in the middle part of the lung.
Small cell cancer develops from neuro-endocrine cells. High associated with smoking. SCLC is
resistant over time to chemotherapy.
Immunotherapy:
Mutation in EGFR gene in tumors, which correlate with the clinical responsiveness to the tyrosine
kinase inhibitor. These mutations lead to increased growth factor signalling. Screening for this
mutation will lead to patients that response to gefitinib.
Mutational load = lung cancer and skin cancer have high mutational load because of UV light and
cigarette smoke.
Checkpoint inhibitor: PDL1 expression on tumor cells is used by tumor cells to inhibit T-cell
activation. Make antibody on PDL receptor, so that PDL1 cannot bind and T cell can be activated.
