Lung cell biology Flashcards
- How many generations of gas exchange units are there?
23
- What proportion of epithelial cells are goblet cells?
1 goblet for 5 epithelial
- How do goblet cells and mucus change in smokers?
Normally mucus is mucin, serum protein like albumin, antiportases and antioxidands. Normally mucus forms a nice thin sol phase over cell, thick gel at the iar interface
In smokers, goblet cells at least double, secretions sit thicker and increase in quantity-traps cigarette smoke but also microbes for infection
- Describe the structure of the mucus layer that lies on top of the epithelia.
Normally made of mucin, serum proteins, antiproteinases and antixodidants
Forms a thin layer over cells that is thicker at the air interface
- What does mucus contain?
Mucin, serum proteins like albumin or antitrypsin, antiproeases, antioxidants
- What proportion of epithelial cells are ciliated cells
About 80% of epithelial cells are ciliated-with metachronous beating-move mucus towards epiglottis
- How do ciliated cells change in smokers?
Cilliated cells are depleted, move asynchonouslt, sound in bronchioles (reduced airways)-unable to transport all the mucus
- Give two characteristics of small airways.
Small and non cartilaginous. In COPD, airway narrows, enzymes and inflammatory cells reduces gas exchange and can cause collapse
- What are clara cells?
Clara cells -non ciliated epithelia found in large, central and small airwat-increase as you go down
Main role is xenobiotic metabolism through phase 1 enzymes (main role is try to solubilise, often transform precarcinogen to carcinogen) and phase II ebzyme-which aime to transfer the offending agent to excretion
Also antiproteases and lyzyzyme
- How are alveoli different in emphysema?
Holes might appear, and alveoli is larger-reduce the surface area for has exchange-increase dead space
- How do Type I and Type II cells differ in their susceptibility to damage?
Type II cells are more suspltible to damage, but type I are still damaged more often (because more common)
- Describe the role of Type II cells.
Contain lamella bodies that store surfactants-phospholipid rich which prevents alveoli collapse. Also has antiproteases
Type II cells are precurors of the Type I cells, the thing squamous cells that line the airway-type 1 covers 95% of the cell surface
- What is the ratio of Type II to Type I cells?
A 2:1 ratio but type 1 cover 95% of the surface-large and flat
- What do stromal fibroblasts do?
Make ECM as the lung cement, elatic, and can divide to repair
- What do alveolar macrophages do and what proportion of total phagocytic cells in the large/conducting airways are macrophages?
Make up about 70% of lung macrophages-increase 10 times in smokers. Scavenging cells that sit in alveoli and clear debris. Request chemokine aid from neutrophils
Kills debris with proeteinases, but also antixodifants, and can metabolise toxicants
- How do numbers of macrophages and neutrophils change in smokers and during infection?
Normally not too abundant, macro x10 and neutron x10 (normally neurto only 5% of lung phagocytes). Higher prortion of neutron in conducting airways. Can go up ti 70% in smokers. Smokers lung has lots of proteases-too much for the cells to neutralise-damages own cells
- Describe the histopathology of emphysema.
Its center-lobular. Fibroblasts adhacent to epithelial cells repair after infection and T1 cell. Lead to increase to T2 cells and fibroblasts. Large fibrotic regions-irreversible
- Describe normal and abnormal repair.
Normal repair-type 1 deth causes growth factors to increase T2 prolif and replacement
Abnormal(excess breakdown and growth factor)-fibrotic effect which causes fibrotix regions
- Describe the effect of smoking on the proliferation and differentiation of alveolar epithelial cells.
Blocks proliferation of Type 2 cells AND their differentiation into t1
- What do phagocytes produce that increase alveolar inflammation?
Macrophages secrete serine proteinases and mettalloproteases-normally can be counteracted by cells in alveoli but too much produced
- Describe the normal metabolism of procarcinogens and how this changes in smokers.
Normally, procacinogen are 1st made to carcinogens by phase 1, then evacuated by phase 2. As the smoking continues, it overloads and the phase 2 can deactivate-causing only procarcinogen to be converted to carcinogen but not evacuated
