Trachea divides in two-dichrotomous branching. As they branch they get smaller and narrower. Goes from primary bronchi to secondary (lobar), then teriary (segmental). Rigth primary bronchi is wider, shorter and goes down more
Held open by cartilage rings-shaped in C. Trachea, oesophagus, bronchi. C shape allows stretching allowing food to go down. Also slightly offset from one another to allow greater tensile strength (at an angle)
Found underneath the epithelial layer, usually nest within the smooth muscle. Made of a lot of goblet cells nested in a gland. Mucus is there to trap microbes and toxin in airway, and its constantly pushed out by cilae. Nearly 10ml mucus produced per day.
Airway lumen, then epithelial layer of ciliated cells and goblet cells with mucus. Deeper in, you have submucosal glands within a smooth muscle cell layer. Outside of that you get cartilage
Mucin granules come to the apical surface and fuses with it-little pores form allowing water in. This makes mucin expand rapidely, and as pore opens more the mucus pops out-expands hundreds of time witrh water
Linked to epithelia by ciliated duct, then collecting duct. Cells are mixes of functional units (Acinii)-serous and mucous. Serous are peripheral to mucus acini. Produce watery mucus and its flushed through the duct into airway. Also secretes water, lysosymes
9+2 pattern – 9 outside and 2 inside. Ciliae are transmembrane with hooks at the end. The rod turns to move-need lot of energy. About 200 per cell
Metachronal rhythm-one field beats and the next one then catches up, then the next etc. As its slightly delayed, mucus is moved along
NO, CO, Arachnoidic acid metabolites (prostaglandins), chemokines, cytokines, proteases. Role of epithalia, secretion of mucsin, movement of mucus, physical barrier, and those mediators
Epithalia has a lot of NOS and maybe NO-which might have a role in increasing speed of beating
SMC role-structure, tone and secretion
Can secrete medators, cytokines and chemokines. Mostly NOS upregulation
As normal through systemic veins
Returns to blood to both sides of the heart through systemic AND pulmonary veins
One of best perfused tissue-many capillaries. Helps in gas exchange, warming and humidifcation of air
Clears mediators and inhaled drugs, and good supply of Immune cells and protein plasma
In post capillary venules-the endothelial cells can contract-creates gaps and openings, leading to plasma leakage. This is a normal process, and mediated by sensory nerves, histamines and other mediators. In disease like asthma, this can be excessive, producing excess histamine and sensory nerve activatoon
Causes a large increase of plasma exudation-happens in asma
Cholinergic nerves, that go straight to brain stem (afferent and efferent, though vagus). Other controles are refulatory mechanism (histamine, etc), reactive gas species, proteinases
As something large enter the airways, activates sensory pathway of cholinergic nerves, causing cholinergic effect-bronchoconstriction to stop from going in. But we don’t have sympathetic release-rely on adrenaline to relax airway. Also has a neuronal pathway, not sympathetic, which produces NO, relaxing NO
We don’t have sympathetic pathways to relax. Instead rely on adrenaline to relax muscle AND some innervation that produces NO to relax SMC
After sensory nerve activation, vagus nerve to parsympathetic ganglion, then contracts SMC wit Ach, increase mucus secretion (also Ach) and maybe mild vasodilation (muscarinsic)
Asthma, COPD and Cystic Firbosis
Clinical syndrome characterised by increased airway responsiveness to stimuli-but its REVERSIBEL (with adrenaline)-causes dyspnea, wheezing, cough. Constant inflammation causes remodelling. Can get mucus plugs in lumen with a lot of eosinophils, epithelial fragility, ticker Basment membrane, large blood vessels
Mucus plug in lumen, epithelial fragility, thicker Basement membrane, large blood vessels and MASSIVE EOSINOPHIL INFITRATION
Eosinophils