Respiratory System- Burns; from GH, new BC, and notes-JS


2 parts:  conducting portion (gets air in and out) and respiratory portion (gas passing)

Conducting portion:  no gas exchange; nasal cavity, nasopharynx, larynx, trachea,

intrapulmonary bronchii, and conducting bronchii conduct air to and fro alveoli

            -Nasopharynx- wear and tear area is covered by stratified squamous epi (wet), or

             oral epi, not respiratory (pseudostratified).  Inspired air is moistened by watery

             secretions of nasopharynx and warmed by blood vessels; covered by olfactory

epithelium, which has nerves passing through it with axons extending towards    brain and dendrites towards surface w/olfactory cilia (good picture on GH 347)

-Larynx- voicebox, responsible for phonation and prevents food/liquid from entering trachea, supported by hyaline and elastic cartilages.  Covered by anterior extention (the epiglottis) when we swallow, snaps back out.  Tip of epiglottis is covered by oral epi, called digestive part; lower part called respiratory part, covered by respiratory epi; larynx’s respiratory epi’s cilia beats towards pharynx 

            -vocal cords- 2 folds of laryngeal mucosa, superior pair of folds is false

             vocal cords (no role in phonation, respiratory epi), inferior pair of folds

             are true vocal cords (produce sound when air passes over them, stratified

             squamous WET epi, which is located at areas of wear and tear in body, no        glands, skeletal muscle in here to assist phonation)

-Trachea- C shaped hyaline cartilage around (cart also on bronchii), lined by resp. epithelium (contains pseudostratified ciliated columnar epi, composed of 30% goblets, 30% ciliated cells, 30% basal cells, and rest composed of brush cells, serous cells, and DNES cells.

            -goblets- secrete mucous, trap junk in resp. tract

            -ciliated cells- move mucous towards pharynx from below and naso above

            -basal cells- at basal lamina, replace cells above when sloughed; stems

            -serous cells- have microvilli, secrete serous fluid, 3%

            -DNES cells- release chemicals that affect other cells in resp. epi, 3%

            -brush cells- small granule mucous cells, tall microvilli apically, 3%

            -trachea’s layers include, from lumen in: respiratory epi, basement

             membrane, lamina propria, elastic lamina, submucosa layer (seromucosal

             glands in here), perichondrium, hyaline cart, perichondrium.

            -C shaped cart opens posteriorly, toward esophagus, opening bridged by

             trachealis muscle

-Intrapulmonary bronchii- divides off of trachea (primary bronchii: right is shorter and straighter, aspirated stuff goes in this one mainly), bronchii divide many times, cart. breaks up along the way and resp. epi diminishes as it goes on (bronchial tree does a strip tease- loses cartilage and epi. thickness as it moves on)

-Conducting bronchioles- no cartilage, has smooth muscle that determines thickness of bronchioles (affected in asthma), relaxes w/epinephrine.  Goblet cells disappear as they get smaller, epithelium transitions from pseudostratifiedàcilia

columnaràciliated cuboidalànonciliated cuboidal.  Always branches of pulm. artery running with bronchioles; contains Clara cells as ciliated cells decrease which secrete lipoprotein that prevents collapse of terminal bronchioles as exhale

-Terminal bronchioles- distal most part of conducting tree, no goblets, some ciliated cuboidals, terminate when alveoli seen at border of bronchiole, then called respiratory bronchioles


***Smoking causes changes in respiratory epithelium:  PseudostratifiedàWet stratified

            squamous epi (metaplasia)àugly wet stratified squamous (atypical size, shape,

            organization; dysplasia)àreal ugly (cancer; anaplasia)àinvasive carcinoma…

            bottom line, don’t smoke.


Respiratory portion:  respiratory bronchioles are first in line upàalveolar ductsà

            alveolar sacsàalveoliàgas exchange w/RBC’s through alveolar walls

            -resp. bronchioles- continuation of terminal bronchioles

            -alveolar ducts- no walls of their own, just pass b/w alveolar sacs

            -alveolar sacs- clusters of alveoli in region, separate from each other by septa

            -alveoli- small air sacs that “pass gas”, separated by interalveolar septa (CT,

             contain capillaries)

            -alveolar walls- lined by epi that contain 2 types of pneumocytes, type I and II

-type I pneumocytes- 95% of alveolar surface, simple squamous, tight junctions b/w them, macros go in and out through these, “cleaning crew of macrophages,” this is the only place where macrophages can “crawl” up and down the epi

                        -type II pneumocytes (great alveolar cells)- bulge out into lumen, 5% of

the alveolar surface, secrete surfactant (or tubular myelin) that reduces surface tension in alveoli, can divide and replace type I’s; low type II-RDS

                                    ***no surfactant = RDS in infants, often in premature infants

            -pulmonary emphysema- hyperinflation, leads to decrease in vital capacity and

            increase in total lung capacity.  Have decrease in elasticity of alveolar wallsà

            ruptures.  Either from smoking or lacking antitrypsin with protects elastic fibers

            from degredation.

            -gaseous exhange:  know and understand this flow pattern: 

                        SurfactantàType I pneumocyteàBasal lamina of type I pneumocyte

                        àBasal lamina of capillary endothelial cellàEndothelial cellàBlood

                        plasmaàPlasmalemma of RBC

            -alveolar macrophages (dust cells)- from monocytes, wonder over to alveolar

            septa and look for things to eat

                        -pneumoconiosis- any disease caused by accumulation of airborne,

                        non-degradable particles in lungs, macro’s lack crapase and crudase!

1.      anthracosis- coal miner’s lung, emphysema and pulm fibrosis


2.      silicosis- deposition of silica dust, leads to pulm. edema, alveolar damage, and massive fibrosis

3.      asbestosis- cancers from deposition of asbestos fibers

-heart failure cells- macrophages eat RBC’s b/c right side of heart not

pumping hard, RBC’s get out, macros eat, hemosiderin is breakdown prod of hemoglobin, look brownish

            -visceral pleura- mesothelium encloses pleual cavity, rubs against parietal pleura