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Histology - Respiration Part 2

Anatomy and Physiology22 CardsCreated about 1 month ago

This deck covers key concepts related to respiratory histology, including developmental periods, cell types, and common malformations.

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most common Tracheoesophageal malformation

Esophageal atresia with Tracheoesophageal fistula (TEF)
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Key Terms

Term
Definition
most common Tracheoesophageal malformation
Esophageal atresia with Tracheoesophageal fistula (TEF)
Canalicular period
16 weeks = 26-28 weeks
Surfactant production begins at
20 weeks
Terminal sac period
(26-28 weeks – birth) Capillaries now associated with primitive alveoli, blood-air barrier established.
Alveolar period
More primitive alveoli develop & mature into adult alveoli. Lung takes on open, “lacy” appearance .At end of 300 million alveoli present
Trends in Respiration from Upper to Lower Tracts
Lower portions of the respiratory tract show progressive loss of the various components characteristic of the trachea; that is, less and less cartilag...
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Histology - Respiration Part 2
TermDefinition
most common Tracheoesophageal malformation
Esophageal atresia with Tracheoesophageal fistula (TEF)
Canalicular period
16 weeks = 26-28 weeks
Surfactant production begins at
20 weeks
Terminal sac period
(26-28 weeks – birth) Capillaries now associated with primitive alveoli, blood-air barrier established.
Alveolar period
More primitive alveoli develop & mature into adult alveoli. Lung takes on open, “lacy” appearance .At end of 300 million alveoli present
Trends in Respiration from Upper to Lower Tracts
Lower portions of the respiratory tract show progressive loss of the various components characteristic of the trachea; that is, less and less cartilage, progressively lower epithelium, gradual loss of goblet cells, and finally loss of cilia and smooth muscle.
Where do Clara cells begin? Where do they end?
BEGIN: Primary bronchioles; END: Alveolar ducts
Separates the trachea (anterior) from the esophagus (posterior). Formed by fusion of two longitudinally-oriented ridges (or folds).
Tracheoesophageal septum
Type I cells
(97% of alveolar surfaces) line the alveoli. Squamous; thin for optimal gas diffusion.
Type II cells
(3%) secrete pulmonary surfactant (dipalmitoyl phosphatidylcholine), which increases the alveolar surface tension. Cuboidal and clustered. Also serve as precursors to type I cells and other type II cells. Type II cells proliferate during lung damage.
Airway Submucosa Components
Loose Commective Tissue (Elastic fibers, larger blood & lymphatic vessels.); Smooth muscle or Glands
Most common tracheoesophogeal abnormality (90%) VACTERL association.
Esophageal atresia with ; Tracheoesophageal fistula (TEF)
VACTERL
Vertebral defects; Anal atresia; Cardiac defects; TEF; Esophageal atresia; Renal defects; Limb defects
Ends 16 weeks = 4 months; Terminal bronchioles (cuboidal epithelium); Capillaries present (not associated); No respiratory bronchi or alveoli
Pseudoglandular period
Canalicular period
16 weeks = 26-28 weeks; Terminal bronchioles (cuboidal epi.); Respiratory bronchioles (cuboidal epi.); Capillaries present (not associated); No alveoli
Terminal sac period
26-28 weeks – birth; Blood-Air-Barrier established.; Terminal sacs or Primitive alveoli lined by simple squamous cells.; Capillaries now associated with primitive alveoli; Surfactant secretion greatly increases
Alveolar period
Birth - 8 - 10 years More primitive alveoli develop & mature into adult alveoli; Lung takes on open, “lacy” appearance.; At end of alveolar period: 300 million alveoli present
Visceral Pleura Origin
Sphlanic Mesoderm
Parietal Pleura Origin
Somatic Mesoderm
Large Cell Undifferentiated Carcinoma
Mutations in stem cells of the epithelium due to persistent exposure to carcinogens (smoking)
Small Cell Carcinoma
Mutations in epithelial neuroendocrine cells from persistent exposure
Mutations of ciliated cells and mucous cells can cause…
Adenocarcinoma