w6 histology Flashcards
where does the elastin lie
lamina propria
PT presents with crushing’s like symptoms from ectopic ACTH secrection. Where is the likely source?
Tumor can cause crushing’s like symptoms, ACTH secrection in the respiratory epithelium
there is a mutation in the serous secretions of the submucousal glands. What layer is most likely disturbed?
if the patient was not able to create glycoproteins what layer would be distrubed
Sol layer
gel layer
- Gel layer: Mucous layer derived from goblet cells and mucous portion of submucosal glands; Viscous, lubricating properties due to mucins(hydrophilic glycoproteins that are hydrated to form mucus)
- Sol layer: Watery, periciliarylayer derived from serous portion of submucosalglands
a male patient presents to the infertility clinic with infertility issues and has a long history of chronic respiratory infections. what is likely the source of his problem?
Primary ciliary dyskinesia (or Immotile Cilia Syndrome) from a dyein mutation
if the patient also presented with: (1) dextrocardia with or without situsinversus, (2) chronic sinusitis, and (3) bronchiectasis = •Kartagener’ssyndrome:
situs invertus is only some times because the beating of the cillia determines the orientation in embryology
compare and contrast COPD from metaplasia
metaplasia
Goblet cell hyperplasia increased cell number; increased mucous secretions protect surface from physical stress & mucosal irritants
Basal cell hyperplasia indicates stem cell proliferation and differentiation to replace cells that are damaged
Squamous cell metaplasia offers better protection against increased airflow that may be associated with “smoker’s cough”, bronchiectasis
COPD
hypertrophy of glands in trachea and bronchi
goblet cell hyperplasia extending into small bronhioles
where are the stem cells within the lung
basal cells
type II pneumocytes (can diff into type 1 so more plastic)
patient presents with edema contained to the superficial lamina propria, what is this called?
a Cyst or Reinke’s edema
what area of the submucousa is subject to changes with age
the hyaline cartilage in the anterior and lateral edges can essify with age
Posterior wall contains trachealissmooth muscle, fibroelastic ligamentconnecting ends of rings
what is the smooth muscle called in the trachea and in the bronchus
trachealis and muscularis
is this an extrapulmonary or intrapulmonary artery and how do you know
extrapulmonary because it has complete rings of cartilage while intrapulmonary cartilage has discontinous rings
a baby is born with a lung that is not working, what is likely the problem
Congenital neonatal emphysema
Congenital absence of bronchial cartilage formation
air can enter but cannot exit
cartilage rings help prevent collapsing of bronchi during exhalation
differentiate between restrictive and obstructive lung diseases
obstructive–> cant get air out (dysnea and wheezing)
restrictive–> cant get air in
Restrictive lung diseases decrease the lung volume and the compliance
Obstructive lung diseases increase the lung volume and the compliance
patient presents with signs of COPD how can we quickly estimate the pathology
Reid Index to analyze the gland hypertrophy
Ratio of seromucous gland acini to wall from epithelial basement membrane to inner surface the cartilage (A/B);normal value is 0.4; measurements of > 0.55 seen in many patients with chronic bronchitis
what conditions present with wheezing
Asthma, emphysema, and chronic bronchitis (COPD)
where do goblet cells stop
brionchiole, none in terminal bronchiole
what is the source of problems in asthma
bronchioles
Parasympatheticstimulation of muscarinic receptors causes bronchiolar smooth muscle contraction and stimulates submucosal gland secretion
Sympatheticstimulation of β-2 receptors causes bronchiolar smooth muscle relaxation(e.g., during exercise)
patient presents with pneumonia, what was the likely source through which this spread
pores of kohn
These openings serve to equalize pressure and increase collateral ventilation of air. If obstructive disease blocks normal airflow to distal regions, undamaged alveoli aerated by the blockage airway can still communicate, to a limited extent, with the airways of an adjacent lobule or acinus.
A disadvantage is that these small openings can also serve as avenues of dissemination of infections.
what does an oxygen molecule have to diffuse through to get to the blood vessel
Type 1 pneumocyte (occluden junctions- tight junctions), BM (type 4 collagen) and endothelial
what occurs in pulmonary edema
Increase in capillary, hydrostatic pressure or inflammation increases fluid exiting capillaries, exceeds lymphatic drainage capacity tight junctions between pneumocytes initially confine fluid to interstitium, if not resolved fluid eventually seeps into alveolar lumen
what makes up the interalvelar septa
Contained within thick segment connective tissue are reticular fibers (type III collagen) that supports the connective tissue and elastic fibers prividing recoil properties to the interalvelarsepta.
differentiate Centriacinar Emphysema and Panacinar Emphysema
Centriacinar Emphysema is usually confined to an area and is the result of smoking wherare panacinar is usually entire area arising from a1 antitrypsin deficiency. Both have excess elastase degredation
what is an acini
portions of lung consisting of a terminal bronchiole and the respiratory airways it aerates.
outline what happens in emphysema
macrophages –> neurophils –> elastase –> overwhelms the protective effect of a1 antitrypsin and neutralize the basal cells
LOSS OF RECOIL
ØIrreversible distention of respiratory airways (i.e., loss of recoil, elasticity, elastance)
–
what cells produce surfactant
how do you measure it in amnotic fluid
what is the pathogenesis of neonatal respiratory distress syndrome
type II cells and club cells non-ciliated bronchiolar cells
type II cells –> Dipalmitoylphosphotidylcholineaccounts for almost all surface-tension reducing properties of surfactant
a phosphotidylcholine: sphingomyelin ratio lower than 2:1 and the absenceof phosphatidyl glycerol = not developed
•Pathogenesis: lack of surfactant production by type II pneumocytes→ increased surface tension→ collapse of smaller alveoli and dilation of alveolar ducts and respiratory bronchioles → stretch damages the epithelium and vasculature→ deposition of intraluminal fibrin and platelet aggregation (eosinophilic staining = “hyaline membrane”)
