Alveolar gas exchange - Cole, Karius Flashcards

(36 cards)

1
Q

respiratory system consists of three portions:

A
  • an air conducting portion (also conditions inspired air)
  • resp. portion for gas exchange b/w blood and air
  • mechanism of ventilation, controlled by inspiratory and expiratory muscles of the thoracic cage
    • also phonation and olfaction
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2
Q

conducting portion composed of

A
nasal cavity
nasopharynx
larynx
trachea
bronchi, bronchioles and terminal bronchioles
[ In H and N]
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3
Q

respiratory portions extend from

A

respiratory bronchioles to alveoli

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4
Q

Fx of nasal cavity and paranasal sinuses

A

warming and moistening air

filtering dust particles present in inspired air

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5
Q

resp. portion lined by ? and fx?

A

psuedostratified ciliated epithleium w/ goblet cells supported by a lamina propria with seromucous glands (moisturizing secretions) and a rich superficial venous plexus (warms incoming air)

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6
Q

create turbulence to help warm and moisten air

A

superior, middle and inferior conchae

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7
Q

paranasal sinuses are lined by

A

thin pseudostratified columnar ciliated epithelium with few goblet cells

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8
Q

adventitia layer has

A

collagen and elastic fibers

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9
Q

lamina propria contents

A

loose C.T. containing seromucous glands, elastic fibers, bone/ cartilage and sm. m.
–composition changes throughout length!

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10
Q

goblet cells contains and what they produce

A

contain large, light-staining granules
hydrophilic glycoproteins called mucins - hydrated extracellularly to form mucus
[their populaiton tapers off in terminal bronchioles]

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11
Q

3 secretory cell types producing airway mucus

A

1) goblet cells
2) clara cells of the terminal bronchioles
3) serous cells of the submucosal glands

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12
Q

mucus contains [4]

A

1) mucins (>30 diff. types)
2) antimicrobial molecules (defensins, lysozyme and iG A) - mucins bind most bacteria, viruses and inhaled particles
3) immunomodulatory molecules (secretoglobin and cytokines)
4) protective molecules (trfoil proteins-sere barrier function, others heal epithelia- and heregulin)

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13
Q

2 layers of airway mucus

A

1) a periciliary layer
2) a mucos gel layer atop the periciliary layer [polymeric MUC5AC and MUC5B continously made and secreted to replenish as ciliary beat it and its trapped contents upwards]

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14
Q

implicated in bronchial carcinoid tumors, small cell lung carcinoma; serete peptide hormones (serotonin.. somatostatin.. calcitonin.. ADH..)

A
neurendocrine cells (NE, cells of Kulchitsky) 
- NE cells and basal cells rest on basal lamina
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15
Q

benign focal pigmentations of oral mucosa that tend to increase significantly with tobacco consumption

A

Smoker’s melanosis

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16
Q

what is metaplasia and in what pathology does it occur

A
  • change to STRATIFIED SQUAMOUS [better protection]
  • DECREASE in ciliated columnar cells [get decreased movement of mucus]
  • INCREASE in goblet cells [protect against pollutants]
  • congestion of smaller airways
17
Q

Trachea characteristics [3]

A
  • 15-20 C-shaped rings of hyaline cartilage
  • resp. epithelium lines most of tract (pseudostratified columnar epi. w/ goblet)
  • has lamina propria..
18
Q

in trachea, the open posterior portion of the ring is bridged by

A

FIBROELASTIC LIGAMENT - collagen and elastic fibers [prevents overdistension of the lumen]
TRACHEALIS MUSCLE - sm m. results in narrowing during cough reflex [smaller diameter increases velocity of expired air, clears air passage]

19
Q

aggregates of lymphoid tissue in the bronchi are known as

A

BALT

Bronchial-associated lymphoid tissue

20
Q

secondary (lobar) bronchi have wall structure similar to main bronchi except

A

supporting cartilages form irregular plates or islands rather than rings

21
Q
bronchioles; describe their:
epithelium
goblet cells
lamina propria
cartilage and glands
A
  • resp. epithelium that gradually reduces in thickness; becomes simple ciliated columnar
  • lose goblet cells as go further down, replaced by clara cells (less viscous secretion); terminal bronchioles have no goblet cells
  • lamina propria dominatd by spiraling layer of muscularis mucosa in the terminal bronchioles
  • bronchioles don’t have cartilage and glands; only thin layer of adventitia remaining in terminal bronchioles
22
Q

Asthma - mechanism and symptoms

A
  • characterized by reversible bronchoconstriction of sm. m. bundles encircling the bronchiolar lumen
  • mucus hypersecreiton by goblet cells
  • symp: wheezing, cough, dyspnea
23
Q

pulmonary lobule def.

A

a terminal bronchiole and the associated regions of pulmonary tissues that it supplies

24
Q

club/ clara cells description and role

A
  • epithleial cells w/ dome-shaped apical domain lacking cilia
  • found in terminal and resp. bronchioles
  • represent 80% of epithelial cell populaiton there
  • secrete surfactant that differs from that produced by type II alveolar cells
25
club cells protective mechanisms
ALVEOLAR BRONCHIOLIZATION - after airway injury, club cells can prolfierate and migrate to replenish alveolar epithelial cells - engulf airborne toxins and break them down iva cytochrome P-450 enzymes (present in their smooth ER)
26
cystic fibrosis description, mechanism, symptoms
- CF results in production of abnormally thick mucus by glands lining the resp. and gastrointestinal tracts - CFTR gene mutations result in defective Cl- transport and increased Na+ absorption - bacterial infections associated with thick mucus plugs consisting of MUC5AC and MUC5B polymers - symp: cough, purulent secretions, dyspnea
27
respiratory portion epithelium, walls
terminal bronchioles DONT have alveoli - sm. m. fiber bundles form knobs bulging into lumen - the epithelium is cuboidal-to-simple squamous - elastic fibers important in bronchioles and alveolar walls
28
alveoli diameter, separated by?
- thin-walled structures about 0.2mm in diameter - separated by interalveolar septa that consists of two simple squamous epithelial layers with interstitium (nonfenestrated capillaries embedded in an elastic connective tissue) b/w them
29
alveolar epithelial cell Type I
represents 40% of the epithelial cell population; covers 90% of the surface; really the one making up the wall
30
alveolar epithelial cell Type IIl; location?
- 60% of cell population, cover only 10% of the alveolar surface - preferentially located at angles formed by adjacent alveolar septa - produce surfactant!
31
alveolar macrophages (dust cells) function, location, migration
- mononuclear phagocyte - found along alveolar surface, within interstitiutm - detached in alveolar lumen histological sections - remove debris that escapses mucus and cilia in the conducting portion fo the system - migrate to bronchi and transported via ciliary action to pharynx to be swallowed or expectorated
32
why are dust cells called heart failure cells?
- in congestive heart failure, LV fails to keep pace with venous return from lungs - lungs become congested with blood - RBCs pass into alveoli and are phagocytosed
33
emphysema disease mech, biochem behind it
- caused by permanent enlargement of the air spaces distal to the terminal bronchioles due to progressive, irreversible destruction of elastic tissue of the alveolar walls - can be destroyed by elastase released by neutrophils present in alveolar lumen - normally serum a1-antitrypsin (serum trypsin inhibitor) neutralizes elastase - if absent, lose elastin, lung elasticity, get COPD, emphysema - damaged elastic fibers can't recoil when stretched, as a result adjacent alveoli become confluent, produce large air spaces or blebs, the structural landmark of emphysema! - loss of elastic tissue also affects terminal and respiratory bronchioles
34
blood air barrier refers to the structures O2 and CO2 must cross during gas exchange, it contains:
- cytoplasm of squamous eptihelial cells (Type I alvoelar cells/ pneumocytes) - fused basal lamina of type I alveolar cells and capillary endothelial cells - cytoplasm of capillary endothelial
35
Acutre Respiratory Distress Syndrome (ARDS), causes, disease mech, can result in..
- form of pulmonary edema resulting form increased permeability of alveolocapillary membrane - cause can be cardiogenic: increase in hydrostatic pressure in alveolar capillaries - noncardiogenic: damage to alveolar epithelial lining caused by bacterial endotoxins or trauma - fluid accumulates in interstitium, alveolar spaces, small airways, stiffening the lung; impairs ventilation, adequate oxygenation of pulmonary capillary blood - can cause intractable and fatal hypoxemia - if recovered, little permanent damage
36
neonatal respiratory distress sundrome
neonates born without surfactant (before week 24, 25) - alveolar surface tension increases - results in hypoventilaiton causing low oxygen (hypoxemia) and CO2 retention - pulmonary hypoperfusion - endothelial cell damage - ifbrin and other proteins form a hyaline membrane exudate