Histo block I: resp sys- alveoli Flashcards

1
Q

what are alveolar ducts and their epithelium?

A

are linear arrangement of alveoli with “knobs” of smooth muscle and simple cuboidal epithelium present between alveoli

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2
Q

what are alveolar sacs?

A

clusters of alveoli at the end of alveolar ducts

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3
Q

what are alveolar pores of Kohn?

A

openings between adjacent alveoli

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4
Q

which are the sites of gas exchange ?

A

Alveolus (Alveoli is plural)

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5
Q

alveolus constitutes for how many structural units?

A

The terminal air spaces, primary structural and functional units (150-250 million per adult /lung).

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6
Q

what is the interstitium?

A

in the alveolus; interalveolar septum abundant continuous capillaries.

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7
Q

The alveolar epithelium is composed of:

A
  1. Type I pneumocytes or alveolar cells (40%)
  2. Type II pneumocyte or alveolar cell (also called septal cell) (60%)
  3. Brush cells
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8
Q

describe the Type I pneumocytes or alveolar cells and function

A

Extremely thin squamous cells with many
occluding junctions. Line most (95%) of
surface area. Gases diffuse through the cell.

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9
Q

describe Type II pneumocyte or alveolar cells also called septal cell and function

A

Are secretory cells.
Cover only 5% of surface area.
Cuboidal cells at septal junctions.
Secrete surfactant from lamellar bodies (decreases surface tension).
Four types of surfactant proteins and phospholipids

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10
Q

which are the progenitor cells for type I alveolar cells?

A

Type II alveolar cells

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11
Q

function of brush cells in alveolus

A

(very few) They may serve as receptors that monitor air quality in the lung.

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12
Q

identify

A

alveolus

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13
Q

which is the most important lipidic component of the surfactant?

A

Dipalmitoylphosphatidylcholine (DPPC)

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14
Q

WHich surfactant proteins are present and their function

A

(SP- A,B,C,D); organize surfactant secreated and immunologic function to attack microorganisms in that region

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15
Q

what is the function of surfactant?

A

decreases the alveolar surface tension and actively participates in the clearance of foreign materials.

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16
Q

identify

A

type II pneumocyte alveolar cell with lamellar bodies

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17
Q

identify

A

SC= septal cells = Type II alveolar = Type II pneumocyte

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18
Q

where does the actual site of gas exchange occur?

A

In the blood-air barrier present in the alveolar septum

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19
Q

the blood-air barrier is made of?

A

Is made of thin layer of surfactant, type I pneumocyte and basal lamina and endothelium of capillaries and basal lamina.

20
Q

what are the regions of the blood-air barrier?

A
  1. thin
  2. thick
21
Q

describe the thin region of the blood-air barrier

A

thin layer of surfactant, type I pneumocyte and basal lamina and endothelium of capillaries and 2 basal lamina fused; passive difussion gases

22
Q

describe the thick region of the blood-air barrier

A

some connective tissue (CT) between basal lamina, site of fluid transfer. Lymphatic vessels in the CT of the terminal bronchioles drain fluid that accumulates in the thick portion of the septum

23
Q

identify

A

Electron micrograph of the interalveolar septum

24
Q

Describe the alveolar macrophage and where is it found

A

Part of the mononuclear phagocytotic system. Can be found in the septum and in the lumen of the alveolus

25
Q

What are the functions of the alveolar macrophage or dust cell?

A


Phagocytize particles. In congestive heart failure phagocytize RBC, sometimes called congestive heart failure cells. Swept to pharynx and swallowed along with mucous

Alveolar macrophages also phagocytose infectious organisms such as Mycobacterium tuberculosis. These bacilli are not digested by macrophages; conditions that damage alveolar macrophages can cause release of the bacteria and recurrent tuberculosis.

Recent evidence suggests that apoptosis of septal macrophages contributes to the development of emphysema

26
Q

macrophages migrate to where?

A

back to the alveolar septa where they remain through life

27
Q

presence of lymphocytes indicates?

A

inflammatory response

28
Q

Septal macrophages are loaded with _______ __________ _________

A

black cytoplasmic inclusions

29
Q

hemosiderin comes from?

A

phagocytosed red blood cells

30
Q

innervation to the airways and blood vessels (smooth muscle_ are:

A
  1. sympathetic
  2. parasypathetic
31
Q

how is the blood supply of the respiratory system?

A

 Pulmonary arteries (gas exchange)
 Bronchial arteries (nutrients to parenchyma of lung)

32
Q

what is the pleura?

A

visceral and parietal mesothelium and connective tissue

33
Q

describe lymphatics of the respiratory system

A

Dual systems parallel blood vessels
Extensive in pleura and lungs
(particularly at time of birth)

34
Q

explain cystic fibrosis

A

Cystic fibrosis (CF, mucoviscidosis) It is an autosomal recessive disorder caused by a mutation in a gene called thecystic fibrosis transmembrane conductance regulator (CFTR)located on chromosome 7.
*
The product of this gene, theCl−channel protein, is involved in final alteration of mucus.
*
All mutations of CFTR gene result in abnormal epithelial transport of Cl−that affects the viscosity of the secretion of the exocrine glands.
*
Individuals with cystic fibrosis have frequent respiratory tract infections.
*
Gene therapy treatment: recently a type of virus called a lentivirus, has been used to deliver a healthy copy of a gene called CFTR

35
Q

what is Chronic obstructive pulmonary disease (COPD)?

A

pulmonary condition characterized by chronic obstruction of airflow

36
Q

What are the subtypes of COPD and causes

A

Subtypes of COPD include: chronic bronchitis, chronic obstructive asthma, and emphysema. The destruction of the alveolar wall may be associated with excess lysis of elastin and other structural proteins in the interalveolar septa.

37
Q

explain emphysema

A

Elastase and other proteases are derived from lung neutrophils, macrophages, and monocytes. A specific genetic disease, α1-antitrypsin deficiency, causes a particularly severe form of emphysema. Its severity can be reduced by supplying the enzyme inhibitor exogenously

38
Q

explain pneumonia

A

Pneumonia is a generic term that describes inflammation of the lung. It is often caused by viruses and bacteria. Some drugs (immunosuppressive agents) and autoimmune diseases increase the risk of certain types of pneumonia
*
In the earliest stage of bacterial pneumonia, protein-rich fluid containing numerous microorganisms fills the lung alveoli. Marked enlargement of the capillaries surrounding the alveoli is followed by a massive migration of neutrophils and erythrocytes into the alveolar air space.
*
In the later stage, macrophages phagocytose the fragmented neutrophils and other cellular and tissue debris; the alveolar exudate is then removed, the alveolar spaces gradually become refilled with air, and the lungs return to their normal function.

39
Q

identify

A

Emphysema is a condition of the lung characterized by permanent enlargement of the air spaces distal to the terminal bronchiole. The changes in the lung parenchyma are accompanied by thickening of the wall of the pulmonary vessels (arrows) and the presence of numerous cells within the air spaces. It is characterized by exhalation being twice as long as inhalation

40
Q

identify

A

Pneumonia image of the lung of an individual in the early stages of acute pneumonia (inflammation of the lung). The air spaces are filled with exudate containing white blood cells (mainly neutrophils), red blood cells, and fibrin.

41
Q

when does surfactant synthesis occur in fetuses?

A

The surfactant produced by type II alveolar cells reduces the surface tension. Surfactant synthesis in the fetus occurs after the 35th week of gestation and is modulated by a variety of hormones, including cortisol, insulin, prolactin, and thyroxine. Without adequate secretion of surfactant, the alveoli would collapse on each successive exhalation.

42
Q

Which is the most critical agent for air space stability?

A

a specific phospholipid called dipalmitoylphosphatidylcholine (DPPC), which accounts for almost all surface tension–reducing properties of surfactant.

43
Q

what happens to preterm infants?

A

there is not enough surfactant production and neonatal respiratory distress syndrome (RDS) can occur. It is also know as Hyaline Membrane Disease. Administration of exogenous surfactant at birth to preterm infants reduces the incidence of RDS.

44
Q

what can decrease neonatal mortality?

A

antenatal administration of corticosteroids (glucocorticoids) to women with threatened preterm delivery

45
Q

identify

A

Respiratory Distress Syndrome = Hyaline Membrane Disease