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CardioPulmRenal Final > Pulmonary Defense Mechanisms > Flashcards

Pulmonary Defense Mechanisms Flashcards

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1
Q

How does the gross structure of the airway serve as a mechanical defense?

A

angulation helps particulates settle out

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2
Q

What is the cough reflex?

A
  • a type of mechanical defense
  • sudden release of trapped air at an increased pressure

-triggered by chemicals, mechanical stimulation, inflammation, or can be voluntary

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3
Q

What defense characteristics are present on the surface of airway epithelial cells?

A
  • cilia
  • tight junctions

-adhesion molecules and TLR’s (ICAM-1, VCAM, selectins) that can be upregulated d/t threats

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4
Q

What secretory products do airway epithelial cells use as defense?

A
  • defensins and cathelicidins
  • Surfactants A & D
  • cytokines, chemokines, and leukotrienes
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5
Q

Which immunoglobulin is associated with airway epithelial cells?

A

IgA

-airway epithelial cells translocate IgA

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6
Q

True or False: airway epithelial cells support the microbiome

A

True

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7
Q

What are the two layers of the airway mucus?

A 
sol layer (closest to epithelium)
gel layer (on top of sol layer)
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8
Q

What are the characteristics of the sol layer of mucus?

A
  • thin, aqueous, closest to epithelium
  • produced by serous cells
  • cilia are in this layer
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9
Q

In certain pathologies, the sol layer is less aqueous. How would this affect the pulmonary defense mechanisms?

A

-if the sol layer is less aqueous, the cilia can’t move well

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10
Q

What are the characteristics of the gel layer of mucus?

A
  • on top of the sol layer
  • cilia draws back and strikes the mucus layer
  • mucus moves upward to trigger cough
  • produced by goblet cells
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11
Q

What immune molecules are present in the mucus?

A
  • IgA
  • defensins
  • cathelicidins
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12
Q

What are defensins and cathelicidins?

A

-small, antimicrobial peptides that can also fxn as opsonins

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13
Q

What types of cells form the majority of immune cells in the airway?

A

T-reg cells

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14
Q

What are the main cytokines secreted by immune cells in the airway?

A

IL-10
TGF-beta

(the “shut-it-down-o-kines”)
keep the airway in a state of tolerance

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15
Q

In addition to T-reg cells, what other immune cells are present in the airway?

A
  • dendritic cells
  • interstitial macrophages
  • alveolar macrophages
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16
Q

What are alveolar macrophages?

A
  • mainly an immunosuppressant, Type II macrophage profile, but can respond if threatened
  • tissue-resident, self-renewing
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17
Q

What surfactant proteins are present in the airway?

A

Surfactant Protein A

Surfactant Protein D

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18
Q

What are the characteristics of Surfactant Proteins A & D?

A
  • function as a major opsonin
  • don’t cause inflammation
  • synthesized by Type II pneumocytes and Clara cells
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19
Q

What products are present in the airway that can initiate the complement system?

A
  • IgG

- mannose-binding lectin

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20
Q

What types of immune cells migrate into the airway from the capillaries?

A
  • macrophages

- neutrophils

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21
Q

What do macrophages secrete to aid in pulmonary defense?

A

leukotrienes, that cause mucus hyper secretion

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22
Q

What do neutrophils do to aid in pulmonary defense?

A

-NET deployment and fibrin deposition

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23
Q

What fills the alveolar space during pulmonary defense?

Study These Flashcards
A

protein-rich edema fluid

24
Q

What is the mechanism to slow the rolling of leukocytes during an adaptive immune response in pulmonary defense?

Study These Flashcards
A

IL-1 and TNF increase expression of P & E selectins

25
What signals neutrophils to enter into pulmonary defense?
IL-8
26
What types of cells are the first to respond in adaptive immunity?
neutrophils, they arrive only a few hours
27
When do macrophages respond in adaptive immunity?
a few days later, following CCR2
28
What is the purpose of edema, in regards to the inflammatory exudate?
it brings the plasma proteins into intimate contact w/ the damaged area
29
What is the purpose of the kinin cascade, in reference to its presence in inflammatory exudate?
- vasodilation - increase blood vessel permeability - stimulates pain receptors
30
What is the purpose of fibrinolytic protein, in regards to inflammatory exudate?
-degrades clots when the wound is healed
31
What products and/or processes are present in the airway d/t inflammatory exudate?
- edema - clotting proteins - complement - kinin cascade - fibrinolytic protein
32
What are the consequences of chronic inflammation in the airway if the pulmonary threat isn't cleared?
- infiltration of activated T-cells and M1 macrophages - -macrophages secrete leukotrienes - --mucus hypersecretion -remodeling of tissues leads to fibrosis
33
What happens within the first several minutes of a Type I Hypersensitivity?
- cross-linking of membrane-bound IgE - degranulation of Mast Cells - -IL-4, IL-5, leukotrienes - -sneezing, pruritis, rhinorrhea
34
What is the role of IL-4 secreted by a Mast cell in a Type I hypersensitivity?
recruit Type II helper cells
35
What is the role of IL-5 secreted by a Mast cell in a Type I Hypersensitivity?
recruit eosinophils
36
What is the role of leukotrienes secreted by Mast cells in a Type I Hypersensitivity?
- mucus hypersecretion | - bronchospasms
37
What happens within the first few hours of a Type I Hypersensitivity?
-influx and activations of Type II helper cells, eosinophils, basophils and neutrophils Symptoms: fatigue, myalgias, asthma
38
What are some characteristics of an eosinophil response to a Type I Hypersensitivity?
-eosinophils are pro-inflammatory mediators -eosinophils can cause local tissue damage -eosinophils can cause sinus infections (Chronic Hyperplastic Eosinophilic Sinusitis)
39
What immune molecules are active in chronic asthma-related airway remodeling?
- leukotrienes C4, D4, and E4 | - prostaglandins D2, E2, and F2
40
What are the physical consequences of leukotrienes being active during chronic asthma-related airway remodeling?
- bronchospasms - vascular permeability - mucus hypersecretion
41
What are the physical consequences of prostaglandins being active during chronic asthma-related airway remodeling?
- bronchospasm | - vasodilation
42
In chronic asthma-related airway remodeling, the recruitment of smooth muscle cells and fibroblasts leads to what?
-collagen deposition in the submucosa
43
What is the treatment for chronic asthma-related airway remodeling?
- corticosteroids | - leukotriene antagonists
44
What is the mechanism of disease of COPD?
- epithelial cells secrete IL-8 which recruits neutrophils - neutrophils secrete IL-17 and IL-22 -IL-17 and IL-22 recruit inflammatory macrophages and more neutrophils
45
What triggers asthma versus what triggers COPD?
asthma: allergens COPD: cigarette smoke
46
What types of innate immune cells are responsible for acting in asthma versus in COPD?
asthma: Mast cells COPD: alveolar macrophages
47
What adaptive immune cells are active in asthma versus in COPD?
asthma: CD4 (Th2 cells) COPD: CD8 (Th1 cells)
48
What types of leukocytes are responsible for acting in asthma versus in COPD?
asthma: eosinophils COPD: neutrophils
49
What is the main end action of asthma versus COPD?
asthma: bronchoconstriction COPD: alveolar destruction
50
Are the consequences of asthma reversible or irreversible?
reversible
51
Are the consequences of COPD reversible or irreversible?
irreversible
52
Clinical: Ventilator-Associated Lung Injury
-physical damage: over-inflation, mechanical stress - biodamage: hyperoxygenation leads to free radicals - -influx of neutrophils leads to NET's - --platelet activation and clotting
53
Clinical: Vaping-Associated Lung Injury
- presents w/ acute respiratory distress syndrome - b/l infiltrates on chest x-ray - -but w/o infection - vaping use within the previous 90 days
54
Clinical: Lipoid PNA
- caused by inhalation of lipids (vaping CBD) - -vitamin E acetate (a lipid) - -essential oils (castor oil, mineral oil, etc.) - macrophage + lipid = foam cells
55
What is the treatment for Lipoid PNA?
- supportive care - steroids - antibiotics for secondary complications

CardioPulmRenal Final (13 decks)

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