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CardioPulmRenal Final > Pulmonary Defense Mechanisms > Flashcards

Pulmonary Defense Mechanisms Flashcards

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?

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?

A

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

25
Q

What signals neutrophils to enter into pulmonary defense?

A

IL-8

26
Q

What types of cells are the first to respond in adaptive immunity?

A

neutrophils, they arrive only a few hours

27
Q

When do macrophages respond in adaptive immunity?

A

a few days later, following CCR2

28
Q

What is the purpose of edema, in regards to the inflammatory exudate?

A

it brings the plasma proteins into intimate contact w/ the damaged area

29
Q

What is the purpose of the kinin cascade, in reference to its presence in inflammatory exudate?

A
  • vasodilation
  • increase blood vessel permeability
  • stimulates pain receptors
30
Q

What is the purpose of fibrinolytic protein, in regards to inflammatory exudate?

A

-degrades clots when the wound is healed

31
Q

What products and/or processes are present in the airway d/t inflammatory exudate?

A
  • edema
  • clotting proteins
  • complement
  • kinin cascade
  • fibrinolytic protein
32
Q

What are the consequences of chronic inflammation in the airway if the pulmonary threat isn’t cleared?

A
  • infiltration of activated T-cells and M1 macrophages
  • -macrophages secrete leukotrienes
  • –mucus hypersecretion

-remodeling of tissues leads to fibrosis

33
Q

What happens within the first several minutes of a Type I Hypersensitivity?

A
  • cross-linking of membrane-bound IgE
  • degranulation of Mast Cells
  • -IL-4, IL-5, leukotrienes
  • -sneezing, pruritis, rhinorrhea
34
Q

What is the role of IL-4 secreted by a Mast cell in a Type I hypersensitivity?

A

recruit Type II helper cells

35
Q

What is the role of IL-5 secreted by a Mast cell in a Type I Hypersensitivity?

A

recruit eosinophils

36
Q

What is the role of leukotrienes secreted by Mast cells in a Type I Hypersensitivity?

A
  • mucus hypersecretion

- bronchospasms

37
Q

What happens within the first few hours of a Type I Hypersensitivity?

A

-influx and activations of Type II helper cells, eosinophils, basophils and neutrophils

Symptoms: fatigue, myalgias, asthma

38
Q

What are some characteristics of an eosinophil response to a Type I Hypersensitivity?

A

-eosinophils are pro-inflammatory mediators
-eosinophils can cause local tissue damage
-eosinophils can cause sinus infections
(Chronic Hyperplastic Eosinophilic Sinusitis)

39
Q

What immune molecules are active in chronic asthma-related airway remodeling?

A
  • leukotrienes C4, D4, and E4

- prostaglandins D2, E2, and F2

40
Q

What are the physical consequences of leukotrienes being active during chronic asthma-related airway remodeling?

A
  • bronchospasms
  • vascular permeability
  • mucus hypersecretion
41
Q

What are the physical consequences of prostaglandins being active during chronic asthma-related airway remodeling?

A
  • bronchospasm

- vasodilation

42
Q

In chronic asthma-related airway remodeling, the recruitment of smooth muscle cells and fibroblasts leads to what?

A

-collagen deposition in the submucosa

43
Q

What is the treatment for chronic asthma-related airway remodeling?

A
  • corticosteroids

- leukotriene antagonists

44
Q

What is the mechanism of disease of COPD?

A
  • 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
Q

What triggers asthma versus what triggers COPD?

A

asthma: allergens
COPD: cigarette smoke

46
Q

What types of innate immune cells are responsible for acting in asthma versus in COPD?

A

asthma: Mast cells
COPD: alveolar macrophages

47
Q

What adaptive immune cells are active in asthma versus in COPD?

A

asthma: CD4 (Th2 cells)
COPD: CD8 (Th1 cells)

48
Q

What types of leukocytes are responsible for acting in asthma versus in COPD?

A

asthma: eosinophils
COPD: neutrophils

49
Q

What is the main end action of asthma versus COPD?

A

asthma: bronchoconstriction
COPD: alveolar destruction

50
Q

Are the consequences of asthma reversible or irreversible?

A

reversible

51
Q

Are the consequences of COPD reversible or irreversible?

A

irreversible

52
Q

Clinical: Ventilator-Associated Lung Injury

A

-physical damage: over-inflation, mechanical stress

  • biodamage: hyperoxygenation leads to free radicals
  • -influx of neutrophils leads to NET’s
  • –platelet activation and clotting
53
Q

Clinical: Vaping-Associated Lung Injury

A
  • 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
Q

Clinical: Lipoid PNA

A
  • caused by inhalation of lipids (vaping CBD)
  • -vitamin E acetate (a lipid)
  • -essential oils (castor oil, mineral oil, etc.)
  • macrophage + lipid = foam cells
55
Q

What is the treatment for Lipoid PNA?

A
  • supportive care
  • steroids
  • antibiotics for secondary complications

CardioPulmRenal Final (13 decks)

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