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CPR Final Exam > Pulmonary Defense > Flashcards

Pulmonary Defense Flashcards

1
Q

What are the immune mechanisms for the upper airways and bronchi?

A
  • Generally innate but some adaptive
  • Anatomic barriers
  • Angulation
  • Cough reflex
  • Mucociliary apparatus
  • Airway epithelium
  • Secretory IgA
  • Dendritic cells lymphocytes and neutrophils
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2
Q

What are the immune mechanisms for the alveolar spaces?

A
  • Alveolar macrophages
  • Type I/ II/ III alveoalr cells
  • Club cells
  • Surfactant and opsonins
  • Complement
  • Neutrophils and eosinophils
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3
Q

What is the sequence of events for the cough reflex?

A
  • Deep inspiration
  • Trapping of air by shutting off exit
  • Initiation of expiratory effort raising the intrathoracic pressure
  • Buildup of pressure
  • Sudden release of trapped air at a high pressure
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4
Q

How is the airway epithelium part of defense?

A
  • It acts as a barrier
  • It also releases bacteriostatic molecules
  • Regulates immune response by containing receptors and producing cytokines
  • Supports the microbiome
  • Translocates IgA
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5
Q

What defense molecules does the mucus contain?

A
  • IgA
  • Lysozyme
  • Lactoferrin
  • Peroxidases
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6
Q

Describe the mucus blanket and how cilia relates to it.

A
  • Aqueous Sol layer
  • Mucus layer
  • The cilia move through the sol layer strinking the mucus layer above it and propels it forwards
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7
Q

What conditions can alter the mucociliary clearance?

A
  • Asthma
  • Chronic bronchitis
  • CF
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8
Q
A
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9
Q

In the conducting airway spaces what are the active immune responses?

A
  • Intraepithelial and submucosal lymphocytes
  • DC
  • Cytokines
  • Lots of Treg cells
    • these produce the largest response
    • IL-10 and TGF-B are big players as the environment is immunoregulatory
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10
Q

What is the first line of defense in the alveoli?

A
  • Alveolar macrophages
  • Tissue residents and they are long lilved self renewing cells
  • Generally an M2 response and they help maintain tolerance
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11
Q

What is the primary cell that goes into the alveolar space?

A
  • Primary responder to threats in the alveolus
  • Highly inflammatory but they can get into lumen of airway and deploy NET to trap particles
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12
Q

What are the tissue residents of the alveolar space?

A
  • Alveolar Macrophages
  • They are M2 and secrete IL10 and TGF-B for maintenancec of tolerance in the iar space
  • They can change their phenotype based on TLR binding and change to M1
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13
Q

What are the surfactant proteins and their significance with immuno?

A
  • SP-A and SP-D act as opsonins
  • They bind wide range of pathogens and can suppress microbial growth, as well as damage bacterial membrane and modulate macrophage phagocytosis
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14
Q

What are the immunoglobins found in the alveolar space?

A

IgA and IgG

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15
Q

what are the non immune opsonins found in the alveolar space?

A
  • Surfactant
  • Fibronectin
  • MBL
  • CRP
  • Type II alveolar
  • Microbiome
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16
Q

What does the acute inflammatory response require?

A
  • IL-1 and TNF increase adhesion molecules on endothelium
  • End result is the slowing down of neutrophils which will follow IL8
17
Q

What is in the inflammatory exudate?

A
  • Clotting proteins
  • Complement
  • Kinin cascade
  • fibrinolytic protein
18
Q

Describe the chronic inflammatory response.

A
  • Infiltration of activated T cells and M1
  • Mucus gets hypersecreted
  • Substantial remodeling of tissues occurs leading to fibrosis
19
Q

What happens in the early phase acute atopic response?

A
  • Cross linking of the mIgE
  • Degranulation of mast cells
    • sneezing, pruritis, rinorrhea, congestion
  • Preformed mast cell cytokines and inflammatory proteins recruits inflammatory cells to area
20
Q

Describe the late phase chronic atopic response.

A
  • Influx of eosinophiols, neutrophils, basophils and Th2 cells
  • 10 fold increase in mast cell and increased expression of Fce receptors
  • Eosinophils are proinflammatory mediators causing local tissue damage
21
Q

Describe the cells found in chronic asthma related airway remodeling and what they do.

A
  • Leukotrienes C4, D4 and E4 induce bronchospasm, vascular permeability and mucus production
  • Prostaglandins D2 E2 and F2 induce bronchospasm and vasodilation
  • Recruitment of sm mm cells and fibroblasts occurs leaidng to deposition of collagen in the submucosa
22
Q

What cell type mediates COPD?

A
  • Th17
  • These induce IL-8 secretion from airway epithelial cells
  • Recruitment of large population of inflammatory macrophages and neutrophils into the area
23
Q

What is ventilator associated lung injury?

A
  • Physical damage occurs due to over inflation and mechanical stress
  • As well as biodamage due to hyperoxygenation, free radical prouction, influx of neutrophils into tissue to activate endothelium
    • neutrophil netosis leading to platelet activation and clot formation
24
Q

What is vaping associated lung injury?

A
  • Presents with ARDS
  • Bilateral CXR infiltrates
  • Absence of infection
  • Vaping use within last 90 days
    • NO OTHER POSSIBLE CAUSE FOR DISTRESS
25
Q

What causes lipoid pneumonia?

A
  • Caused by inhalation aspiration of lipids
  • Usually very rare but increased due to vaping CBD THC bc of the vitamin E acetate
  • Essential oils (Chronic)
    • vicks, castor oil, olive oil, minereal oil, petroleum jelly,
    • Tx: supportive care steroids antimicrobials secondary complication

CPR Final Exam (16 decks)

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