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CPR Exam 2 > 6. Pulmonary Defense Mechanisms > Flashcards

6. Pulmonary Defense Mechanisms Flashcards

1
Q

lung defense can be divided into –

A

2 locations

upper airway/bronchi & alevolar spaces

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2
Q

what defense mechanisms take place in the upper airway & bronchi

A

anatomic barriers

angulation

cough reflex

mucociliary apparatus

airway epithelium

secretory IgA

dendritic cells, lymphocytes and neutrophils

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3
Q

what defense mechanisms take place in alveolar spaces

A

alveolar macrophages

type II alveolar cell

surfactant & opsonins

complement

neutrophils & eosinophils

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4
Q

what assists in removal of particulate matter in the resp system

A

mucus in nose, orpharynx all the way down to bronchi - trap particles

branching of bronchi up prevents particle from getting to ends

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5
Q

what are the sequence of events that lead up to the cough reflex

A
  1. deep inspiration
  2. trapping of air by shutting off its exits (glottis in the case of cough)
  3. initiation of expiratory effort, raising the intrathoracic P
  4. build up P
  5. sudden release of trapped air at high P
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6
Q

what can trigger a cough

A

chemicals

mechanical stimulation

inflammation

voluntary

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7
Q

what are the physical barriers present in the airway epithelium

A

cilia/mucociliary escalator

tight jxns

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8
Q

what membrane receptors are found in airway epithelium

A

adhesion molecules (ICAM-1)

preotease receptors

Toll-like receptors - response to outside threats and secrete beta-defensins

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9
Q

what antimicrobial substances are present in the airway epithelium

A

beta-defensins

phospholipase A2

SPA & SPD - surfactant

cationic peptides

ROS & RNS

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10
Q

what inflammatory mediators are present in airway epithelium

A

cytokines, chemokines, leukotrienes, ROS & RNS

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11
Q

what translocates IgA

A

airway epithelium

-translocate from plasma cell –> across cell –> into airway lumen w/o degradation

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12
Q

what defense molecules does mucus contain

A

IgA

lysozome

lactoferrin

peroxidases

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13
Q

what are the layers of the mucus blanket

A

sol layer (aq)

(inbtn = cilia)

mucus layer

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14
Q

what is the mucus elevator

A

cilia moving thru sol layer striking mucus layer above and then propel it forward

-move mucus up to trigger cough reflex

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15
Q

what can alter mucociliary clearance

A

asthma, chronic bronchitis, CF

-sol layer becomes less aq & cilia cant move as well so they get stuck in mucus

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16
Q

what is the fxn of the Treg cells

A

make IL-10 & TGF-beta

keep at immunosuppressive state

17
Q

what is the fxn of dendritic cells in the airway

A

extend processes thru tight jxn to sample lumen

present sample to interstial macrophages - make IL-10, TGF-beta & IL-27

18
Q

what are alveolar (airway) macrophages

A

first line of defence in alveoli

tissue residents - long lived & self renewing

  • plasticity of responses - generally an M2 profile & maintain tolerance
  • secrete IL-10 & TGF-beta
19
Q

what are SPA & SPD

A

surfactants

  • synthesized by type II alveolar cells & Clara cells
  • bind pathogens, supress microbial growth, damage bacterial membranes & modulate macrophage phagocytosis

=major opsonin

20
Q

what are other defense mechanisms of alveolar space

A

IgA (noninflam- no complement receptor) & IgG (cause inflam)

type II alveolar cells make nonimmune opsonins: surfactant, fibronectin, MBL & C-reactive protein

microbiome

21
Q

how is tolerance maintained in the airway

A

alv macrophages provide cytokines

-retnoic acid helps to make/support FOXP3 Treg cells

surfactant

interstitial space immune cells that respond to threat if triggered

22
Q

what is the acute immune response

A

activation of immune response by exogenous trigger

influx of inflam cells (neutrophils & macrophages) from caps into air space

deployment of neutrophil nets

23
Q

how are leukocytes recruited

A
  1. activte endothelium by cytokines (which are secreted by resident macrophages & mast cells in periphery)
  2. acute phase cytokines - IL1, IL6 & TNF upregulated adhesion molecules (P & E selectins)
  3. leukocytes bind and slow down
  4. chemokines increase affinity & clustering of integrins
  5. leukocytes firmly attach, cytoskeleton reorganize & endothelium flattens
24
Q

Neutrophils and macrophages arrive at different times and respond via different mechanisms- what are they?

A

neutrophils - hrs –> IL8L receptor on neutrophil responds to IL* & use ICAM1 to go thru membrane

macrophages - days –> CCL2 receptor on macrophage responds to CCR2 & enters via VCAM1

25
Q

what proteins are included in inflammatory exudate

A

clotting proteins - blood clot

complement - destroy bacteria

kinin cascade - vasodilate, increase permability & stimulate pain receptors

fibrinolytic- degrade clot when healed

26
Q

what happens during chronic inflammatory response

A

increased expression of chemotactic factors –> increase modulatory proteins & lipids (inflitration of activated T cells & M1 macrophages) –>

mucus hypersecretion

emphysema

27
Q

what happens during the early phase acute atopic response

A

w/i mins:

  1. cross-linking of mIgE
  2. degranulation of Mast cells
  3. sneezing, pruritis, rhinorrhea, congestion
  4. preformed mast cells (IL4 - recruite & sustain type 2 T helpers & IL5 - eosinophils and chemotatic proteins)
28
Q

what occurs during the late phase chronic atopic response

A

4-12 hours

  • influx & activation of eosinophils, neutrophils, basophils and lymphocytes (Th2)
  • increase Mast cells & expression of Fc-epsilon receptors
  • systemic symptoms: fatigue, myalgias, asthma
29
Q

what is the fxn of eosinophils

A

proinflam mediators

local tissue damage, sinus infection

chronic hyperplastic eosinophilic sinusitis (CHES)

30
Q

what do leukotrienes C4, D4 & E4 do

A

induce bronchospasm, vascular permeability & mucus production

31
Q

what do prostaglandins D2, E2 & F2 do

A

induce bronchospasm and vasodilation

32
Q

what leads to deposition of collagen in sub mucosa during chronic asthma related remodeling

A

recruitment of Sm M cells and fibroblasts

33
Q

what is the treatment for bronchial asthma

A

corticosteroids - reduce inflam

leukotriene antagonists - relax Sm M - reduce inflam

phosphodiesterase inhibitors - relax Sm M

34
Q

how does Th17 mediated inflammation in COPD occur

A

Th17 cytokine induce IL8 & G/GM-CSF secretion from epithelial cells via stimulation from IL17 & IL22

increase neutrophils –> nets form –> clotting –> overtime damage

35
Q

whats the difference in inflammation btn asthma and COPD

A

asthma: reversible - allergen –> epithelial & mast cell –> CD4+ –> eosinophil –> bronchoconstriction

COPD: irreversible; smoke - alv macrophage & epithelial cells –> CD8+ and neutrophils (stimulate more epithelial cells) –> CD8 stimulates small airwary narrowing & alveolar destruction

36
Q

what is ventilator associated lung injury

A

= iatrogenic

physical damage: over-inflam & mechanical stress

biodamage: hyper-O2 –> free radical production –> influx of neutrophils from activated endothelium –> netosis –> platelet activation & clot formation

37
Q

what is lipoid pneumonia

A

caused by inhalation/aspiration of lipids (vaping THC)

dramatic increase bc vaping - (Vitamin E acetate) & essential oils

CPR Exam 2 (20 decks)

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