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Respiratory > 9. Lung Defence I > Flashcards

9. Lung Defence I Flashcards

1
Q

What does the MUCOCILIARY ESCALATOR consist of

A
  • CILIATED airway Epithelial Cells
  • AIRWAY SURFACE LIQUID (over cilia)
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2
Q

layers in the AIRWAY SURFACE LIQUID

A

upper: GEL / MUCOUS

below: PERI-CILIARY SOL LAYER - LIQUID

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3
Q

what does MUCOCILIARY ESCALATOR do

A

SELF-CLEARING Mechanism of the AIRWAYS (DEFENCE)

as CILIA BEAT they CARRY/PULL MUCOUS away

MOVE PARTICLES to top of Trachea (SWALLOWED) to PREVENT them ENTERING LUNGS (from distal to apical airway)

  • all beat in same direction (coordinated)
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4
Q

SPEED at which CILIA BEAT Per Second

A

10-15 BEATS PER SECOND

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5
Q

how much time does the MUCOCILIARY CLEARANCE mechanism have/give (before entering lungs)

A

15 minutes

passage time length so 15 min time zone of mucociliary escalator to clear pathogens

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6
Q

MAINTENANCE of …. is CRITICAL - key physiological mechanism to achieve MUCOCILIARY CLEARANCE of the airways

A

AIRWAY SURFACE LIQUID (ASL) HEIGHT
- PERI-CILIARY LIQUID (PCL) at 7 μm

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7
Q

ASL is made in the LUNGS and PULLED UP into Trachea (like a FUNNEL)
- what prevents ‘DROWNING’ of airways

A

VOLUME ABSORPTION
- LIQUID PULLED OUT of the ASL as it moves up

  • by NA TRANSPORT
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8
Q

what is VOLUME/LIQUID ABSORPTION of the ASL DRIVEN by

A

NA+ TRANSPORT

  • as Na+ travels through ENaC (Epithelial NA CHANNEL)
    it PULLS WATER WITH IT (osmosis)

(TRANSEPITHELIAL ION TRANSPORT)

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9
Q

how do we have a shift from fluid absorption to FLUID PRODUCTION ie if airways are dry

A

CFTR
- DOWNREGULATES NA+ ABSORPTION
- causes CHLORIDE SECRETION (CL- CHANNEL)

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10
Q

how do we have a shift from fluid absorption to FLUID PRODUCTION ie if airways are dry

A

CFTR
- DOWNREGULATES NA+ ABSORPTION
- CHLORIDE SECRETION (CFTR CL- CHANNEL)

Cl- outside cells attracts layer of WATER

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11
Q

INNATE DEFENCE factors in AIRWAYS

A

in ASL:
DEFENSINS & OPSONINS

scavenging cells (engulf & digest):
- ALVEOLAR MACROPHAGES
- NEUTROPHILS
- CHRONIC INFLAMMATORY CELLS

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12
Q

INNATE DEFENCE MOLECULES present/made in ASL

A

DEFENSINS
OPSONINS

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13
Q

a significant component of AIRWAY DEFENCE is the PHYSICAL BARRIER provided by the…

A

AIRWAY SURFACE LIQUID

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14
Q

what is the CFTR GENE

A

makes CFTR protein:
CYSTIC FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR

  • MUTATIONS in this gene cause CYSTIC FIBROSIS (CF)
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15
Q

what does the CFTR PROTEIN do when switched on

A
  • NA+ DOWN REGULATOR
  • acts as CHLORIDE CHANNEL for Cl- SECRETION outside cell (attracts water)
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16
Q

what is the name of the MOST COMMON GENE VARIENT that can AFFECT CF GENE

A

F508del

17
Q

what 2 mechanisms does AIRWAY HEALTH depend on

A
  • MUCOCILIARY ESCALATOR
  • INATE DEFENCE
18
Q

what many things happen WITHOUT CFTR

A
  • HYPERABSORPTION of NA+
  • HYPERABSORPTION of FLUID from ASL
  • ASL becomes very SMALL and Crushes down on CILIA
  • CILIA CANNOT FUNCTION PROPERLY (need peri-sol layer)

BODY RESPONSE: MORE MUCOUS SECRETION
(more mucous layer, less sol layer)

in CF: more PRONE to AIRWAY INFECTION

NEUTROPHILS come in and explore causing INFLAMMATION etc.

19
Q

how does the BODY RESPOND when CILIA CANNOT FUNCTION PROPERLY due to LOW LIQUID in ASL

A

SECRETE MORE MUCOUS (mucosal glands)

20
Q

example of a BACTERIA that causes characteristic LONG TERM AIRWAY INFECTION if appears in CF

A

PSEUDOMONAS AERUGINOSA

21
Q

what TYPE of BACTERIA is PSEUDOMONAS AERUGINOSA (+/-)

A

GRAM NEGATIVE

22
Q

what happens to the PHENOTYPE of PSEUDOMONAS AERUGINOSA when present in CF and how does it lead to ANTIBIOTIC RESISTANCE

A

CHANGING PHENOTYPE
- QUORUM SENSING
(when bacteria change phenotype in presence of other bacteria)

  • leads to ALGINATE PRODUCTION

-> INCREASED ANTIBIOTIC RESISTANCE

23
Q

what does the MUCUS BUILD UP in CF mean for BACTERIA

A

PROVIDE IDEAL ENVIRONMENT
- more inclined to BACTERIAL ADAPTATION

24
Q

what are the SHORT TERM CONSQUENCES for a person with CF

A

INTENSE NEUTROPHIL MEDIATED INFLAMMATION
- LOCALISED in AIRWAYS

Downward spiral of Airway Destruction:
- Proteases, Cytokines/Chemokines, Chondrolysis (loss of articular cartilage)

-> REMODELLING OF LUNGS

25
Q

what is a Common LONG TERM CONSEQUENCE / AIRWAY DISEASE that appears in people with CF

A

BRONCHIECTASIS
- Permanent WIDENING / DILATION of AIRWAYS

26
Q

more LONG TERM pathological CONSQUENCES that can occur in CF

A
  • Biofilms, Quorum Sensing, Sputum
  • Haemoptysis, Venous Malformations
  • Pneumothorax (Apical blebs, poor prognosis)
  • increased PULMONARY HYPERTENSION
    -> HYPOXIA and VENTILATORY FAILURE (DEATH)
27
Q

CF is a … RESPIRATORY DISEASE with an …. profile

A

CHRONIC respiratory disease
ACCUTE INFLAMMATION profile (neutrophils)

28
Q

people with CF mount a considerable … RESPONSE to PSEUDOMONAS

A

ANTIODY RESPONSE

29
Q

ALTERNATIVE PROTEINS/MECHANISMS can give LIQUID SECRETION into ASL (not only CFTR)

  • These work under what conditions
A

under SHEAR PRESSURE/STRESS

eg EXERCISE

-> STIMULATES AIRWAY CELLS to SECRETE LIQUID

30
Q

what can STIMULATE AIRWAY CELLS to SECRETE LIQUID
(WITHOUT the need for CFTR)

A

EXERCISE

(under shear pressure)

31
Q

in CF what is there DISRUPTION of

A

MUCOCILIARY ESCALATOR

32
Q

in CF how is the INFLAMMATION

A

INTENSE ‘ACUTE’ INFLAMMATION

which is CHRONIC and LOCALISED

33
Q

how is the ENVIRONMENT for BACTERIA in CF

A

PREDISPOSES (more inclined to) BACTERIAL ADAPTATION

Respiratory (16 decks)

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