Pulmonary Defense Mechanisms - Bowden Flashcards

1
Q

immunological barriers at the upper airway

A
Anatomical barriers 
Cough Reflex
Angulation
Mucociliary apparatus
airway epithelium 
IgA
DC, N, lymphocytes
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2
Q

immunological barriers at the Alveolar spaces

A
Alveolar M (usually M2)
Type 1 an dType 2 cells
Clara cells (club cells)
Surfactant
Complement 
N and E
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3
Q

branching of the bronchi and the bronchioles causes what

A

more deposition of the substance

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4
Q

Cough Reflex

A
  1. deep inspiration
  2. glottis closes to trap air inside
  3. rise in intrathoracic P (while trying to expire)
  4. P buildup
  5. sudden release of trapped air at high P = COUGH
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5
Q

3 major functions of the epithelium

A
  1. barrier
  2. Defense towards pathogens : release of cytokines, bacteriostatic molecules
  3. Translocate IgA (which is in mucus and binds to pathogens)
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6
Q

Mucociliary Clearence

A

particles 2-3um to 10um get deposited in mucus (upper Airway)
Mucus has
1. IgA, lysozyme, lactoferrin, perioxidases
2. cilia on aqueous layer propelling stuff upward to be coughed or swallowed

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7
Q

mucus contanis what

A
  1. IgA, lysozyme, lactoferrin, perioxidases

2. cilia on aqueous layer propelling stuff upward to be

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8
Q

defected mucociliary clearance is present in what

A

Asthma
COPD
chronic bronchitis
cystic fibrosis

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9
Q

the airway normal has what immune cells present

A

Tregs (IL10, TGF-B)
DC (IL27, IL10, TGF-B)
M1 (IL10, TGF-B, IL27)

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10
Q

first immune cell to appear during any kind of respiratory condition

A

NEUTROPHILS (acute and fast and first)

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11
Q

what comes to the alveoli after the Neutrophil

what can they eventually do

A

M2 (TGF-B, IL10)
they can become smoke filled alveolar Macrophages (unable to digest what is inside) = scavenger cells
can also recruit M1

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12
Q

surfactant A and D function

A

from type 2 cells and club (Clara) cells
opsonize bacteria
activate macrophages for phagocytosis of BACTERIA

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13
Q

Alveolar macrophages activate what type of cells

A

FOX3P (Treg) cells

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14
Q

what is the first thing that happens during acute inflammatory response

A

IL1 and TNF cause IL8 to be secreted from endothelial cells + alveolar macrophages (some IL6)
this bring neutrophils

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15
Q

how does edema happen at the inflammatory site

A

plasma protiens brought into the contact of damaged area causes fluid buildup

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16
Q

what to the proteins at the site of damage activate

A
  1. Clotting factors : blood clot
  2. Complement : destroy bacteria
  3. Kinin cascade : vasodilation , increase permeability stimulate pain receptors
17
Q

Fibroinolytic protein

A

degrades the blood clot when the wound is healed

18
Q

Acute inflammatory response steps

A
  1. neutrophils recruited
  2. edema and vasodilation
  3. epithelium dies and sheds off
  4. only BM holds around alveoli
  5. NETs cast form neutrophils
19
Q

acute inflammatory response what causes this and outcome

A

allergen of some sort or pathogen

if the allergen is effectively removed then all goes back to normal = fast recovery

20
Q

Chronic Inflammatory response
what comes
what happens

A

chronic acute response causes this

  1. M1 and Th1, Th17, CTL come
  2. hypersecretion of mucus
  3. activate proteases
  4. tissue remodeling and can lead to fibrosis
21
Q

ex of type 1 hypersensitivity in this lecture

A

Asthma

22
Q

Early phase for Type 1 HS
what is brought
what happens

A
Acute Atopic response
IgE 
MAST cell degranulation 
(IL4, IL5, Histamine)
= sneezing , pruritis, rhinorrhea, congestion
23
Q

Late phase for Type 1 HS
what is brought
what happens

A

after 4-12 hrs
N, E, B, Th2 cells*
MANY MORE MAST cells with Fce receptor

24
Q

what do the eosinophils cause for chronic inflammatory response

A

local tissue damage and inflammation

fatigue, asthma, myalgias

25
Q

what does the Eosinophils causes for remodeling

A
  1. LEUKOTRIENES C4, D4, E4 : bronchospasm, vascular permeability, mucus made
  2. PROSTAGLANDINS D2, E2, F2 : bronchospasm, vasodilation
    = SM and fibroblasts come and deposit collagen and tissue damage
26
Q

what do Th2 cells secrete for chronic inflammatory response

A

secretion of IL4, IL5, IL13

27
Q

COPD cytokines involved

A
  1. TGF-B + IL6 causes the IL17, IL22 release
  2. IL17 causes
  3. IL8 secreted from epithelial cells
  4. causes N to come
  5. many M an dN try to get rid of the carbon smoked
28
Q

smokers who dont get COPD or are immunosuppressent COPD pts with low Tregs have what kind of cells

A

anti-inflammatory :
TGF-B + IL2 —->
nTreg, Tr1, iTreg

29
Q
SIMPLE COMPARISON BETWEEN ASTHMA AND COPD
ASTHMA : 
1st cells
2nd cells
leading to
A
  1. Ep cells + mast cells (IL4, IL5, IL13), IgE
  2. Eosinophils + CD4+ Th2 cells , N
  3. Bronchoconstriction (and other stuff is chronic )
    = reversible with inhaler)
30
Q
SIMPLE COMPARISON BETWEEN ASTHMA AND COPD
COPD : 
1st cells
2nd cells
leading to
A
  1. Avl M + Ep cells
  2. Neutrophils, CD8+cells
  3. small airway narrowing from mucus and deposition, alveolar destruction
31
Q

Ventilator Associated Lung injury

happens from what

A

being on a ventilator causes lung damage due to

  1. over-inflation
  2. mechanical stress
  3. Hyper-oxygenation
  4. free radicals
  5. NEUTROPHILS COME **
32
Q

Ventilator Associated Lung injury steps

A
  1. endothelium gets activated
  2. Neutrophils come
  3. Neutrophil NETs
  4. platelet activation
  5. blood clot formation
    = thickening of BM and capillaries break
33
Q

Vaping associated with lung injury
what is caused
what is seen

A

causes ARDS (Acute Respiratory Distress Syndrome)
Bilateral infiltrated on CXR
NO infection

34
Q

Vaping associated with lung injury

HOW ARDS is caused

A
  1. inhlation of lipids and oils (VIT E is vaporized in the lungs to an oil
  2. causes lipid pneumonia
  3. Foam cells develop (M that take up many ipids and cant break them down)
35
Q

other things causing lipid pneumonia

A

Essenial oils chronically used (petroleum)

Vicks, Olive oil, mineral oil

36
Q

Lipid Pneumonia Tx

A

steroids
Antimicrobials (for secondary complications)
supportive care