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TMS exam > 6 - lung fibrosis mechanisms > Flashcards

6 - lung fibrosis mechanisms Flashcards

1
Q

variety of cells lining the respiratory airways

A 
ciliated cells
goblet cells
basal cells 
alveolar T1 
alveolar T2
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2
Q

role of alveolar T1 cells

A

squamous pneumocytes that make up 90% of lung surface area

forms structure of alveolar walls

flat and thin for gas exchange

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3
Q

role of alveolar T2 cells

A

secrete lipoprotein called surfactant to reduce surface tension in the alveoli

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4
Q

how much air do we breathe in daily

A

10, 000 L

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5
Q

factors that may expose the lungs to predispositions for disease

A 
smoking
type of workplace (carpenter)
oxygen (can produce ROS)
genetics
viruses breathed in in air
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6
Q

how many viruses do we breathe in a day

A

500 million

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7
Q

what does IPF stand for

A

idiopathic pulmonary fibrosis

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8
Q

what is idiopathic pulmonary fibrosis

A

end stage of a heterogenous group of interstitial lung diseases
accounts for >5000 deaths a year

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9
Q

overall fibrosis aspect of IPF

A

caused by scar tissue –> collagen (ECM) depositing and building up

which prevents breathing over time

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10
Q

symptoms of IPF

A 
dyspnoea (shortness of breath)
coughing
fever
weight loss
clubbing
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11
Q

what is clubbing

A

thickening of finger tips

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12
Q

dyspnoea

A

shortness of breath

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13
Q

what does a physical examination look for to diagnose IPF

A

sounds in the lungs e.g. crackling

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14
Q

overall/general mechanism of IPF development

A

fibroproliferative response to lung injury

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15
Q

order of steps underlying IPF development from initial injury to organ failure

A
  1. epithelial cell injury
  2. activation of coagulation cascade –> inflammation
  3. establishment of chemokine networks, leukocyte infiltrations and activation
  4. fibroblast recruitment, proliferation and differentiation
  5. loss of organ function
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16
Q

order of events during an active breathing cycle

A
  1. diaphragm contracts (flattens, increases thoracic volume)
  2. external intercostal muscles contract (rip cag moves up and out)
    - -> air is sucked in
  3. diaphragm relaxes (dome-shaped)
  4. internal intercostal muscles contract
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17
Q

what might cause bronchiolar tissue damage

A 
trauma
infection 
physical/chemical agents 
tissue necrosis
foreign bodies (asbestos)
immune reactions (hypersensitvity)
18
Q

how is bronchiolar tissue repaired

A

by regeneration of damaged tissue by paranchymal cells of the same type
or by replacement by connective tissue (scar formation)

19
Q

4 steps for tissue repair

A
  1. haemostasis
  2. inflammation
  3. proliferation
  4. remodelling
20
Q

haemostasis and inflammation steps of tissue repair

A
  1. haemostasis
    - -> blood vessels constrict to keep blood within damaged vessel
    - -> platelets stick together, fibrin activated to reinforce plug (clotting cascade)
    - -> growth factors and cytokines recruited
  2. inflammation
    - -> immune cell recruitment, 1st macrophages then neutrophils
    - -> wound debridement (removal of damaged tissue by phagocytes)
21
Q

which cytokines are recruited during tissue repair

A

TGF-a
PDGF
VEGF

22
Q

PDGF

A

platelet derived growth factor

  • regulates cell growth and division.
23
Q

VEGF

A

vascular endothelial growth factor

  • stimulates formation of blood vessels
24
Q

proliferation and maturation/remodelling steps for tissue repair

A

step 3: proliferation

  • re-epithelisation –> proliferation of epithelial cells
  • angiogenesis
  • fibroplasia –> myobibroblasts activated by PAMPs to make collagen
  • ECM deposition to make tissue

4: maturation/remodelling
- scar formation
- collagen remodelled from TIII to TII
- collagen realigned along tension lines
- apoptosis removes unneeded cells

25
Q

aberrant wound healing

A

not normal

scar formation

26
Q

cell types important in aberrant wound healing

A 
epithelial cells
macrophages
fibroblasts
myofibroblasts
endothelial cells
27
Q

role of platelets in wound healing

A

recruit inflammatory cells and growth factors

form fibrin plug

28
Q

extracellular matrix function

A

provides structural support

regulates movement and growth of cells

29
Q

components of extracellular matrix

A

collagen –> provides tensile strength
elastin –> provides elastic strength and recoil
proteoglycans –> regulate structure and permeability
adhesive glycoproteins
integrins –> cell surface receptor that mediate cell adhesion

30
Q

importance proper regrowth of ECM

A

if pattern of ECM remains then restitution of normal tissue structure can occur

31
Q

keloid scar

A

thickened/raised scar tissue

32
Q

viruses implicated in IPF

A

herpes simplex virus

hep C

33
Q

types of herpes simplex virus

A

human herpes virus 7 and 8
cytomegalovirus
epstein-barr virus (EBV)

34
Q

key physical features of gammaherpesvirus

A

dsDNA genome
envelope protein e.g. integrins
latency in cell bodies of neurons

35
Q

immune response to viral infection

A

Th1 cells:
- activate macrophages –> use MHC I to help cytotoxic T cells using perforins and granzymes

Th2 cells:
- make cytokines to help B cells produce antibodies

36
Q

problem caused by fibroblasts

A

tissue is less expandable

37
Q

problem with herpes virus

A

reprograms lung epithelial cells to produce fibrotic factors
makes lung more susceptible

38
Q

mechanism of viral infection

A

virus enters by endocytosis and replicates
host cell presents viral peptides via MHC I
infected cells release cytokines into blood
viruses kill infected cells —> DC cells recruited
DCs migrate viral peptides to lymphatics and present to naive T cells

CD4 activated via MHC II:

  • Th1 –> activates CD8 T cells
  • Th2 –> activates B cells to produces antibodies

NK cells –> monitor amount of MHC I on cells

39
Q

secondary condition usually developed after IPF

A

interstitial pneumonia

40
Q

effect of viral infections on IPF

A

initiate the disease
exacerbate the disease progression
cause rapid decline

TMS exam (22 decks)

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