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lecture 3 Flashcards

1
Q

how many isoforms does carbonic anhydrase have?

A
  • 11
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2
Q

why is carbonic anhydrase important?

A
  • generates bicarbonate
  • allows protection of tissues
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3
Q

when is carbonic anhydrase III expression increased?

A
  • in gastrooesophageal reflux disease
  • increased in inflamed mucosa
  • moves to cells lower in mucosa to form a barrier
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4
Q

what disease completely loses carbonic anhydrase III?

A
  • LPR
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5
Q

where is the 20 minute acid exposure shown?

A
  • in larynx (pH2 has greatest effect)
  • has no effect on oesophagus
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6
Q

what happens when pig oesophagus is treated with both acid and pepsin?

A
  • becomes damaged
  • less expression at more acidic pHs
  • oesophagus expression recovers if incubation at pH 7.4 (recoverable reduction)
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7
Q

what happens when pig larynx is treated with acid and pepsin?

A
  • doesn’t recover
  • damage with both
  • decreases CA III expression permanently
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8
Q

what mucus is expressed in the larynx?

A
  • MUC 4 (membrane bound mucin) - MUC5AC (gel forming surface mucin)
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9
Q

what mucus is expressed in LPR?

A
  • expression of MUC 5AC is lost
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10
Q

what does this show MUC 5AC to have a role in?

A
  • protection
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11
Q

what is OME?

A
  • otitis media with effusion (glue ear)
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12
Q

what is OME thought to be due to?

A
  • respiratory viruses
  • allergy
  • Eustachian tube obstruction
  • bacterial infections
  • dysfunctional mucocilliary clearance
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13
Q

what is OME actually caused because of?

A
  • reflux of gastric juice
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14
Q

what were the results from the effusions tested?

A
  • acidic protease activity found in 19/65
  • 59/65 contained pepsin or pepsinogen protein
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15
Q

what pH does pepsin damage tissues at?

A
  • high pHs
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15
Q

what was concluded from this experiment?

A
  • 91% effusions contain pepsin/pepsinogen so source certainly gastric juice
  • gastric reflux may be primary factor in OME
  • reflux instigates cascade of inflammatory events
16
Q

why are they called allografts?

A
  • not perfectly matched to the patient
17
Q

what lung conditions are applicable for lung transplants?

A
  • emphysema
  • idiopathic pulmonary fibrosis (destruction of lungs, fibrous tissue forming instead)
  • cystic fibrosis
18
Q

what is the survival rate 1 year post transplant?

19
Q

what is the mortality rate?

A
  • 50%
  • due to allograft failure
  • epithelial damage and scarring occurs
20
Q

how does bronchiolitis obliterates syndrome (BOS) improve years after transplant?

A
  • with anti-reflux surgery at same time shows cured from BOS
  • rest lead to deterioration of lungs
  • patients with no history of reflux also have low survival rate after BOS surgery
21
Q

how do you prevent reflux?

A
  • fondoplication
22
Q

what occurs in fondoplication?

A
  • fundus of stomach wrapped around bottom of oesophagus
  • strengthens cardiac sphincter
  • reduces chance of reflux
  • protection of lungs
23
Q

what does BOS result from?

A
  • fibrosis
  • lots of inflammatory cells and collagen
  • no room for air to pass through
  • loses airway ability to exchange gases
  • loss of FEV1 (forced expiratory volume) over time
24
what might cause BOS?
- measured bile acids in lung lavage samples - high levels of bile acids in BOS
25
what is a lung lavage?
- put fluid (saline) into lung - aspirated back out - measure bile acids
26
what is measured in lavage fluid?
- large amounts of pepsin - protease activity
27
why do some samples have no values?
- due to different patients conditions - shows reflux is transient event (dependent on when lavage is taken)- evidence of reflux could be cleared from lungs
28
does it relate to evidence of inflammation?
- no - neutrophil levels don't directly link at same time point to pepsin - reflux causes response to increase neutrophils (lagging) - high neutrophils means low pepsin as reflux already occurred
29
what are the conclusions of this experiment?
- 75% had detectable pepsin levels - 79% had detectable pepsin like activity - pepsin detected in induced sputum samples - reflux plays role in lung allograft rejection
30
what is the paradigm (pattern) for chronic allograft rejection?
- alloreactivity - response to injury - causes acute rejection, inflammation, CD4 T cell infiltrate
31
what is the result of this?
- chronic, cytokine driven changes - chronic intraepithelial CD8 lymphocytosis (lots of killer T cells, inflammatory response) - transition of epithelia to myofibrilasts - matrix changes - collagen scarring
32
what does this cause?
- allograft loss (death)
33
what is bronchiolitis obliterates syndrome?
- results from immunological and non immunological mechanisms - acute rejection is linked - pathophysiology is poorly understood - gastro-oesophageal reflux is contributing factor
34
what was the aim of the pepsin as a marker of gastric aspiration study?
- to. measure pepsin as marker of gastric aspiration in lung transplant recipients with acute rejection and BOS
35
what subjects were included in study?
- 4 normal volunteer controls - 17 unexplained chronic cough patients - 36 transplant patients

psc2016 (12 decks)

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