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psc2016 > lecture 4 > Flashcards

lecture 4 Flashcards

1
Q

how was the pepsin measured?

A
  • slot blot ELISA
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2
Q

how does slot blot ELISA work?

A
  • primary specific antibody (anti pepsin)
  • secondary antibody (anti sheep goat)
  • secondary recognises first, conjugated to peroxidase
  • repeat washing
  • colour development
  • substrate added, dab with H2O2
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3
Q

what did we find?

A
  • pepsin levels low in normal
  • chronic cough group have no pepsin
  • lung transplant patients have lots of pepsin (significantly high levels)
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4
Q

which group of transplant patients had highest pepsin levels?

A
  • acute rejectors
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5
Q

what is high levels of pepsin linked with?

A
  • acute rejection
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6
Q

why do BOS patients not have high pepsin levels?

A
  • patients are showing damage to lungs
  • BOS development causes leaky lungs so any pepsin escapes from lungs
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7
Q

why no pepsin in the chronic cough group?

A
  • coughed up so no pepsin in actual lungs
  • aspirate doesn’t get down through lungs
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8
Q

what results were shown from isografts with aspiration?

A
  • more T killer cells when lungs damaged with reflux
  • large number of lymphocytes
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9
Q

how is the rejection process accelerated?

A
  • chronic aspiration of gastric fluid
  • damage to lungs
  • aspiration as immune response stimulated
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10
Q

what is the effect of gastric juice on rat lung allografts?

A
  • pH 2.5 rat gastric juice = damage, open spaces disappeared,
  • low pH isn’t only damaging factor
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11
Q

what is aspiration a source of?

A
  • injury
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12
Q

what antibiotic prevents deterioration of allografts?

A
  • azithromycin
  • FEV is shown to increase
  • not antimicrobial effect
  • reduces amount of neutrophils
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13
Q

what does azithromycin do?

A
  • effects gastric motility
  • prevents reflux by increasing gastric emptying
  • no contents in stomach to reflux as easy
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14
Q

what does azithromycin reduce levels of?

A
  • C reactive protein (inflammatory linked plasma protein)
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15
Q

is azithromycin effective still in patients with lung transplants and BOS?

A
  • bile acid aspiration reduces the survival
  • if bile acid present, deterioration always occurs
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16
Q

what diseases have high pepsin and no other obvious cause?

A
  • OME
  • non-allergic rhinitis
  • sinusitis
  • hoarseness
  • chronic cough
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17
Q

what pH is acid damaging below?

A
  • pH 3.5
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18
Q

how is pepsin reactivated?

A
  • when trapped in tissue reactivated by second exposure to acid
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19
Q

how is chronic cough and reflux related?

A
  • by reflux to top of oesophagus and pepsin in sputum
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20
Q

what is low impedance?

A
  • easy flow through the machine
21
Q

what factors are significant in terms of reflux and chronic cough?

A
  • age
  • pepsinspit
  • gender
22
Q

what is pepsinspit?

A
  • cough up and measure pepsin in sputum
23
Q

what is full column?

A
  • where the refluxate has gone passed all the rings
  • not known if goes out, but like yes cant say for definite
24
Q

why are the pepsin levels in lung lavages low?

A
  • pepsin doesnt reach lungs as cough as soon as exits oesophagus?
25
Q

what does the leading edge of waveform indicate?

A
  • retrograde bolus movement
  • levels gone up
26
Q

what happens when the reflux event passes the rings?

A
  • fall of impedance
27
Q

what shows the height of the reflux?

A
  • multiple channels
28
Q

what does the trialing edge of waveform indicate?

A
  • clearance of the bolus
29
Q

does stopping reflux by anti-reflux surgery benefit the patient?

A
  • after fundoplication the reflux symptom index decreases
  • heartburn and other symptoms decrease
  • quality of life improves
30
Q

what does a reflux symptom index of 13 mean?

A
  • reflux present
31
Q

how does FEV1 change after operation?

A
  • improvement
32
Q

how are bile salt assays tested?

A
  • oxidising them with 3-alpha HSD to remove an OH group so its oxidised
  • dehydrogenase
  • uses NAD+
33
Q

what occurs in kit 2 for measuring bile salt assays?

A
  • reaction to oxidised form
  • can go bckwards as NADH
  • can go forwards too so cycles
  • more development of NAD
  • measure levels of thio-NADH
34
Q

what other method is used to measure bile salts?

A
  • mass spec
  • more sensitive
35
Q

what is the hypothesis of profiles of sputum and gastric juice in cystic fibrosis?

A
  • gastric and lung microbiomes are related
36
Q

how do cystic fibrosis patients become reinfected with the same bacteria?

A
  • present/hiding in stomach
  • found on proton pump inhibitors
  • pH high so bacterial overgrowth
37
Q

what were the results from the experiment?

A
  • 9/14 non CF grew bacteria/funghi (stomach isn’t sterile)
  • all CF sputa and gastric juice grew bacteria/funghi
  • p.aeruginosa in 11/14 CF patients
38
Q

why does non CF patients have more microbial species ?

A
  • most CF patients on long term antibiotic treatment
39
Q

what are the conclusions?

A
  • stomach acts as resiviour for microbes which can be refluxed and aspirated into lungs
40
Q

what can be an issue following this discovery?

A
  • PPIs as reduce acidity of stomach so add to further overgrowth
  • antibiotics
41
Q

how does reflux and covid-19 link?

A

-

42
Q

how does covid enter cells?

A
  • uses ACE2 receptor
  • converts angiotensin from 1 to 2 to affect blood pressure
43
Q

what GI symptoms support clinical diagnosis of covid-19?

A
  • nausea
  • vomitting
  • diarrhoea
44
Q

what theory was made linking covid-19 and reflux?

A
  • reflux and aspiration damages lungs
  • damaged tissue present
  • allows covid access
  • so can infect lungs
45
Q

how was reflux identified?

A
  • uses reflux symptom index (level over 13=reflux)
  • measure salivary pepsin levels using ELISA
46
Q

what results linked pepsin and severe covid?

A
  • pepsin of more than 76ng/ml
  • RSI greater than 13
47
Q

how does severe covid link?

A
  • pepsin levels increasing from mild to severe
  • severity based on pepsin and high reflux
48
Q
A

psc2016 (12 decks)

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