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BMS3052 > Other respiratory conditions > Flashcards

Other respiratory conditions Flashcards

1
Q

COPD

A

:D

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2
Q

COPD:

  • Describe C
  • Describe O
  • Is airway obstruction both reversible (by what?) and non-reversible (due to what?
  • What are the 2 types of COPD
A

Chronic and progressive
Airway is obstructed
Reversible by bronchodilators, non reversible due to airway remodelling
Chronic bronchitis and emphysema

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3
Q

Do you need to know about chronic bronchitis and emphysema?

A

Yes

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4
Q

Do you need to know the risk factors for COPD

/

A

Yes

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5
Q

Chronic and acute aspects of pathophysiology:

  • what immune cell is predominant in each?
  • Do you need to know more detail?
A

ChroNic: Neutrophils
AcutE: Eosinophils
Yes

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6
Q 
Diagnosis: what will happen to:
-FEV1
-FVC
%FEV1/FVC
Peak expiratory flow rate 
-Flow volume diagram
-Do you need to know symptoms and FEV1 decreases for mild/mod/severe COPD?
A 
FEV1 decreases 
FVC doesn't change 
FEV1/FVC decreases 
PEF decreases 
Cove shaped 
Yes
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7
Q

Asthma vs COPD: differences in terms of

  • Nature of airway obstruction
  • Whether airflow obstruction can be improved
  • Age of onset
  • Do you need to know immune cell changes?
A

More intermittent vs progressively worsening
Improvement vs less improvement
Young vs 60+
Yes

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8
Q

Do you need to know COPD epidemiology

A

Yes

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9
Q

What are early interventions for COPD?

A

Encourage smoking cessation
Encourage exercise
Encourage flu and pneumococcal vaccinations
Treat comorbidites

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10
Q

What are the pharmacological therapies for COPD

A

Dilators
Corticosteroids
Alpha-1 antitrypsin replacement

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11
Q

Do you need to know more about dilators?

A

Yes

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12
Q

Corticosteroids: describe efficacy in

  • Chronic vs acute COPD
  • COPD vs asthma
A

Not good in chronic (mainly neutrophils and macrophages), but good for acute (work on eosinophils)
Not as good as in treating asthma

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13
Q

Should corticosteroids by the oral route be used long term, why?

A

No, due to sdie effects

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14
Q

What factors should be considered when prescribing steroids for COPD

A

Frequency of exacerbations

Levels of eosinophils

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15
Q

Alpha 1 antitrpysin:

  • Where is it usually produced?
  • After it is produced, what is its mechanism?
  • What happens with alpha 1 antitrypsin deficiency
A

Liver
Travels to lung and coats it; protects lung elastin from being degraded by neutrophil elastase.
Alpha-1 antitrypsin gets stuck in liver, neutrophil elastase degrades elastin

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16
Q

What medication is used to treat alpha 1 antitrypsin deficiency?

A

Alpha 1 proteinase inhibitor Zemaira

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17
Q

What are late stage interventions

A

Oxygen therapy

Surgery

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18
Q

Surgery

  • Can surgery to reduce lung volume improve breathlessness?
  • Is transplantation viable?
A

Yes

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19
Q

How much oxygen therapy is needed per day?

A

15 hours

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20
Q

Does the evidence say that e cigarettes have helped reduce smoking rates?

A

NO

21
Q

Is vaping safe?

Can vaping make you more susceptible to COVID?

A

No

Yes

22
Q

Do you need to know about

  • Acute and long term effects of vaping?
  • EVALI
A

Yes

Yes

23
Q

IDIOPATHIC PULMONARY FIBROSIS

A

:D

24
Q

Do you need to know

  • Epidemiology
  • Risk factors
  • Symptoms
A

Yes

25
Q

Idiopathic pulmonary fibrosis pathology - first step:

  • What is the trigger?
  • What factors contribute to it?
  • What are the cellular effects?
A

Repetitive microinjuries
Aging, environmental factors and genetic susceptibility
Leads to epithelial cell senescence, apoptosis, proliferation, activation (to form proinflammatory mediators), EMT

26
Q

After this, what do the epithelial cells release?

A

Growth factors and cytokines

27
Q

How do growth factors and cytokines lead to fibrosis?

A

Fibroblast migration and proliferation
ECm accumulation (from above cells)
Differentiation of fibroblasts to myofibroblasts)

28
Q

Is there positive feedback regarding fibrosis formation?

A

Yes

29
Q

What is the histological and functional effect of fibrosis

A

Reduced sruface for gas exchange

30
Q

What are the 2 medical treatments for IPF

A

Pirfenidone (Esbrit)

Nintedanib (Ofev)

31
Q

For Pirfenidone and Nintedanib, do they treat the progression of IPF and reverse established fibrosis?
Are both taken orally?

A

Only prevent progression, cannot reverse.

Yes

32
Q

Pirfenidone: mechanism of action

A

Inhibits TGF-B

33
Q

Nintedanib: mechansim of action?

A

Reduces growth factor signalling

34
Q

D you need to know more about Pirfenidone and Nintedanib?

A

Yes

35
Q

What is the surgical option for treating IPF?

A

Lung transplantation

36
Q

SILICOSIS

A

:D

37
Q

Alternative names for silica?

A

crystalline silica, crystalline silicon dioxide, SiO2

38
Q

Do you need to know

  • Silica content of various stones
  • Daily exposure limit of silica
A

Yes

39
Q

Silicosis:

  • Cause
  • Effect on lung structure and function?
A

Inhaling silica

Pulmonary interstitial fibrosis, progressive loss of lung functino

40
Q

Is there a cure for silicosis?

A

No

41
Q

how can silicosis be prevented?

A

Wet cutting
Proper ventilation
Washing hands and clothes, proper PPE

42
Q

What are the 3 types of silicosis? Do you need to know about them in detail?

A

Acute silicosis
Accelerated silicosis
Chronic silicosis

43
Q

Do you need to know about epidemiology?

A

Yes

44
Q

What are the 3 steps of silicosis pathogenesis?

A

Silica uptake: alveolar macrophagse phagocytose silica particles
Inflammation: macrophages release ROS and cytokines, leading to activation of fibroblasts
Macrophages undergo apoptosis, releasing silica. Silica is taken up by macrophages again, leading to positive feedback

45
Q

Do you need to know studies about these steps?

A

Yes

46
Q

What two drugs treat silicosis?

A

Nintedanib

Relaxin

47
Q

Do you need to know about relaxin?

A

Yes

48
Q

What procedure is used to treat silicosis? How does it work?

A

Whole lung lavage - put saline in lungs, removes silica.

BMS3052 (15 decks)

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