Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Respiratory > Obstructive Airways Disease > Flashcards

Obstructive Airways Disease Flashcards

1
Q

where is the problem in obstructive disease compared to restrictive disease?

A

Obstructive - airways

Restrictive - lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the obstructive airway syndrome? (3 factors) What is ACOS?

A
  • asthma
  • chronic bronchitis
  • emphysema

ACOS: asthma/COPD overlap syndrome - COPD with reversability and eosinophilia who are steroid responsive, more reversably to salbutamol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the asthma triad?

A
  • reversible airflow obstruction
  • airway inflammation
  • airway hyperresponsiveness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q 
In asthma what do:
-Bronchoconstriction
-Chronic airway inflammation
-airway remodelling
Lead to?
A

Bronchoconstriction leads to brief symptoms

Chronic airway inflammation leads to exacerbations of airway hyperresponsiveness

Airway remodelling leads to fixed airway obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q 
What is seen in the:
-basement membrane
-Submucosa
-Smooth muscle
In the remodelling that takes place in asthma?
A
  • Thickened basement membrane
  • collagen deposition in the submucosa
  • smooth muscle hypertrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the four steps of the inflammatory cascade in asthma, where does:

  • avoidance
  • anti-inflammatory drugs: corticosteroids/cromones
  • Anti-leukotriene/histamine, anti-IgE, anti-IL5
  • Bronchodilators: B2-agonists, muscarinic antagonists

Fit in with this?

A

1: genetic predisposition and triggers (virus/allergen/chemical/nutrition)
- avoidance

2: eosinophilic inflammation
- anti-inflammatory

3: mediators and TH2 cytokines
- Anti-leukotriene/histamine
- Anti-IgE
- Anti-IL5

4: hyper-reactive smooth muscle
- bronchodilators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

list some triggers assoc. commonly with asthma (10)

A

Allergens: animal dander, dust mites, pollens, fungi

Others: exercise, viral infection, smoke, cold, chemicals, drugs (NSAIDs/BBlockers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the different clinical features for the clinical syndrome of asthma? (7)

A
  • episodic symptoms and signs
  • diurnal variability (nocturnal or early morning)
  • non-productive cough/wheeze
  • triggers
  • assoc. atopy (eczema/conjunctivitis/rhinitis)
  • FH asthma
  • Wheezing due to turbulent airflow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the five aspects of asthma diagnosis?

A

1: history and examination
2: diurnal variation of peak flow rate
3: reduced forced expiratory ratio - FEV1/FVC < 75%
4: reversability to inhaled salbutamol
5: provocation testing = bronchospasm (exercise/histamine/methacholine/mannitol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the pathophysiology of COPD

A

Noxious particles or gases e.g. smoking lead to the activation of alveolar macrophages and neutrophils that release proteases which causes:
-mucociliary dysfunction
-inflammation
-tissue damage
(mucus hypersecretion, emphysema, mucosal and peribronchial inflammation and fibrosis)
which leads to the development of obstruction and ongoing disease progression to result in:
Characteristics - exacerbations/reduced lung function
Symptoms - breathlessness, worsening QOL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are proteases normally counteracted by? what is the difference in the balance of this in COPD patients

A
  • anti-proteases such as a1-antitripsin
  • usually there is a balance between proteases and anti-proteases however in COPD there is an imbalance: either an increase in proteases or a decrease in anti-proteases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is mucociliary function affected in COPD?

A

-COPD patients have recurrent resp. tract infection which damage the airway tissue leading to loss of ciliated cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the difference between chronic bronchitis (6) and emphysema (4) in COPD

A

Chronic bronchitis:

  • Chronic neutrophilic inflammation
  • Mucus hypersecretion
  • Mucociliary dysfunction
  • Altered lung microbiome
  • Smooth muscle spasm and hypertrophy
  • Partially reversible

Emphysema:

  • Alveolar destruction
  • Impaired gas exchange
  • Loss of bronchial support
  • Irreversible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 4 ways COPD is assessed? What indicates high risk?

A
  • assess symptoms
  • assess degree of airflow limitation using spirometry
  • assess risk of exacerbations
  • assess co-morbidities (IHD/HF)

2 exac. or more within the last year
or
FEV1<50% predicted
= indicators high risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the 7 factors that make up the clinical syndrome of COPD

A
  • chronic symptoms
  • smoking
  • non-atopic
  • daily productive cough
  • progressive breathlessness
  • frequent infective exacerbations
  • chronic bronchitis = wheezing
  • Emphysema = reduced breath sounds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe how COPD leads to cor-pulmonale

A 
Progressive fixed airflow obstruction
Impaired alveolar gas exchange
Respiratory failure: low PaO2 high PaCO2
Pulmonary hypertension
Right ventricular hypertrophy/failure
	(i.e. cor pulmonale)
17
Q

What is the difference between type 1 and type 2 respiratory failure?

A

Type 1 respiratory failure: hypoxaemia with low or normal carbon dioxide levels

Type 2 resp. failure: hypoxaemia with hypercapnia

18
Q 
describe the differences between asthma and COPD:
smoker?
allergic?
onset?
intermittant or chronic?
productive or non productive cough?
eosinophilic or neutrophilic inflamm?
diurnal variability?
-steroid response?
bronchodilatory response
FVC and TLCO changes
Gas exchange normal or abnormal?
A 
Asthma:
Non smokers 
Allergic
Early or late onset
Intermittent symptoms
Non productive cough
Non progressive 
Eosinophilic inflammation
Diurnal variability
Good corticosteroid response
Good bronchodilator response
Preserved FVC and TLCO
Normal gas exchange 
COPD:
Smokers
Non allergic
Late onset
Chronic symptoms
Productive cough
Progressive decline
Neutrophilic inflammation 
No diurnal variability
Poor corticosteroid response
Poor bronchodilator response
Reduced FVC  and TLCO
Impaired gas exchange
19
Q

What are the 6 risk factors for developing asthma?

A

Family history of atopic disease (e.g. asthma, eczema, allergic rhinitis, or allergic conjunctivitis)

Co-existence of atopic disease

Male sex (for pre-pubertal asthma) and female sex (for persistence of asthma from childhood to adulthood)

Bronchiolitis in infancy

Parental smoking, including perinatal exposure to tobacco smoke

Low birthweight and/or Premature birth

20
Q

In COPD is there a higher or a lower residual volume than in normal lungs?

A

-higher

21
Q

what is the treatment for COPD?

A

General management

smoking cessation advice
annual influenza vaccination
one-off pneumococcal vaccination

Bronchodilator therapy

a short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA) is first-line treatment
for patients who remain breathless or have exacerbations despite using short-acting bronchodilators the next step is determined by the FEV1

FEV1 > 50%

long-acting beta2-agonist (LABA), for example salmeterol, or:
long-acting muscarinic antagonist (LAMA), for example tiotropium

FEV1 < 50%

LABA + inhaled corticosteroid (ICS) in a combination inhaler, or:
LAMA

For patients with persistent exacerbations or breathlessness

if taking a LABA then switch to a LABA + ICS combination inhaler
otherwise give a LAMA and a LABA + ICS combination inhaler

Oral theophylline

NICE only recommends theophylline after trials of short and long-acting bronchodilators or to people who cannot used inhaled therapy
the dose should be reduced if macrolide or fluoroquinolone antibiotics are co-prescribed

Mucolytics

should be 'considered' in patients with a chronic productive cough and continued if symptoms improve

Cor pulmonale

features include peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2
use a loop diuretic for oedema, consider long-term oxygen therapy
ACE-inhibitors, calcium channel blockers and alpha blockers are not recommended by NICE

Respiratory (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions