Brainscape's Knowledge GenomeTM

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


See full index

Medicine Year 1 > Week 102 COPD > Flashcards

Week 102 COPD Flashcards

1
Q

What is the composition of air?

A

N2- 78%
O2- 21%
Ar- 1%
CO2- 0.04%

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

What’s the equation for diffusion?

A

Time (t) taken for a molecule to diffuse a specified distance (x) in one direction (from “start” to “end”

x^2 alpha t

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

What is in-between the parietal and visceral pleura of the thorax?

A

Interpleural space containing fluid with a negative pressure

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

Give 3 facts of parietal and visceral pleura of the thorax

A

• Superior and anterior borders of lungs and
pleura → identical

• Cupula of pleura – 1-2 cm above the clavicle; 2-3 cm above the 1st rib ́s border

• Sup. interpleural space at the level of the 2nd
rib ́s cartilage (thymus, Hassal’s corpuscles, connective and fatty tissue)

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

Name pleural recesses of the thorax

A

Right costodiaphragmatic recess of pleural cavity

Left costodiaphragmatic recess of pleural cavity

• Superior and anterior borders of lungs and
pleura → identical

• Cupula of pleura – 1-2 cm above the clavicle; 2-3 cm above the 1st rib ́s border

• Sup. interpleural space at the level of the 2nd
rib ́s cartilage (thymus, Hassal’s corpuscles, connective and fatty tissue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why is the right main bronchus more vulnerable to inhalation injury?

A

Shorter
Straighter
Wider
More vertical

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

What plain film projection is best for an accurate heart size?

A

PA projection (AP projection is not reliable)

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

Name pathological changes that occur in COPD:

A

Chronic bronchitis
Emphysema
Small airways disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the clinical implications for the patient dependent on?

A
  • History
  • Physical signs on examination
  • Radiology
  • Lung function tests
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What 2 disease in COPD go together?

A

Chronic bronchitis

Emphysema

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

Describe the anatomy of the normal human airway

A
  • Cartilage is present to level of proximal bronchioles
  • Gas exchange occurs beyond terminal bronchiole
  • Distal airspaces kept open by elastic tension in alveolar walls
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name the cells found in the normal bronchial epithelium

A
  • Ciliated columnar cells
  • Goblet cells
  • Bronchial gland
  • Basement membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe a major indicative symptom of chronic bronchitis, but what must you beware of?

A

Symptom: cough productive of purulent sputum for at least 3 months of the year for at least 2 successive years

Beware: other chronic conditions with wheeze may fit this definition e.g. asthma, bronchiectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the WHO definition of chronic bronchitis?

A

Chronic bronchitis refers to an inflammatory
process in the wall of the bronchioles with
excessive production of mucus and sputum
from hypertrophic glands. The small airways
are narrow, and there is morning cough more
than 3 months per year

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

What can contribute to the pathology of chronic bronchitis?

A

-Cigarette smoke and other irritants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the pathophysiology of chronic bronchitis

A

Irritated epithelial cells increase numbers of goblet cells, mucous glands and mucous in the airway lumen.

Increased CD8 +ve lymphocytes and neutrophils occur- inflammatory cell infiltration.

Increased inflammatory cells in submucosa.

Excess abnormal mucous “glues” and flattens cilia.

Bacterial adherence to bronchial secretions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What do the submucosal macrophages release in chronic bronchitis?

A

Proteases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Name other pathological changes in bronchial epithelium

A
  • Loss of ciliated cells

- Squamous metaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How are distal airspaces of the airways kept open?

A

By elastic tension in alveolar walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is emphysema?

A 
Destruction
of lung tissue distal to the
terminal bronchioles. There
is degenerative loss of radial
traction of the bronchial walls
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the protease/anti-protease theory of emphysema?

A

Observation

Patients with alpha-1-antitrypsin deficiency (an anti-protease) develop
emphysema

Theory

Smoke causes inflammatory cell infiltration
Cells release proteases (elastase, matrix metalloproteases)
These overwhelm body’s natural anti-proteases (like α-1AT )
Causing destruction of structural proteins in alveolar walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe connective tissue in the normal alveolar wall

A 
Elastin - E
• 30% lung extracellular matrix
• Hydrophobic, highly X-linked
complex, 3D molecule
• Elastic properties
• Sheets surround alveoli
• Stretch & elastic recoil
Collagen - C 
• 60% lung extracellular matrix
• Triple helical structure
• Molecules overlap + X-link to
form fibrils of high tensile
strength
• Meshwork for lung structure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Name structural abnormalities in emphysema

A

Loss of elastin/connective tissue in alveolar walls

Dilated airspaces

Loss of elastic tissue to support small airways

Causes floppy airways which narrow or collapse on expiration (higher intrathoracic pressure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe small airway disease in COPD

A 
Increasingly appreciated
Small airway thickening & fibrosis
(unlike emphysema)
Progression of COPD correlates
with:
  • Wall volume
  • Inflammatory cells
  • Mucous in lumen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are pointers towards asthma?

A 
Never-smokers 
Nasal symptoms
Diurnal variation 
Family history
Exacerbating factors Childhood atopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are pointers towards chronic bronchitis?

A

Smoking history

Purulent sputum > 3 months for > 2years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are pointers towards emphysema?

A

Smoking history, weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are physiological consequences of emphysema?

A
  • Airflow obstruction
  • Gas trapping (can’t get air out)
  • Hyperinflation of the chest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Name physical signs of COPD:

A 
Pursed lip breathing
Hyperexpanded chest
↑ accessory muscles 1
↓ cricoid /sternal notch 2
↓ chest expansion
Intercostal recession 3
Paradoxical costal margin
↓ hepatic /cardiac dullness to percussion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is audible with a stethoscope in COPD?

A
  • Heart sounds in epigastrium
  • ↓ breath sounds
  • Polyphonic wheezes
  • Scanty insp. Crackles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Name physiological consequences of emphysema

A 
Loss of capillary bed
• Reduced blood flow
through the lungs
• Hypoxia & hypercarbia
• Pulmonary hypertension /
cor pulmonale
32
Q

Name physical signs of COPD

A 
Bounding pulse (CO2 retention)
• Flapping tremor (CO2 retention) 
• Cyanosis (from hypoxia)
• ↑ JVP
• Ankle swelling
• Tricuspid regurgitation
• Large (pulsatile) liver
33
Q

What receptor controls broncodilation?

A

Beta 2

34
Q

What receptor controls

bronchoconstriction?

A

M

35
Q

What type of drugs can facilitate bronchodilatation?

A

B2 receptor agonists

36
Q

Explain the physiology when an agonist binds to a B2 receptor in the airwyas

A
  • binds to 7 TMD
  • Activates coupled Gs protein (alpha subunits detethers from beta/gamma and = conformational change)
  • GDP–> GTP
  • ATP–> cAMP by adenylate cyclase

= GI/vascular/bronchial/ciliary/smooth muscle relaxation

37
Q

Name short acting B2 agonists (SABAs)

A

Salbutamol

Terbutaline

38
Q

Name long acting beta2 agonists (LABAs)

A

Salmeterol
Formoterol
Indacaterol
Vilanterol

39
Q

How can beta 2 agonists be administered?

A

By inhalation

40
Q

How long do SABAs work for?

A

Acts within minutes and lasts for 4-6 hours

41
Q

How long do LABAs work for?

A

12-24 hours after acting in minutes

42
Q

What are side effects of B2 agonists?

A

Tremor
Hypokalaemia
Tachycardia

43
Q

What type of antagonist can be used to ease airways?

A

Muscarinic anatagonists because they antagonise Ach to reduce bronchoconstriction

Block M1 and M3 –> bronchodilation

44
Q

What pathway do M1/M3 receptors work by?

A

PLC–> IP3/DAG –> Ca+

45
Q

Name short acting muscarinic antagnoists (SAMAs)

A

Ipratrpoium

46
Q

Name long acting muscarinic antagonists (LAMA)

A

Tiotropium
Umeclidinium
Aclidinium
Glycopyrronium

47
Q

How are muscarinic antagonists administered?

A

Inhalation

48
Q

How long does ipratropium last for?

A

Can be used as and when required

Lasts 4-6 hours

49
Q

How long do LAMAs last for?

A

Should be used regularly\

12-24 hr duration of action

50
Q

What are side effects of LAMAs?

A

Dry mouth
Blurred vision
GI disturbances
Can ppt glaucoma in susceptible individuals

51
Q

What typed of administrations of bronchodilators exist?

A

Inhaler: aerosol, dry powder

Nebuliser

52
Q

Describe the step by step treatment algorithm for COPD

A

Step 1: SABA
Step 2: SABA LAMA
Step 3: SABA LAMA LABA
Step 4: SABA LAMA LABA ICS

At each stage give smoking cessation advice

53
Q

What is most important in advising patients at all stages of COPD?

A

SMOKING CESSATION

• Cannot replace lost
lung function but
reduces rate of decline
• Active programmes +
nicotine replacement
chance of quitting
54
Q

What vaccinations can you give to help manage COPD?

A

Influenza (annual)

Pneumococcus (every 10 years)

55
Q

How can you manage COPD pharmacologically?

A

Rational use of bronchodilators

Inhaled corticosteroids

Mucolytics - carbocisteine

56
Q

What drugs are controversial in managing stable COPD?

A

Inhaled corticosteroids
There is limited evidence for the benefit of inhaled corticosteroids:
• No survival benefit independent of effects of long acting bronchodilators
• No effect in decline in FEV1
• Possible effect of reducing rate of acute exacerbations is unclear
• Substantial adverse effects notably increased risk of pneumonia

57
Q

What hospital investigations take place when managing acute exacerbations of COPD?

A 
Arterial blood gas ideally breathing air - or note
inspired pO2)
• CXR (?pneumonia. ? pneumothorax)
• ECG
• FBC & renal profile
• CRP (crude measure of ‘infection’)
• Theophylline blood level (if taking)
• Sputum for bacteriology – but don’t wait to treat
• Blood culture (if febrile)
58
Q

How can acute exacerbations of COPD be managed?

A
  • Nebulised bronchodilators
  • Controlled oxygen therapy (? risk of CO2 retention)
  • Antibiotics if sputum purulent
  • IV fluids
  • IV or oral corticosteroids
  • Consider iv aminophylline (monitor blood levels beware interactions)
  • Chest physiotherapy
  • Consider Non-Invasive Ventilation (NIV) if CO2 rising
  • Consider ITU if appropriate (? ceiling of treatment)
59
Q

What are advantages of acute Non-Invasive Ventilation (NIV)

for exacerbations of COPD?

A 
• reduces mortality, rate of
intubation & LOS
• more cost effective than
intubation / ventilation on
ITU
60
Q

When do you administer long-term o2 therapy (LTOT)?

A
  • Patients with COPD and cor pulmonale
  • Arterial pO2 < 7.3 kPa – when stable
  • Flow rate to bring pO2 < 10 kPa
  • Without significant ↑ pCO2
61
Q

Name common causes of obstructive lung diseases

A

Asthma
Emphysema
Chronic bronchitis

62
Q

Name less common causes of obstructive lung disease

A 
Bronchiectasis
Cystic fibrosis (inherited form of bronchiectasis)
63
Q

Name rare causes of obstructive lung disease

A

Obliterative bronchiolitis

64
Q

What are common COPD symptoms

A

Cough
Sputum
Wheeze
Breathlessness

65
Q

What does diagnosis of asthma require?

A

demonstration of variability or reversibility
in lung function

e.g. spirometry before and after bronchodilator

66
Q

How can you identify asthma in particular from histology of the bronchial epithelium?

A

Eosinophil infiltration

67
Q

What is stridor?

A

• High-pitched inspiratory wheeze
• Audible at a distance
• Caused by laryngeal oedema, vocal cord
spasm or tracheal obstruction e.g.

68
Q

Describe wheeze

A

Continuous musical sound with a definite pitch
• Generated at site of stenosis when walls of lightly
touching bronchi are set in oscillation by jet of air
• Wheeze frequency is independent of airway size
• Varies with velocity of airflow at point of stenosis
• Most prominent in EXPIRATION

69
Q

What are the types of wheeze?

A

Monophonic

Polyphonic

70
Q

Describe polyphonic wheeze

A

• Common in COPD and asthma
• ‘Polyphonic’ = cluster of harmonically unrelated
sounds
• Regional variations in airway narrowing and
‘floppiness’ result in sequential, dynamic
compression
• May be absent on tidal breathing (if present =
severe disease
• Number increase with forced expiratory effort§

71
Q

Describe monophonic wheeze

A

• Low pitched
• Occurs when bronchus narrowed by critical
stenosis or intrabronchial mass (tumour)
• Tend to be ‘focal’ or at least louder in one
lung than the other
• Relatively uncommon
• Can get transient & random monophonic
wheeze with COPD / Asthma

72
Q

Name some causes of monophonic wheeze

A

Bronchial tumour

Inhaled foreign body e.g. peanut

73
Q

Describe crackles

A 
• Non-musical explosive sounds
• Most common in inspiration
• Airways that have closed during expiration
‘snap’ open on inspiration
• Can be early, middle or late
74
Q

What types of crackles can you get?

A

early
mid
late

75
Q

Describe features of early inspiratory crackles

A
  • Typical of COPD (though rarely appreciated!)
  • Scanty - only present in severe disease
  • Also audible at the mouth (i.e. larger airways)
76
Q

Describe features of mid inspiratory crackles

A
  • Typical of bronchiectasis
  • Also audible at the mouth (i.e. larger airways)
  • May also represent bubbling secretions
77
Q

Describe features of late inspiratory crackles

A 
Generated by small, sub-pleural, fibrotic
airways
Sound like ‘velcro’ and usually profuse
Predominantly basal
Not audible at the mouth

Medicine Year 1 (13 decks)

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