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Obstructive Airways Disease Flashcards

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1
Q

Does asthma affect the small or large airways, or both?

A

It is a chronic inflammatory disease of both the small and large airways.

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2
Q

What are the zones of the bronchial tree called?

A

Acinar/respiratory zone

Conducting zone

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3
Q

In which zone does gas transport take place?

A

Condition zone

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4
Q

In which zone does gas exchange occur?

A

Acinar zone

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5
Q

What are the 3 points of the asthma triad?

A

Airway Inflammation
Reversible Airway Obstruction
Airway Hyper-responsiveness

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6
Q

What are the hallmark changes to the airway of an asthmatic?

A

Basement membrane thickening
Collagen deposition in the submucosa
Hypertrophy of smooth muscle

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7
Q

What allergens could trigger asthma?

A

Animal dander
dust mites
pollens
fungi

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8
Q

What other factors could trigger asthma?

A 
exercise
viral infection
smoke 
cold 
chemicals
drugs (NSAIDs, b-blockers)
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9
Q

What is the clinical presentation of asthma?

A 
Episodic symptoms 
Diurnal variability 
Non-productive cough
Symmetrical wheeze due to turbulent airflow
Triggers
Responsive to beta-blockers or steroids
FH of asthma
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10
Q

Which antibodies would be increased in an asthmatic? And which WBCs would be raised?

A

IgE

Blood eosinophilia >3%

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11
Q

How do you diagnose asthma?

A 
History + exam
Diurnal variation of Peak flow rate
Reduced FEV1/FVC (<75%)
Reversibility to inh. salbutamol (>15%)
Provocation testing -> bronchospasm
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12
Q

Which factors are used in provocation testing?

A

Exercise

Histamine / methacholine / mannitol

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13
Q

What is the neurotransmitter released from parasympathetic post-ganglionic fibres that causes contraction?

A

acetylcholine

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14
Q

Which receptor mediates ASM contraction?

A

muscarinic M3 ACh receptors

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15
Q

Apart from contraction, what else happens when the M3 muscarinic ACh receptors are bound?

A

increased mucosa secretion from receptors on gland (goblet) cells

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16
Q

Which neurotransmitters are released from parasympathetic post-ganglionic fibres that cause relaxation?

A 
Nitric oxide (NO)
Vasoactive intestinal peptide (VIP)
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17
Q

What is the neurotransmitter associated with sympathetic stimulation of bronchial smooth muscle?

A

Adrenaline - released from the medulla of the adrenal gland - enters circulation - binds receptor

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18
Q

Which sympathetics receptor controls bronchial relaxation

A

B2-adrenoceptors on ASM cells

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19
Q

What other effects are caused by sympathetic stimulation of b2-ADR?

A

decreased mucus secretion (goblet cells)

increased mucociliary clearance (epithelial cells) = mucociliary escalator.

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20
Q

Sympathetic stimualtion also causes contraction…where and what receptors mediate this?

A

Vascular smooth muscle contraction

a1-adrenoceptors on vascular smooth muscle cells

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21
Q

A phosphorylated myosin light chain results in…?

A

contraction

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22
Q

Which enzyme dephosphorylates MLC?

A

myosin phosphatase

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23
Q

A de-phosphorylated MLC results in?

A

relaxation

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24
Q

Which enzyme phosphorylates MLC?

A

myosin light chain kinase

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25
Which type of stimulation would result in a greater intracellular concentration of Ca2+?
parasympathetics
26
Which type of stimulation will cause a greater rate of phosphorylation than de-phosphorylation?
parasympathetics -> contraction rate > relaxation rate
27
What are the phases of an asthma attack?
Immediate (bronchospasm) and delayed (inflammatory)
28
From 0-2 hrs post-inhalation of allergen, e.g. pollen, what type of reaction is happening?
Type 1 hypersensitivity
29
What happens in the early phase of an asthmatic attack?
bronchospasm | acute inflammation
30
Hours 6-8 post-inhalation of allergen, is what type of reaction?
Type IV hyper-sensitivity
31
What happens in the late phase of an asthmatic attack?
Bronchospasm | Delayed inflammation
32
What type of immunological response will a non-atopic person have to exposure to an allergen?
Low-level Th1 response | cell mediated immune response involving IgG and macrophages
33
What type of immune response will an atopic person have to an allergen?
Strong Th2 response | antibody mediated response involving IgE
34
What are the features of an acute-severe asthma attack?
``` Unable to complete sentences Resp rate >25 Pulse rate >110 PEFR <50% Characterised by a polyphonic wheeze and dyspnoea. ```
35
What are the signs of a life-threatening asthma attack?
``` PEFR <33% Bradycardia / Hypotension Silent chest Confusion Cyanosis / Hypoxia ABG: PaCO2 >5, PaO2 <8 Previous ITU admission ```
36
Why would you ask an asthmatic if they have had a previous admission to ITU?
Shows they are prone to life-threatening attacks
37
Why would an asthmatic having a life-threatening attack have a silent chest?
Indicates that air entry into the chest is so bad that a wheeze cannot be generated It doesn't mean that there is no bronchoconstriction!
38
Why would a asthmatic patients PaCO2 be high in an attack?
A high PaCO2 suggests fatigue and imminent respiratory failure. You would expect it to be low because of hyperventilation but it isn't.
39
What are the complications of an acute asthma attack?
Pneumothorax | Emphysema
40
Who would have a primary pneumothorax?
Otherwise healthy individuals so not if they have asthma. Common in young adult smokers
41
An asthmatic (or any lung disease) is most likely to have this kind of pneumothorax?
secondary
42
When does a tension pneumothorax occur?
When there is one-way movement of air into the pleural space, leading to respiratory or cardiovascular compromise
43
What is emphysema?
pathological destruction of alveoli - loss of elastic recoil
44
What is the effect of emphysema on lung volumes and compliance?
Residual volume increases. | Compliance increases
45
What is compliance?
A measure of effort gone into stretching the lungs
46
What does it mean for the patient if compliance increases?
It is more effort for the patient to empty their lungs. Patients tend to start the next inhale before the last breath has been fully exhaled. Lungs eventually become hyper-inflated.
47
Which storage disease is associated with emphysema?
alpha-1-anti-trypsin deficiency; autosomal recessive disorder. A1AT is supposed to protect the lungs from neutrophil elastase - an enzyme that disrupts connective tissue.
48
What is the effect of smoking + the deficiency emphysema?
Smoking makes the deficiency have a worse effect on the lungs -> Panacinar emphysema
49
What is panacinar emphysema?
A type of emphysema where the entire acinus is enlarged from the respiratory bronchiole to the distal alveoli.
50
Mnemonic for the treatment of acute asthma?
``` O - oxygen S - salbutamol (nebulised) H - hydrocortisone (IV) I - Ipratropium (nebulised hrly) T - Theophylline (oral) M - Magnesium sulphate (IV) An - Anaesthetist ```
51
What does COPD stand for?
Chronic Obstructive Pulmonary Disease
52
What are the 2 main syndromes COPD encompasses?
Emphysema | Chronic bronchitis
53
COPD is characterised by?
Airflow obstructions that is partially reversible in some patients (with bronchodilators) but which worsens progressively, as assessed with FEV1.
54
In the disease process of COPD, what doesn't smoking stimulate?
Resident alveolar macrophages
55
These alveolar cells stimulate the production of which cytokines?
``` IL-8 Leukotriene B4 (LTB4) ```
56
In the disease process fo COPD, the cytokines activate what?
Neutrophils, CD8+ T cells, and increase macrophage numbers
57
The proteinases and free radicals released in the disease process of COPD cause...?
The destruction of alveolar walls -> emphysema | Hyper-secretion of mucus ->chronic bronchitis
58
What is the clinical presentation of chronic bronchitis?
Cough + wheeze Clear mucoid sputum normally, purulent when infected Increasing breathlessness
59
What are some of the cellular dysfunctions of chronic bronchitis?
Inflammation of bronchi + bronchioles chronic neutrophilic infiltration mucus hyper-secretion mucociliary dysfunction
60
What are the cellular dysfunctions of emphysema?
``` Distention + damage to alveoli Destruction of acing pouching in alveolar sacs Loss of elastic recoil Irreversible Impaired gas exchange ```
61
How do you diagnose COPD?
History: smoking / history of chronic symptoms / FH (A1AT deficiency) Investigations: Lung function tests, CXR, ABGs
62
What are the expected results of lung function tests in a COPD patient?
Reduced FEV1 Reduced FVC FEV1/FVC ratio tends to be <75% Reduced PEFR
63
What would you see on a CXR of a COPD patient?
Nothing, it is classically normal
64
What does FVC mean?
Forced Vital Capacity | The maximum volume forcibly expelled following a maximum inspiration.
65
What is FEV1?
Forced Expiratory Volume in 1 second. | Volume of air that can be expired in the 1st second of expiration in an FVC determination.
66
In obstructive airway diseases, which lung volume measure is affected?
FEV1 decreased (therefore ratio is too)
67
In a restrictive lung disease, which lung volume measure is affected?
FVC reduced (ratio normal)
68
What does peak flow rate assess?
Airway function
69
What are the typical blood gas results for a COPD patient?
raised PaCO2 levels, low PaO2
70
What is the main drive for breathing in a COPD patient?
low PaO2 levels
71
Do COPD patients typically have respiratory/metabolic acidosis/alkalosis? And is it compensated or not?
Compensated respiratory acidosis; | Increased renal reabsorption of HCO3- into blood
72
How do you mange COPD?
3 ways: pharmacological non-pharmacological (smoking cessation etc) surgically
73
What are the things a patient can do themselves to deal with their COPD?
Smoking cessation weight loss (if needed) physical activity (pulmonary rehab) physiotherapy - to clear secretions
74
What are the pharmacological interventions you could give to help a COPD patient?
``` Immunisations - influenza/pneumococcal Bronchodilators + Inhaled corticosteroids Oral prednisolone for exacerbations Diuretics if they have cor pulmonale Oxygen if long-term hypoxic (at home) ```
75
What is the order of Bronchodilators + Inhaled corticosteroids you would give a COPD patient?
LAMA / LABA LAMA+LABA combo LAMA+ICS combo LAMA+ICS+LABA combo
76
How would you treat an acute exacerbation of COPD?
``` iSOAP i - ipratropium S - salbutamol O - oxygen A - amoxicillin (if purulent sputum) P - prednisolone ```
77
How does ipratropium act?
Blocks muscarinic ACh receptors in ASM (not specific) - inhibits bronchoconstriction and mucus secretion
78
What is the deciding factor for antibiotics in a COPD exacerbation?
If the sputum is purulent or not, if not = no antibiotics

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