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Resp > Obstructive Airways Disease > Flashcards

Obstructive Airways Disease Flashcards

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
Q

Which type of stimulation would result in a greater intracellular concentration of Ca2+?

A

parasympathetics

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26
Q

Which type of stimulation will cause a greater rate of phosphorylation than de-phosphorylation?

A

parasympathetics -> contraction rate > relaxation rate

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27
Q

What are the phases of an asthma attack?

A

Immediate (bronchospasm) and delayed (inflammatory)

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28
Q

From 0-2 hrs post-inhalation of allergen, e.g. pollen, what type of reaction is happening?

A

Type 1 hypersensitivity

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29
Q

What happens in the early phase of an asthmatic attack?

A

bronchospasm

acute inflammation

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30
Q

Hours 6-8 post-inhalation of allergen, is what type of reaction?

A

Type IV hyper-sensitivity

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31
Q

What happens in the late phase of an asthmatic attack?

A

Bronchospasm

Delayed inflammation

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32
Q

What type of immunological response will a non-atopic person have to exposure to an allergen?

A

Low-level Th1 response

cell mediated immune response involving IgG and macrophages

33
Q

What type of immune response will an atopic person have to an allergen?

A

Strong Th2 response

antibody mediated response involving IgE

34
Q

What are the features of an acute-severe asthma attack?

A 
Unable to complete sentences
Resp rate >25
Pulse rate >110
PEFR <50%
Characterised by a polyphonic wheeze and dyspnoea.
35
Q

What are the signs of a life-threatening asthma attack?

A 
PEFR <33%
Bradycardia / Hypotension
Silent chest 
Confusion
Cyanosis / Hypoxia
ABG: PaCO2 >5, PaO2 <8
Previous ITU admission
36
Q

Why would you ask an asthmatic if they have had a previous admission to ITU?

A

Shows they are prone to life-threatening attacks

37
Q

Why would an asthmatic having a life-threatening attack have a silent chest?

A

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
Q

Why would a asthmatic patients PaCO2 be high in an attack?

A

A high PaCO2 suggests fatigue and imminent respiratory failure.
You would expect it to be low because of hyperventilation but it isn’t.

39
Q

What are the complications of an acute asthma attack?

A

Pneumothorax

Emphysema

40
Q

Who would have a primary pneumothorax?

A

Otherwise healthy individuals so not if they have asthma. Common in young adult smokers

41
Q

An asthmatic (or any lung disease) is most likely to have this kind of pneumothorax?

A

secondary

42
Q

When does a tension pneumothorax occur?

A

When there is one-way movement of air into the pleural space, leading to respiratory or cardiovascular compromise

43
Q

What is emphysema?

A

pathological destruction of alveoli - loss of elastic recoil

44
Q

What is the effect of emphysema on lung volumes and compliance?

A

Residual volume increases.

Compliance increases

45
Q

What is compliance?

A

A measure of effort gone into stretching the lungs

46
Q

What does it mean for the patient if compliance increases?

A

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
Q

Which storage disease is associated with emphysema?

A

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
Q

What is the effect of smoking + the deficiency emphysema?

A

Smoking makes the deficiency have a worse effect on the lungs -> Panacinar emphysema

49
Q

What is panacinar emphysema?

A

A type of emphysema where the entire acinus is enlarged from the respiratory bronchiole to the distal alveoli.

50
Q

Mnemonic for the treatment of acute asthma?

A 
O - oxygen 
S - salbutamol (nebulised)
H - hydrocortisone (IV)
I - Ipratropium (nebulised hrly)
T - Theophylline (oral)
M - Magnesium sulphate (IV)
An - Anaesthetist
51
Q

What does COPD stand for?

A

Chronic Obstructive Pulmonary Disease

52
Q

What are the 2 main syndromes COPD encompasses?

A

Emphysema

Chronic bronchitis

53
Q

COPD is characterised by?

A

Airflow obstructions that is partially reversible in some patients (with bronchodilators) but which worsens progressively, as assessed with FEV1.

54
Q

In the disease process of COPD, what doesn’t smoking stimulate?

A

Resident alveolar macrophages

55
Q

These alveolar cells stimulate the production of which cytokines?

A 
IL-8
Leukotriene B4 (LTB4)
56
Q

In the disease process fo COPD, the cytokines activate what?

A

Neutrophils, CD8+ T cells, and increase macrophage numbers

57
Q

The proteinases and free radicals released in the disease process of COPD cause…?

A

The destruction of alveolar walls -> emphysema

Hyper-secretion of mucus ->chronic bronchitis

58
Q

What is the clinical presentation of chronic bronchitis?

A

Cough + wheeze
Clear mucoid sputum normally, purulent when infected
Increasing breathlessness

59
Q

What are some of the cellular dysfunctions of chronic bronchitis?

A

Inflammation of bronchi + bronchioles
chronic neutrophilic infiltration
mucus hyper-secretion
mucociliary dysfunction

60
Q

What are the cellular dysfunctions of emphysema?

A 
Distention + damage to alveoli
Destruction of acing pouching in alveolar sacs
Loss of elastic recoil
Irreversible 
Impaired gas exchange
61
Q

How do you diagnose COPD?

A

History: smoking / history of chronic symptoms / FH (A1AT deficiency)

Investigations: Lung function tests, CXR, ABGs

62
Q

What are the expected results of lung function tests in a COPD patient?

A

Reduced FEV1
Reduced FVC
FEV1/FVC ratio tends to be <75%
Reduced PEFR

63
Q

What would you see on a CXR of a COPD patient?

A

Nothing, it is classically normal

64
Q

What does FVC mean?

A

Forced Vital Capacity

The maximum volume forcibly expelled following a maximum inspiration.

65
Q

What is FEV1?

A

Forced Expiratory Volume in 1 second.

Volume of air that can be expired in the 1st second of expiration in an FVC determination.

66
Q

In obstructive airway diseases, which lung volume measure is affected?

A

FEV1 decreased (therefore ratio is too)

67
Q

In a restrictive lung disease, which lung volume measure is affected?

A

FVC reduced (ratio normal)

68
Q

What does peak flow rate assess?

A

Airway function

69
Q

What are the typical blood gas results for a COPD patient?

A

raised PaCO2 levels, low PaO2

70
Q

What is the main drive for breathing in a COPD patient?

A

low PaO2 levels

71
Q

Do COPD patients typically have respiratory/metabolic acidosis/alkalosis? And is it compensated or not?

A

Compensated respiratory acidosis;

Increased renal reabsorption of HCO3- into blood

72
Q

How do you mange COPD?

A

3 ways:
pharmacological
non-pharmacological (smoking cessation etc)
surgically

73
Q

What are the things a patient can do themselves to deal with their COPD?

A

Smoking cessation
weight loss (if needed)
physical activity (pulmonary rehab)
physiotherapy - to clear secretions

74
Q

What are the pharmacological interventions you could give to help a COPD patient?

A 
Immunisations - influenza/pneumococcal
Bronchodilators + Inhaled corticosteroids
Oral prednisolone for exacerbations
Diuretics if they have cor pulmonale
Oxygen if long-term hypoxic (at home)
75
Q

What is the order of Bronchodilators + Inhaled corticosteroids you would give a COPD patient?

A

LAMA / LABA
LAMA+LABA combo
LAMA+ICS combo
LAMA+ICS+LABA combo

76
Q

How would you treat an acute exacerbation of COPD?

A 
iSOAP
i - ipratropium
S - salbutamol
O - oxygen
A - amoxicillin (if purulent sputum)
P - prednisolone
77
Q

How does ipratropium act?

A

Blocks muscarinic ACh receptors in ASM (not specific) - inhibits bronchoconstriction and mucus secretion

78
Q

What is the deciding factor for antibiotics in a COPD exacerbation?

A

If the sputum is purulent or not, if not = no antibiotics

Resp (8 decks)

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