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MB1: Respiratory > Obstructive airways disease > Flashcards

Obstructive airways disease Flashcards

1
Q

large airways are how big and in what zone?

A

> 2mm

Conducting zone

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2
Q

small airways are how big and in what zone?

A 
<2mm
Acinar zone (gas excahnge
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3
Q

what is the exception to the rule of airway size and zone

A

They are small airways but in the conducting zone

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4
Q

4 causes of obstruction in asthma and COPD

A

Infolding of mucosa due to oedema and hypertrophy
lumen obstruction
spasm of outer smooth wall
Tear of alveolar walls

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5
Q

The infolding of musosa due to hypertrophy and oedema is inflammatory. in asthma this is eosinophilic/neutrophilic and in COPD it is eosinophilic/neutrophilic

A

Asthma - eosinophilic

COPD - both but mainly neutrophilic

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6
Q

What is the asthma triad

A

airway inflammation
airway hyperresponsiveness
reversible airflow obstruction

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7
Q

What are the 3 stages of asthma dynamically evolving

A

Bronchoconstriction
Chronic inflammation
Airway remodelling

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8
Q

What is the clinical syndrome of asthma (signs)

A 
Diurinal variability 
Non productive cough and wheeze 
Triggers - allergen or other 
Family history 
Blood eosinophilia >4%
Responsiveness to beta agonists
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9
Q

what is the disease process of COPD

A

smoke and other irritants activate macrophages and airway epithelial cells - release IL-* and leukotrine B4. these cause chemotaxis of neutrophils and macrophages that secrete proteases to break down connective tissues.
Cytotoxic t cells destroy alveolar walls

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10
Q

What counters the protease production triggered by cigarette smoke

A

Antiprotease, from genes. it is rarely fully effective

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11
Q

what does chronic bronchitis cause

A

Chronic neutrophilic inflammation
smooth muscle spasm and hypertrophy
Altered microbiome
Mucus hypersecretion and mucociliary dysfunction

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12
Q

What does emphysema cause

A

impaired gas exchange due to alveolar destruction

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13
Q

How is COPD diagnosed?

A

Gold grading - FEV1 graded 1-4

Grid plotting of exacerbation vs symptoms

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14
Q

What is ACOS

A

COPD with blood eosinophilia >4%
more reversible to salbutamol
hard to distinguish from asthmatic smokers

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15
Q

Name an effort dependent test

A

Spirometry

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16
Q

Name 4 effort independent tests

A

Relaxed vital capacity
Nitrogen washout
exhaled breath nitric oxide
Impulse oscillometry

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17
Q

Name 3 gas diffusion tests

A

CO transfer factor
ABG
SaO2 during exercise

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18
Q

What is bronchial challenge testing

A

use of exercise or allergens to cause a decrease in FEV1

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19
Q

how much should FEV1 decrease by in bronchial challenge testing

A

20% reduction

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20
Q

how do methacholine and mannitol cause airway hyperresponsiveness

A

mannitol - destroys mast cells to degranulate - so immune mediators released
Methacholine stimulates the parasypathetic system via M3

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21
Q

A person can have asthma without hyperreactivity. true/false

A

false - they must be hyperreactive

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22
Q

how does DLCO measure gas diffusion across the alveolar-arterolar barrier

A

small dose Co is given and observed how much is absorbed into blood as Hb has high affinity for it

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23
Q

What conditions cause DLCO to decrease

A

anaemia, emphysema, interstitial lung disease, pulmonary oedema, PE

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24
Q

what interleukin mediates nitric oxide production

A

IL-13

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25
Q

what do high levels of exhaled nitric oxide suggest

A

uncontrolled asthmatic inflammation

Patients not correctly taking ICS medication

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26
Q

where is exhaled breath NO not useful

A

Smokers or patients with COPD as cigarette smoke suppresses NO

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27
Q

Where can ICS be used

A

Asthma

ECOS (eosinophilic COPD)

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28
Q

What can ICS cause and why

A

Pneumonia

Causes local immunosuppression and impaired mucociliary clearance

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29
Q

Where can prednisolone be used

A

acute asthma exacerbations

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30
Q

Oral steroids have a low/high therapeutic ratio and ICS have a low/high therapeutic ratio

A

Oral - low

ICS - high

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31
Q

ICS is used in combination with what in COPD

A

ICS/LAMA/LABA

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32
Q

true/false - ICS work in eosinophilic and neutrophilic COPD

A

false - it only works in eosinophilic COPD

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33
Q

How small does a particle have to be to get past the carina

A

less than 5 microns

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34
Q

How small does a particle have to be to get past generation 7 of the respiratory tree

A

less than 2 microns

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35
Q

Why is a spacer good to use?

A

it reduces oropharyngeal and laryngeal side effects and reduces systemic absorption of drug

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36
Q

What drug is good as an add on for exercise induced bronchoconstriction

A

Cromones

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37
Q

In who are cromones most effective

A

atopic children

38
Q

Roughly how do cromones work

How good are they in terms of duration and efficacy

A

stabilise mast cells

Short acting and poor efficacy

39
Q

What is the main leukotriene in asthma and what does it do?

A

LTD4
Chemotaxis of eosinophils
Oedema
Bronchoconstriction

40
Q

Name the main LTRA used, how it is taken

High/low therapeutic ratio

A

Montelukast, oral and once daily

High

41
Q

how does omalizumab work to treat asthma

A

Inhibits IgE binding to IgE receptor to prevent TH2 response as well as basophil and mast cell mediator release

42
Q

Where would anti-IgE be used

A

severe persistent allergic asthma (raised IgE)

43
Q

how does benralizumab work to treat asthma

A

blocks effects of IL-5, responsible for eosinophilic inflammation

44
Q

Where would anti IL-5 be used

A

severe refractory eosinophilic asthma (blood eosinophil >300 cell/ul)

45
Q

how does dupilumab work to treat asthma

A

Block effects of TH2 cytokines IL-4/13, which produce eosinophilic inflammation, IgE, airway hyperreactivity and mucin production

46
Q

where would anti IL-4a be used

A

severe refractory eosinophilic asthma (blood eosinophil >150 cells/ul and a FeNO>25ppb)

47
Q

What does anti IL-4a suppress

A

IgE and FeNO

48
Q

beta agonists are combined with ____ to make a duo

A

ICS

49
Q

beta agonists can be combined with what for COPD

A

ICS/LAMA/LABA - eosinophilic COPD

LABA/LAMA - neutrophilic COPD

50
Q

how does tachyphylaxis play a part in beta agonists

A

Chronic use of LABAs can cause a tolerance

51
Q

Name a short and long acting muscarinic antagonist

A

SAMA - ipratropium

LAMA - Tiotropium

52
Q

true/false - muscarinic antagonists can be used for COPD and asthma

A

true - usually used in COPD as a LAMA/LABA or ICS/LAMA/LABA but tiotropium can also be used in more severe asthma as triple therapy

53
Q

how does theophylline work and what is it used for

A

inhibits PDE to sustain cAMP levels. maintenance therapy in asthma

54
Q

where is IV aminophylline used

A

acute asthma attack

55
Q

xanthines - high/low therapeutic ratio

Contraindications?

A

contraindicated with P450 drugs

low therapeutic ratio

56
Q

What is roflumilast and when is it used

A

PDE4 inhibitor used in COPD as an add on to LABA/LAMA

Rarely used due to adverse effects

57
Q

what is carbocisteine and erdosteine and when are they used?

A

COPD - reduces sputum viscosity to aid ejection

Rarely used

58
Q

Name 2 non-pharmacological ways of reducing COPD exacerbation

A

Smoking cessation

Vaccination against flu and pneumonia

59
Q

how can acute COPD be treated?

A 
nebulised salbutamol and ipratropium
24-28% oxygen titrated against SaO2 for T2 resp failure 
prednisalone (oral)
NIV to create higher FiO2
Consider antibiotic in infection
60
Q

How can acute asthma be treated?

A

Nebulised salbutamol and maybe ipratropium
High flow oxygen above 60%
IV aminophylline (maybe)
Prednisalone (oral)
PO2 down and PCO2 up consider intubation with mechanical ventilation

61
Q

Easiest way of measuring improvement in community for an asthmatic?

A

Peak flow chart

62
Q

What dosage would you increase if an asthmatic has repeated exacerbations?

A

Increase ICS dose

63
Q

The gold guideline states all potential COPD patients must have what?

A

Spirometry, it is graded 1-4 if FEV1/FVC<0.70

64
Q

symptoms on the gold grid scale of COPD are measured on what scale?

A

mMRC scale of 0-4

65
Q

what is the only treatment for pulmonary hypertension

A

lung transplant

66
Q

What is type 1 respiratory failure

A

Low PO2

67
Q

What is type 2 respiratory failure

A

Low PO2 and high PCO2

68
Q

Describe mechanism of T1 resp failure

A

patient begins hyperventilation to reduce PCO2 and increase PO2

69
Q

Why can overoxygenation easily occur

A

the top of the O2 Hb dissociation curve can show large drops in PO2 without large SaO2 drops

70
Q

A patient on O2 should never have SaO2 greater than _____

A

98%

71
Q

what conditions predispose T2 resp failure

A 
COPD
Cystic fibrosis 
Kyphoscoliosis 
MS
Obesity 
Motor neurone
72
Q

Causes of hypercarbia

A

V/Q mismatch
Haldane effect
Hypoxic drive (uncommon)

73
Q

describe how a V/Q mismatch causes hypercarbia

A

oxygenation causes vasodilation of blood vessels in poorly ventilated alveoli. CO2 exits the blood in these alveoli but cannot be expelled so remains in lung

74
Q

describe how the haldane effect causes hypercarbia

A

Oxygenation causes all 4 binding sites of Hb to be oxygenated and liberates CO2, which is released into alveolus and reabsorbed into the blood

75
Q

describe how hypoxic drive causes hypercarbia

A

desensitisation to CO2 chemoreceptors causes oxygen chemoreceptors to be the primary respiratory drive

76
Q

how can you spot an oxygen sensitive patient

A

look for chronic CO2 retention as it signifies poor ventilation

77
Q

Can patients without CO2 retention become acidotic with excess oxygenation

A

Yes!

78
Q

How can hypercarbia be treated

A

increase Vt with NIV

Aim for SaO2 of 88-92%

79
Q

What is tissue hypoxia

A

where tissues are so deprived of oxygen they switch to anaerobic respiration for energy, become acidotic and die

80
Q

what conditions cause hypoxia

A 
circulatory hypoxia 
anaemic hypoxia 
toxic hypoxia 
Hb to met-Hb
alveolar hypoventilation
hypoxaemic hypoxia 
V/Q mismatch
impaired diffusion
81
Q

Ventilation without perfusion is _____

A

dead space

82
Q

perfusion without ventilation is _____

A

shunting

83
Q

What can cause impaired diffusion

A

interstitial thickening

Vasculr dysfunction

84
Q

What causes alveolar hypoventilation

A 
Opiate use 
Kyphoscoliosis
Bronchial obstruction
laryngeal obstruction
obesity
Anaesthesia
85
Q

What causes hypoxaemic hypoxia

A

anaesthetic gases

Low barometric pressure

86
Q

Oxidation of iron in Hb produces ____

A

met-haemoglobin, which cannot bind oxygen

87
Q

Why does anaemic hypoxia cause hypoxaemia

A

iron deficiency so less oxygen can be bound to Hb

88
Q

Circulatory hypoxia causes 2 types of reduction in oxygen delivery. what are they are example

A

Global reduction - heart failure

Local reduction - compartment syndrome, vessel occlusion, oedema

89
Q

How does CO cause toxic hypoxia

A

Co irreversibly binds to Hb at high affinity to prevent oxygen release

90
Q

How does cyanide cause toxic hypoxia and how is it treated

A

inhibits ATP so cells shift to anaerobic respiration, do not take up oxygen so it remains in the blood
Treated with amyl nitrite

91
Q

Where is high flow oxygen beneficial

A

non drained pneumothorax
CO poisoning
Sickle cell crisis
Cluster headaches

MB1: Respiratory (15 decks)

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