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MBBS - Year 2 > Respiratory - Breathlessness: Airflow Obstruction > Flashcards

Respiratory - Breathlessness: Airflow Obstruction Flashcards

1
Q

Overview of mechanical respiration

A

Inspiration & expiration
Gas conduction
Gas transfer
Exhalation

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2
Q

What does inhalation and exhalation require

A

Organised MSK function (diaphragm, IC muscles and rib cages) of the thorax to draw in air and return it to atmosphere
Function of pleural space to enable the expansion of the lung

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3
Q

What kind of things compromise inhalation and exhalation

A

Muscle wasting and neurodegenerative disease

Pleural disease - fibrosis, PTX

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4
Q

Where is the conducting zone

A

From nose to bronchioles

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5
Q

What is found in conducting zone

A

Resp type mucosa

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6
Q

Function of conducting zone

A 
Passage of air from environment to lungs 
Airways protection 
Air humidification and warming 
Smell 
Speech
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7
Q

How does the conducting zone protect the airway

A

Through mechanical and immunological removal of pathogens

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8
Q

How does the conducting zone allow the passage of air

A

Made of cartilage and muscle
Allows rigidity but flexibility of airways
Resistant to compression and collapse
Allows expansion during breathing

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9
Q

Why is the trachea C shaped

A

To allow swallowing

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10
Q

Mechanical (cellular) mechanisms of airway protection by the conducting zone

A

Cilla and mucus (mucocilliary escalator)

Physical barrier between external environment and tissue

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11
Q

Immunological mechanisms of airway protection by the conducting zone

A

Identification and removal of pathogens

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12
Q

Mechanical (anatomical) mechanisms of airway protection by the conducting zone

A

Reflex protection

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13
Q

How does nasal hair protect the airway

A

Remove larger particulate material

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14
Q

Movement of mucocilairy escalator

A

Moves mucus up the airways to pharynx to remove particles

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15
Q

What is cilia action independent of

A

Nervous control

May persist for several hrs after death

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16
Q

What is cilia rate dependent on

A

Temp (falls when colder)

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17
Q

Mucus secreting cells

A

Seromucinous glands within submucosa

Goblet cells within epithelium

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18
Q

Comparison of mucus produced by different cells

A

Seromucinous glands produce more watery, thin mucous whereas the goblet cells and mucous cells produce thicker mucous

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19
Q

When are neuroendocrine cells involved in the growth and envelopment of the airways

A

In utero

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20
Q

MALT

A

Mucosa Associated lymphoid Tissue

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21
Q

When is MALT acquired

A

In response to antigenic stimuli

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22
Q

Why can immunological identification and removal of pathogens occur in the nasopharynx

A

Dense lymphoid tissue

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23
Q

Serous cell secretions that destroy potential pathogens

A 
Lysosome 
Lactoferrin 
Antiprotease 
IgA 
Epithelial peroxidase
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24
Q

Examples of reflex airway closure and removal of foreign bodies

A

Cough reflex
Swallow reflex
Gag reflex

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25
Q

What are pulmonary irritant receptors stimulated by

A

Both mechanical (light touch) or chemical stimuli

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26
Q

Swallow reflex

A

Enables epiglottis to cover larynx to prevent aspiration

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27
Q

What nerve is involved in the cough reflex

A

Vagus nerve

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28
Q

Gag reflex (pharyngeal reflex or laryngeal spasm)

A

Reflex contraction of back of throat

Prevents foreign bodies entering upper wiarways

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29
Q

Stimulus of gag reflex

A

Touch from back of throat, tonsils, uvula, roof of mouth or base of tongue

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30
Q

Mucous involvement in smell

A

Dissolve odours to allow detection

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31
Q

Phases of speech

A

Respiration - lung function
Phonation - laryngeal function
Articulation - vocal tract (upper airways)

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32
Q

Where does the laryngeal cavity extend from

A

The tip of the epiglottis to the lower edge of the cricoid cartilage

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33
Q

False vocal cords vs true vocal cords

A

Resp epithelium vs squamous epithelium

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34
Q

Why do the true vocal cords adjust to a more robust epithelium

A

True vocal cords are subject to more mechanical trauma from phonation

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35
Q

Barriers to tumour spread in the larynx

A

Intrinsic and extrinsic connective tissue bands

Thyroid and cricoid cartilage

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36
Q

Intrinsic connective tissue bands in the larynx

A

Quadrangular membrane

Conus elastics

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37
Q

Extrinsic connective tissue bands in the larynx

A

Thyroid membrane

Cricothyroid membrane

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38
Q

What is the interstitium

A

Lungs connective tissue scaffolding

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39
Q

What does interstitial comprise of

A 
Collagen 
Elastin fibres 
Fibroblasts 
Myofibroblasts 
Pericytes 
Histiocytes 
Mast cells 
Neuroendocrine cells
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40
Q

Where are Clara cells (bronchiolar exocrine cells) most numerous in

A

Terminal bronchioles

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41
Q

What are Clara cells important in modulating

A

Bronchiolar infl

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42
Q

What can Clara cells secrete

A

Endothelin - powerful broncho and vasoconstrictor

Protease inhibitors

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43
Q

Cells found in alveoli

A 
Type 1 pneumocytes
Type 2 pneumocytes 
Alveolar macrophages 
Pores of Kohn 
Lambert's canal
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44
Q

Pores of Kohn

A

Small gaps between alveoli

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45
Q

Lambert’s canal

A

Tubular connections which connect terminal and resp bronchioles w. adjacent peri bronchial alveoli

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46
Q

Nuclei in pneumoncytes

A

Type 1 - flattened

Type 2 - larger, darker

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47
Q

What do Type 1 pneumocytes do

A

Thin for increased gas exchange

Forms a barrier to prevent fluid loss

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48
Q

What do Type 2 penumocytes do

A

Surfactant protection - reduced surface tension in order to facilitate lung expansion

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49
Q

Pulmonary vasculature

A 
Pulmonary arteries 
Pulmonary capillaries 
Pulmonary veins 
Bronchial arteries 
Lymphatics
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50
Q

Where do pulmonary veins tend to be found

A

In the interlobar septa

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51
Q

Blood supply of lungs

A

Bronchial arteries arising from systemic circulation

Pulmonary arteries

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52
Q

What is the pleura

A

A pair of serous membrane lining the thoracic wall (parietal) and lungs (visceral)

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53
Q

Structure of pleura

A

Meosthelial cell lining

Connective tissue sub mesothelium

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54
Q

Elastin layer variation in visceral and parietal layers of pleura

A

Visceral layer is double and thicker - account for lung movement
Parietal - single layer and thinner

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55
Q

What is the most readily preventable cause of death in humans

A

Smoking

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56
Q

Which components of tobacco have a carcinogenic effect

A

Tar
Polycyclic aromatic hydrocarbons
Nitrosamine

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57
Q

What causes the a/c effects of smoking

A

Nicotine - increase in HR and BP, CO and elevation of cardiac contractility

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58
Q

Effects of smoking in resp system

A

Mucosal irritant —> bronchitis & RBILD/ DIP
Destruction of alveolar walls —> emphysema
Carcinogenesis –> lung cancer

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59
Q

RBILD

A

Resp bronchial ILD

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60
Q

DIP

A

Desquamative interstitial pneumonia

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61
Q

What diseases are included in COPD

A

C/c bronchitis
Emphysema
(a/c obstructive bronchiolitis but diff pathology)

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62
Q

Main risk factor of COPD

A

Smoking - 80% of cases are smokers

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63
Q

Oher risk factors for COPD

A

Environmental/ occupational pollution
Airway hyper-responsiveness
Genetic factors

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64
Q

Zones affected in COPD

A

Conducting zone

Gas exchange zone

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65
Q

How is the conducting zone affected in COPD

A

C/c bronchitis - hypersecretory
Obstructive bronchiolitis - obstructive

These pathological processes may lead to cyanosis

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66
Q

How are large airways affected in c/c bronchitis

A

Mucus hyper secretion

Infl

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67
Q

How are small airways affected in c/c bronchitis

A

Peribronchiolar fibrosis
Airway obstruction - infl thickening
Goblet cell hyperplasia
Loss of Clara cells

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68
Q

How is the gas exchange zone affected in COPD

A

Emphysema - loss of elastic recoil in alveoli

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69
Q

Symptoms of a blue bloater (c/c bronchitis)

A 
C/c productive cough 
Purulent sputum 
Haemoptysis 
Cyanosis (due to hypoxia)
Peripheral oedema 
Crackles, wheeze
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70
Q

Complications of c/c bronchitis

A 
Pulmonary HTN 
Cor pulmonale (form c/c pulmonary HTN)
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71
Q

Symptoms of a pink puffer (emphysema)

A 
Dyspnoea 
Minimal cough 
Pink skin, pursed lip breathing 
Accessory muscle use 
Cachexia 
Hyperinflation (barrel chest)
Tachypnoea
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72
Q

Complications of emphysema

A

PTX (due to bullae)

Wt loss

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73
Q

Change in mucin type in c/c bronchitis

A

Thicker, more viscous

Increased seromucinous glands

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74
Q

Change to goblet cells in c/c bronchitis

A

Hyperplasia - reduced capacity to remove mucus (increased susceptibility to infection)

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75
Q

Emphysema

A

Irreversible abnormal increase in the size of air spaces beyond the terminal bronchioles w/ destruction of air space walls w/ out obvious fibrosis

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76
Q

What do proteases cause

A

Tissue degeneration

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77
Q

What does elastase do

A

Break down elastin

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78
Q

Why must there be a balance between proteases and antiproteases

A

Allows any tissue damage which may have occurred to be removed and repaired in a controlled manner whilst limiting damage to surrounding tissue

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79
Q

Pathogenesis of emphysema

A

Smoking causes antiprotease inactivation and causes uncontrolled activity of proteases –> destruction of elastin causes alveoli to become brittle preventing deflation on expiration

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80
Q

Process of emphysema development

A

Harmful particles from smoking trapped in alveoli
Infl response triggered
Infl chemicals dissolve alveolar septum
Large air cavity filled w/ carbon deposits formed

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81
Q

Patterns of emphysema

A

Centrilobular
Paracinar
Paraseptal
Irregular

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82
Q

Centrilobular emphysema

A

Central/ proximal alveolar unit involved, distal alveoli spared
Most commonly seen in smokers
More severe in upper lobes

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83
Q

Paracinar emphysema

A

Whole alveolar unit involved
More commonly in lower lobes
Associated w/ alpha1-antitrypsin deficiency

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84
Q

Paraspetal emphysema

A

Proximal alveolar unit normal, emphysematous change more evident near the pleura, along septa and margins of lobules
Seen in upper half of lungs

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85
Q

Emphysema histology

A

Airspace enlargement
Fractured alveolar walls
+/- infl

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86
Q

Smoking related ILD

A

Resp bronchiolitis
Resp bronchiolitis associated ILD
DIP

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87
Q

Resp bronchiolotis vs resp bronchiolitis associated ILD

A

Pts may not be symptomatic w/ resp bronchiolitis and wont always develop RBILD
Pts are symptomatic w/ resp bronchiolitis associated ILD - persistent cough and/ or mild breathless

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88
Q

Lung function test in resp bronchiolitis associated ILD

A

Normal or mildly restrictive defect

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89
Q

Mx of resp bronchiolitis associated ILD

A

Resolves completely on quitting smoking

May require corticosteroids

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90
Q

Typical pts of DIP

A

Middle-aged cigarette smokers who complain of breathlessness and cough of insidious onset

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91
Q

Prognosis of DIP

A

Responds well to steroid and smoking cessation but can progress to interstitial fibrosis

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92
Q

Effects of tobacco in epthelial lining of resp tract

A

Metaplasia
Dysplasia
Carcinogenesis

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93
Q

Metaplasia in the resp tract

A

Noxious tobacco smoke not tolerated by columnar epithelium

Squamous epithelium more resistant to thermal and chemical damage

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94
Q

Consequences of metaplasia in resp tract

A

Reduced function

Increased propensity for malignant transformation

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95
Q

Is metaplasia in the resp tract reversible

A

Yes on smoking cessation

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96
Q

What is squamous dysplasia in the resp tract a precursor lesion for

A

Squamous cell carcinomas

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97
Q

What is squamous dysplasia in the resp tract characterised by

A

The presence of disordered squamous epithelium w/ loss of pleomorphism

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98
Q

Most frequently diagnosed major cancer in the world

A

Lung cancer

Also most common cause of cancer mortality worldwide

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99
Q

What % of lung cancers are in active smokers or those who’ve stopped recently

A

80%

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100
Q

What age is lung cancer most common in

A

40 and 70yrs w/ peak incidence in 50s/60s

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101
Q

Prognosis of lung cancer

A

Poor - survival <50%

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102
Q

Other factors affecting lung cancer

A 
Industrial exposure - asbestos, uranium , arsenic, nickel 
Radiation 
Air pollution 
Molecular genetics 
EGFR mutations
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103
Q

Types of lung tumours

A

90-95% are carcinomas
5% carcinomas
2% mesenchymal and other types

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104
Q

Classical features of squamous cell carcinomas

A

Malignant cells w/ keratinisation and intercellular bridges

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105
Q

Pathological feature for lung adenocarcinomas

A

Gland or duct formation w/ mucin

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106
Q

Lung tumours of seromucinous glands

A

Salivary type tumours such as mucoepidermoid carcinoma and adenoids cystic carcinoma

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107
Q

Lung tumours of blood vessels

A

Haemoangiomas

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108
Q

Lung tumours of mesothelium

A

Mesothelioma

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109
Q

Determining if a lung mass is a metastasis

A

Lung is a common site

Can see single lesions but often multiple, well circumscribed nodules

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110
Q

Common cancers that may metastasise to lung

A 
Colorectal 
Renal 
Breast 
Melanoma 
Direct spread from oesophagus
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111
Q

Dx of lung cancer

A

Bronchial washings and brushings
EBUS TBNA
Lung biopsy
Bronchial biopsy

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112
Q

EBUS TBNA

A

Endobronchial ultrasound guided transbronchial (fine) needle aspirations

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113
Q

Reporting of lung excisions - providing prognostic info

A 
Type of tumour 
Size 
Margins 
Pleural involvement 
Vascular invasion 
Involvement of adjacent structures e.g. hearts, pericardium, diaphragm 
Lymph node involvement
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114
Q

Types of air movement in lung

A

Convection

Diffusion

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115
Q

What part of the conducting zone is most susceptible to collapse during expiration

A

Bronchioles and alveolar ducts

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116
Q

What does the pulmonary arteries carry

A

Deoxygenated mixed venous blood from RV to alveoli of lungs

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117
Q

Where does blood drain from the lungs

A

Pulmonary vein and azygous vein

Minority of blood in bronchial veins

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118
Q

Systems innervating resp tract

A

Cholinergic
Adrenergic
Peptidergic

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119
Q

Cholinergic effect on smooth muscle of bronchioles

A

Constrict

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120
Q

Adrenergic effect on smooth muscle of bronchioles

A

Dilate

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121
Q

Petidergic effect on smooth muscle of bronchioles

A

Dilate

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122
Q

Spirometry

A

Method for studying pulmonary ventilation

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123
Q

Tidal volume

A

Volume of air inspired or expired w/ each normal breath (500ml)

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124
Q

Inspiratory reserve volume

A

Extra volume of air that can be inspired over and over normal TV (2500ml)

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125
Q

Expiratory reserve volume

A

Extra volume of air that can be expired by forceful expiration after end of normal TV (1100ml)

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126
Q

Residual volume

A

Volume of air remaining in lungs after most forceful expiration (1200ml)

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127
Q

Calculating total lung capacity

A

IRV + TV + ERV + RV

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128
Q

Factors affecting IRV

A 
Current lung volume 
Lung compliance 
Muscle strength 
Comfort 
Flexibility of the skeleton 
Posture
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129
Q

Lung compliance

A

Measurement of lung expandability

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130
Q

Does all the air that is breathed in reach gas exchange area

A

No - some fills resp passages

Dead air space - 150mls

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131
Q

Intrapulmonary pressure

A

Pressure in alveoli, which rises and falls during respiration but always equalises w/ atmospheric pressure

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132
Q

Muscles that arise from the rib cage

A

External IC
Sternocleoimastoid
Anterior serrati (lift many ribs)
Scaleni (lift 1st 2 ribs)

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133
Q

Muscles moving lower rib cage

A

Abdominal recti

Internal IC

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134
Q

In which ways can lungs be expanded and contracted

A

Downward (inspiration) and upward (expiration) movement of diaphragm
Elevation and depression of the ribs to increase the diameter of chest cavity

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135
Q

Transpulmonary pressure

A

Pressure difference between alveoli and pleura

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136
Q

What is lung compliance determined by

A

Elastic force of the lung tissue itself

Elastic fibres caused by surface tension of fluid lining alveoli

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137
Q

Lung compliance in pulmonary fibrosis (restrictive lung disease)

A

Decreased –> smaller changes in lung volume for small changes in trans pulmonary pressure

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138
Q

How does decreased lung compliance affect pts breathing

A

More shallowly and rapidly

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139
Q

How does decreased lung compliance affect spirometry measurements

A

Decreases seen in RV, FRC, TLC

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140
Q

How does lung compliance change in emphysema

A

Increases –> larger changes in lung volume for small changes in trans pulmonary pressures

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141
Q

How does increased lung compliance affect pts breathing

A

Pts breathe more slowly and deeply

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142
Q

How does increased lung compliance affect spirometry measurements

A

Increases seen in RC, FRC, TLC

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143
Q

Lung compliance in c/c bronchitis

A

Normal but will still see increases in RV, FRC and TLC

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144
Q

If 2 alveoli are connected but have diff diameters, where will the air flow

A

From small to large

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145
Q

Alveolar macrophages and surfactant

A

Help degrade surfactant

Type II pneumocytes take up rest and recycle or destroy it

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146
Q

Role of lung surfactant

A

Increased lung compliance so easier to inflate
Reduces pressure and fluid accumulation in alveoli
Helps keep alveoli’s size relatively uniform during resp cycle

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147
Q

How does airway resistance change w/ disease

A

Increases in disease

At any given lung volume, resistance in COPD is higher

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148
Q

What is the glottis formed by

A

Vocal cords (folds)

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149
Q

How are food and saliva prevented from entering resp tract

A

Sphinchteric action of vocal chords and epiglottis

150
Q

What is the pharynx nerve supply

A

Nerves from pharyngeal plexus

151
Q

Innervation of laryngeal muscles

A

Recurrent laryngeal nerve (except cricothyroid)

152
Q

Which nerve provides sensation to the glottis and sub glottis

A

Recurrent laryngeal nerve

153
Q

Which nerve provides sensation to supra glottis

A

Superior laryngeal nerve

154
Q

What is the larynx adapted to act as in phonation

A

A vibrator

Vibrating element is vocal folds (vocal cords)

155
Q

Position of vocal cords during normal breathing

156
Q

What happens to the vocal cords during phonation

A

Cords move together so passage of air between them causes vibrations

157
Q

What is our pitch determined by

A

Degree of stretch of cords

158
Q

Which organs of articulation allows us to change sound

A

Lips
Tongue
Soft palate

159
Q

Which organs act as resonators

A

Mouth
Nose and associated nasal sinuses
Pharynx
Chest cavity

160
Q

Allergens responsible for asthma

A 
Pets 
Eosinophils 
Dust mites 
Fungus
Pollen
161
Q

Mediators of asthma attack

A

B lymphocyte produces IgE which causes release of histamine, leukotriene, bradykinins, prostaglandins which cause immediate allergic symptoms

162
Q

What happens to the airways in asthma

A

Airways get inflamed and constricted

163
Q

Pathological changes in asthma

A 
Thickening of basement membrane 
Mucous gland hyperplasia 
Desquamation of epithelium 
Hypertrophy of smooth muscle 
Oedema of mucosa and submucosa - due to infiltration 
Mucosal plug
164
Q

Symptoms seen in asthma

A

Wheeze
Cough
Breathlessness

165
Q

Things to look for in the hx of an asthma pt

A

Fhx of atopy
Samter’s triad
Occupation (work related/ exacerbated asthma)

166
Q

What might come up in Fhx of atopy for asthma pts

A

Eczema
Allergic rhinitis
Nasal polyps
Aspirin intolerance

167
Q

Samter’s triad

A

Asthma
Nasal polyps
Aspirin sensitivity/ intolerance

168
Q

Why is occupation important for asthma pts

A

Could be cause of late onset asthma

169
Q

Reversibility testing

A

Way of measuring if pt has asthma or not
Ask pt to stop taking all med and take an FEV1 measurement then give them 2 puffs of salbutamol through a spacer and see if FEV1 improves
FEV1 should improve by 400ml or 12%

170
Q

What is usually used for reversibility testing

A 
Short-acting beta 2 agonists or ICS for longer reversibility tests (6-8 weeks)
Oral steroids (30mg pred for 2/52)
171
Q

How can we measure airway infl

A

Sputum differential counts

Exhaled nitric oxide (FeNO) > 40

172
Q

Allergy testing for asthma

A

Skin prick test
Blood - RAST Total IgE & IgA for seasonal and perennial allergens
Blood eos > 1

173
Q

Measuring disease control in asthma

A

RCP
Asthma Control Questionnaire (ACQ)
Asthma Control Test (ACT)
Mini-asthma QoL Questionnaire (AQLQ)

174
Q

Things to consider in difficult asthma

A

If the dx is really asthma?
Pts adherence

If both these things are fine, you must increase therapy in a step wise fashion

175
Q

Ddx for asthma

A 
Vocal cord dysfunction (paradoxical vocal cord movement)
Dysfunctional breathing (hyperventilation syndrome)
GORD (reflux related cough/ breathelessness)
176
Q

Types of bronchodilators

A

SABA
LABA
LAMA

177
Q

SABA’s

A

Short acting beta 2 agonists

178
Q

Examples of SABAs

A

Salbutomol

Terbutaline

179
Q

LABA

A

Long acting beta 2 agonists

180
Q

Examples of LABAs

A

Salmeterol
Formoterol
Vilanterol

181
Q

LAMA’s

A

Long acting muscarinic antagonist

182
Q

Examples of a LAMA

A

Tiotropium

183
Q

How should drug powder inhalers be taken

A

Fast and furious

184
Q

ICS used in asthma mx

A

Beclomethasone
Fluticasone
Budesonide
Ciclesonide

185
Q

Aetiology of asthma

A

Asthma gene complexes - ADAM 33, DPP10

Hygiene hypothesis

186
Q

Epidemiology of COPD

A

3rd leading cause off death worldwide

Worldwide prevalence of 10.1%

187
Q

What is COPD characterised by

A

C/c resp Symptoms
Structural pulmonary abnormalities (airway and/or alveolar abnormalities)
Lung function impairment (primarily airflow limitation that is poorly reversible)

188
Q

Host risk factors for COPD

A

Genetic

Lung growth, low BW, age

189
Q

Risk factors for COPD - exposure

A 
Tobacco smoke 
Biomass fuels, open fires 
Occupational dusts and exposures 
C/c uncontrolled asthma 
Lower socioeconomic status
190
Q

Dx of COPD

A

Hx and symptoms e.g. SOB/ wheeze, c/c cough, sputum production
Possible risk factors
Spirometry

191
Q

Measurements in spirometry

A 
FEV1
FVC
FEV1/ FVC ratio 
PEFR 
FEF 25%-75%
192
Q

FEV1

A

Forced expired volume in 1 seconds

193
Q

FVC

A

Forced vital capacity

194
Q

PEFR

A

Peak expiratory flow rate

195
Q

FEF 25-75%

A

Forced expiratory flow between 25-75% of the vital capacity

196
Q

How does spirometry measures change according to height

A

Tall people have large lungs

197
Q

How does spiromtry measures change according to age

A

Resp function decline w/ age

198
Q

How do spirometry measures change w/ sex

A

Lung volumes smaller in females

199
Q

How does spirometry measures change w/ race

A

Black people and asians have smaller lung volumes (-12%)

200
Q

How does spirometry measures change w/ posture

A

Little difference between sitting and standing

Reduced in supine

201
Q

How long to wait when giving a SABA for bronchodilatory reversibility testing

A

20 mins before retesting

202
Q

How long to wait when giving a LABA for bronchodilatory reversibility testing

A

2hrs before retesting

203
Q

Criteria for GOLD 1

A

FEV1 > 80% predicted

204
Q

Criteria for GOLD 2

A

50% < FEV1 < 80% predicted

205
Q

Criteria for GOLD 3

A

30% < FEV1 < 50% predicted

206
Q

Criteria for GOLD 4

A

FEV1 < 30% predicted

207
Q

Key indicators for a dx of COPD

A 
Dyspnoea 
C/c cough 
C/c sputum production 
Recurrent LRTI 
Hx of risk factors 
Fhx of COPD
208
Q

Dyspnoea in COPD

A

Progressive over time
Characteristically worse w/ exercise
Persistent

209
Q

C/c cough in COPD

A

May be intermittent and may be unproductive

Recurrent wheeze

210
Q

Intrathoracic causes of c/c cough

A 
Asthma 
Lung cancer 
TB 
Bronchiectasis 
Left HF 
ILD 
CF
Idiopathic cough
211
Q

Extrathoracic causes of c/c cough

A

C/c allergic rhinitis
PND Syndrome
GORD
Medication e.g. ACEi

212
Q

What should be looked for in initial assessment of COPD pts

A 
FEV1 - GOLD 1-4
Exacerbation hx 
Smoking 
Alpha1-antitrypsin 
Comorbidities
213
Q

Initial mx of COPD pts

A 
Smoking cessation 
Vaccination 
Active lifestyle and exercise 
Initial pharmacotherapy 
Self-mx education 
Mnage comorbidities
214
Q

Self-mx education for cOPD

A

Risk factor mx
Inhaler technique
Breathlessness
Written action plan

215
Q

How do we aim to reduce symptoms in stable COPD

A

By relieving symptoms
Improving exercise tolerance
Improving health status

216
Q

How do we aim to reduce risk in stable COPD

A

Prevent disease progression
Prevent and treat exacerbations
Reduce mortality

217
Q

What needs to be taken into account for mx of COPD

A

Degree of airflow obstruction
Exacerbation
Symptoms

218
Q

Initial pharmacological treatment of COPD for those w/ no exacerbation hx

A

SABA or LAMA

LABA or LAMA if CAT < 10

219
Q

When would you consider giving a LAMA and LABA for COPD

A

If highly symptomatic

220
Q

When would you consider giving ICS and LABA for COPD

A

If Eos > 100

221
Q

Effects of LABA/ LAMA combinations in COPD pts

A

Increases FEV1
Reduces symptoms
Reduces exacerbation rates

222
Q

Non-pharma mx of COPD

A 
Smoking cessation 
Pulmonary rehab 
Nutrition incl vit D supplementation 
Vaccinations 
Candidate for long-term oxygen therapy
223
Q

What is an exacerbation of COPD defined by

A

Increase in dyspnoea
Increase in cough
Increase in sputum volume/ purulence
WITH or WITHOUT symptoms of an URTI

224
Q

What % of COPD exacerbations are bacterial

A

30-50% - H.influenza, strep pneumonia

225
Q

What % of COPD exacerbations are viral

A

30% - rhinovirus, influenza

226
Q

Mx of a/c exacerbations of COPD

A

Regular nebulisers - bronchodilators
Abx
Steroids (30mg pred for 5/7 - 7/7)
Consider need for non-invasive ventilation in more severe exacerbations

227
Q

When would you give abx for a/c exacerbations of COPD

A

Usually for pts w/ hx of more purulent sputum, otherwise only if consolidation on CXR or clinical signs of pneumonia

228
Q

Drug treatments used in resp med

A 
Bronchodilators - anti-chilergics, beta-agonists
Corticosteroids 
Leukotriene receptor antagonists 
Cromones
Monoclonal antibodies - asthma 
Methylxanthines 
Phosphodiesterase inhibitors 
Mucolytics
229
Q

SE of beta-2 agonists

A

Tremor
Tachycardia. palpitations
Decreased K

230
Q

Ultra long-acting B2 agonists

A

Indacaterol (Onbrez) - COPD
Vilanterol
Olodaterol

231
Q

Examples of short acting anticholinergics

A

Ipratropium

232
Q

Examples of long acting anticholinergics

A

Tiotropium
Glycopyrronium
Alidinium

233
Q

Role of administration for anticholinergics

234
Q

Indications for Anticholinergics

A

COPD

Severe asthma

235
Q

Beneficial effects of corticosteroids in resp system

A

Reduce infl mediators
Increases anti-infl mediators
Reduce eosinophils, macrophages, lymphocytes

236
Q

Examples of combination inhalers

A 
Seretide 
Symbicort 
Fostair
Relval lepta 
Anoro elllipta
237
Q

Components of Symbicort

A

Budesonide & formoterol

238
Q

Components of Fostair

A

Beclomethaosne & formoterol

239
Q

Components of Flutiform

A

Fluticasone & formaterol

240
Q

Examples of leukrotriene receptor antagonists

A

Montekulast
Zafirkulast
Pranlukast

241
Q

Indication for leukotriene inhibitors

A

Aspirin sensitive asthma

242
Q

Infl effects of leukotrienes in the airways

A

Increased mucus secretion
Epithelial cell damage
Eosinophil recruitment
Increased release of bradykinins

243
Q

What are cromones

A

Mast cell stabilisers

244
Q

Administration of cromones

A

Inhaled

QDS

245
Q

Which group of people are cromones usually given to

246
Q

Omalizumab

A

Monoclonal antibody - binds circulating IgE

Given in anaphylaxis and uncontrolled allergic asthma

247
Q

Mepolizumab

A

Monoclonal antibody - blocks IL-5

Reduces exacerbations but no change in symptoms

248
Q

Administration of mepolizumab

A

4 weekly injections

249
Q

Administration of Xanthines

A

Oral or IV

250
Q

Examples of xanthines

A

Theophylline

Aminophylline

251
Q

Effects of xanthines

A

Inhibit phosphodiesterase

Have bronchodilatory and anti-infl effects

252
Q

SE of xanthines

A

Nausea

Drug interactions - low therapeutic range

253
Q

PDE4 inhibitors

A

New gen “theophyllines”

254
Q

Admin of PDE4 inhibitors

255
Q

Example of PDE4 inhibitors

A

Roflumilast

256
Q

SE of PDE4 inhibitors

257
Q

Examples of mucolytics

A

Carbocysteine
Erdosteine
Mecysteine

258
Q

Administration of mucolytics

259
Q

Indication for mucolytics

A

Pts w/ c/c bronchitis

260
Q

Asthma treatment cascade

A

Allergen/ irritant exposure – avoidance
Infl – anti-infl
Infl mediator please - mediator blockers
Bronchoconstriction - bronchodilators

261
Q

Inh vs po drugs

A

Inhaled drug delivers drugs where required
Reduced systemic exposure
Reduced systemic adverse effects

262
Q

Types of inhalers - structural

A

Nebuliser
Metered dose inhaler
Dry powder inhaler

263
Q

Advantages of spacers

A

Helps co-ordination
Less oropharyngeal deposition
Improved lung delivery
Comparable efficacy to nebulisers

264
Q

Disadvantages of spacers

A

Size
Cost
Assembling - older people
Electrostatic - increased delivery in primed or used spacers

265
Q

Phases of coughing

A

Irritation
Inspiration
Compression
Expulsion

266
Q

Presentation of influenza

A 
Fever 
Non-productive cough 
Myalgia 
Headaches 
Malaise 
Sore throat 
Rhinitis
267
Q

Mx of influenza

A 
Analgesia 
Antipyretics 
Fluids 
O2
Antivirals 
Resp isolation
268
Q

What does alpha-antitrypsin do

A

Neutralises proteases

269
Q

What properties do lysosomes and lactoferrin

A

Bactericidal

270
Q

Examples of URTI

A 
Pharyngitis 
A/c laryngitis
Bacterial epiglottis 
Sinusitis 
Common cold 
Influenza 
Croup 
Pertussis
271
Q

Pharyngitts

A

Inflammation of the nasopharyngeal mucosa with reactive inflammation of the lymph nodes and tonsils.

272
Q

Non infective causes of pharyngitis

A

Allergic rhinitis

Irritative pharyngitis

273
Q

Complications of pharyngitis

A

Abcess formation and tonsil hypertrophy = airway obstruction
A/c rheumatic fever
ReA

274
Q

Features of pharyngitis

A 
Sore throat - worse when swallowing 
Neck pain and swelling 
Fever 
Headache 
Swollen tonsils
275
Q

Symptoms in bacterial vs viral pharyngitis

A

Bacterial - sudden onset, tonsils exudes and fever
Viral - cough, nasal congestion, coryza, oral ulcers
Symptoms resolve in 3-5days in viral and 5-7 days in bacterial

276
Q

Symptoms of a/c laryngitis

A

Flu like: fever, cough, malaise, enlarged lymph nodes, Stridor, hoarseness, pain.

277
Q

Dx of laryngitis

A

Laryngoscopy shows swollen, red vocal folds
Biopsy
Blood culture

278
Q

Mx of laryngitis

A

Analgesics
NSAIDs
Abx
Voice rest

279
Q

What is bacterial epiglottis caused by

A

Caused by inflammatory cell accumulation = airway narrows = airway obstruction
Haemophilus influenzae, Streptococcus pneumoniae, Staph aureus.

280
Q

Complications of bacterial epiglottis

A

Airway obstruction,
Oropharyngeal secretion aspiration
Cardiopulmonary arrest
Death may occur due to occluded airway

281
Q

Features of bacterial epiglottis

A 
Dysphagia
Distress
Tachypnoea
Cyanosis
Sore throat
Fever
Individual refuses to lie down
282
Q

Ix for bacterial epiglottis

A

Laryngoscopy: swollen, red epiglottis
X-ray: shadow of enlarged epiglottis
Lab results: Increased WBC, CRP, Culture.

283
Q

Risk factors for sinusitis

A

Allergies
Dental infections spreading to maxillary sinus
Tumours
Genetic disorders (Kartagener’s CF)

284
Q

Complications of sinusitis

A

Meningitis
Cavernous sinus thrombosis
Abcess

285
Q

Features of bacterial sinusitis

A 
Fever
Headache 
Pain when leaning forward 
Voice change 
Lasts > 10 days
286
Q

Features of viral sinusitis

A 
Self limiting 
Painful sinus on leaning forward 
Discharge
Lasts <10 days 
PND irritate larynx and causes cough
287
Q

Croup

A

Laryngobronchitis

Usually seen in children

288
Q

Viruses causing croup

A 
Parainfluenza virus 
RSV 
Influenza A and B 
Rhinoviruses 
Adenovirus
Measles
289
Q

Px of croup

A

Child develops harsh, barking cough w/ URTI which may progress to stridor

290
Q

Mx of croup

A

Often no treatment required but some children develop more severe LRTI —> intubation and ventilation
Oral pred can be used

291
Q

Duration of acute cough

292
Q

Duration of subacute cough

A

3/52 - 8/52

293
Q

Duration of c/c cough

294
Q

Diurnal variation of asthma symptoms

A

Worse at night/ early morning

295
Q

Stridor vs wheeze

A

Stridor comes from upper airway (obstruction) and is heard on inspiration
Wheeze comes from lower airways and is heard on expiration

296
Q

Examination findings for asthma

A 
Use of accessory muscles 
Tracheal tug 
Expiratory wheeze 
High RR
Tremor, tachy (salbutamol)
Subcostal and IC recession
297
Q

How to take a peak flow measurement

A

Ask pt to stand up
Take a deep breathe in and out
Take another deep breath in
Purse lips around peak flow meter and breathe out as fast as they can

298
Q

CXR findings of COPD

A 
Extra long lungs 
Flattened diaphragm (hyperinflation)
Prominent vascular markings
299
Q

Stages of lung maturation and development

A

Pseudoglandular (5-17 weeks)
Canalicular (16-25 weeks)
Saccular (terminal sac) (24 weeks to birth)
Alveolar (late foetal period to ~8yrs)

300
Q

Clinical problems w/ lung surfactant production

A 
Adequate amounts of surfactant not produced until ~32nd week 
Premature infants (up to prenatal 7 months) – respiratory distress syndrome (RDS) = insufficient surfactant
Resulting in increased surface tension = collapse of alveoli (atelectasis)
301
Q

Types of movement of air in resp system

A

Conduction in larger airways

Diffusion in smaller airways

302
Q

Calculating minute ventilation

A

Tidal volume x RR

303
Q

Alveolar ventilation

A

(Tidal volume - dead volume) x RR

Determine O2 and CO2 conc in blood

304
Q

Functional residual capacity

A

Volume of air already in lung before inspiration

305
Q

Vital capacity

A

Air that can be drawn in from residual volume

306
Q

Hysteresis

A

Difference in compliance between inspiration and expiration

If lungs fill w/ water, the gradient increases as lungs will be more compliant and hysteresis disappears

307
Q

What happens when the vagus nerve is stimulated

A

Bronchoconstriction - parasympathetic fibres

308
Q

What does sympathetic innervation of beta2 adrenergic receptors cause in smooth muscle

A

Bronchodilation

309
Q

Oxygen content vs oxygen saturation

A

Content - amount of O2 carried by 1L of blood

Sat - % of O2 carrying sites on Hb occupied by O2 (should be 100%)

310
Q

Drugs exacerbating asthma

311
Q

What is the physiological mechanism of breathlessness in COP

A

Increased Residual Volume - all the air cannot be expelled due to hyperinflation and gas trapping

312
Q

How does Total Lung Capacity change in emphysema

313
Q

How does Forced Vital Capacity change in lung diseases

A

Normal COPD

Decreased in ILD

314
Q

How many measurements should be taken on a peak flow meter

315
Q

Peak flow diary

A

Usually kept for 2+ weeks
Aim to take measurements QDS
Look for diurnal variation

316
Q

Calculating PEF variability

A

(PEFmax - PEFmin)/ (1/2 (PEFmax + PEFmin))

Variability > 20% - asthma

317
Q

FEV1/FVC ration in obstructive lung disease

318
Q

Why is Asthma worse at night

A

Low cortisol at night

319
Q

Asthma mx algorithm

A

SABA - reliever and low dose ICS (preventer)
Add LABA to ICS (combi inhaler)
Increase ICS to medium dose or add LTRA

320
Q

When are LABA/ LAMA inhalers most used

321
Q

Characteristics of moderate a/c asthma

A

Increasing symptoms

Increasing PEF >50-75% best or predicted

322
Q

Characteristics of a/c severe asthma

A 
Any one of:
PEF 33-50% best or predicted 
RR > 25 
HR > 110
Inability to complete sentences in one breath
323
Q

Clinical signs of life-threatening asthma

A 
Altered conscious level 
Exhaustion 
Arrhythmia 
Hypotension 
Cyanosis 
Silent chest 
Poor resp effort
324
Q

Measurements in life-threatening asthma

A

PEF < 33% best predicted
PaO2 < 92%
Normal PaCO2 (4.6-6.0kPa)

325
Q

Characteristics of near-fatal asthma

A

Raised PaCO2 and/or requiring mechanical ventilation

326
Q

Medications for a/c asthma

A

SABA (nebuliser) 5mg - 2 puffs QDS as well as prn
Ipratropium 500 microgram QDS
Corticosteroids (IV or po)
Oxygen (if sats below 94%)

Continue w/ usual asthma drugs

327
Q

Corticosteroid dosage for a/c asthma

A 
40mg Pred (give in the AM) - 0.5/kg of bw 
IV hydrocortisone 100mg
328
Q

FEV1/ FVC ratio in restrictive lung disease

329
Q

Example of primary concordance

A

Pt doesn’t redeem prescription

330
Q

Example of secondary concordance

A

Pt not taking medication as prescribed

331
Q

What does adherence and compliance look at

A

Pts behaviour and attitudes

332
Q

Concordance

A

Process entertaining pt views on medication-taking; agreement btwn patient + clinician

333
Q

Triggers for asthma

A 
Viral infections 
SMoking 
Pets 
Occupation 
GORD 
Drugs - NSAIDs and BB
OSA 
Pregnancy 
Anapylaxis
334
Q

How do we quantify breathlessness

A

MRC dyspnoea scale
Grades 1 - 5
Not troubled by breathlessness except on strenuous exercise to too breathless to leave the house/ breathless when dressing

335
Q

When is it suggested to measure alpha1 antitrypsin in pts

A

Younger pts w/ COPD (<40)

336
Q

Why might you see elevated Hb (polycythemia) in COPD

A

Hypoxia stimulated formation of erythropoietin in kidneys

337
Q

Inhaled therapies for COPD

A

SABA or SAMA
LABA + LAMA or LABA + ICS (if features suggest steroid responsiveness)
LABA + LAMA + ICS

338
Q

What is most likely to kill COPD pts

A

Hypoxia (resp failure)

339
Q

Type 1 resp failure

A

Hypoxaemia only

Treat w/ O2

340
Q

Type 2 resp failure

A

Hypoxaemia AND hypercapnia

Treat w/ O2 and NIV

341
Q

Why does HCO3 rise in resp failure

A

Attempted compensation by kidneys

342
Q

Contraindications of lung function tests

A 
Pts who are acutely unwell 
PTX (until 6/52 recovery)
Infection 
Haemoptysis 
MI/PE 
Major surgery
343
Q

TLCO

A

Measure of gas transfer

344
Q

When is TLCO < 80%

345
Q

How does ILD affect TLC

A

Reduces it

346
Q

Conditions w/ an obstructive picture on spirometer

A

Asthma
COPD
CF
Bronchiectasis

347
Q

When do we see normal Spiro readings and low TLCO

A

Early ILD

Pulmonary arterial HTN (PAH)

348
Q

Acidotic ABG

349
Q

Alkalotic ABG

350
Q

Metabolic acidosis on ABG

A

CO2 < 4.5 (low)

Bicarb < 22 (low)

351
Q

Resp acidosis on ABG

A

CO2 > 6.0 (high)

Bicarb > 26 (high)

352
Q

Resp alkalosis on ABG

A

CO2 < 4.5 (low)

BIcarb < 22 (low)

353
Q

Metabolic alkalosis on ABG

A

CO2 > 6.0 (high)

Bicarb > 26 (high)

354
Q

Causes of resp acidosis

A

Alveolar hyperventilation
Skeletal - kyphoscoliosis
Critical airway obstruction - asthma, COPD
Mechanical/ neuromuscular - musculodystrophy. myasthenia gravis

355
Q

Causes of metabolic acidosis

A 
M - methanol 
U - uraemia (CKD)*
D - DKA 
P - propylene glycol 
I - infection, iron, isoniazid*, inborn errors of metabolism
L - lactic acidosis 
E- ethylene glycol 
S - salicylates, sepsis*
356
Q

Anion gap

A

(Na + K) - (Cl + HCO3) => 16

357
Q

Cause of normal anion gap depsite deranged ABG

A

Bicarb losses from gut (diarrhoea)

Renal tubular acidosis

358
Q

Causes of raised anion gap

A 
Ketoacidosis 
Renal failure 
Lactic acidosis 
Salicylate toxicity 
Methanol 
Ethylene glycol
359
Q

Causes of metabolic alkalosis

A

Loss of acid e.g. vomiting
Diuretics*
Milk-alkali syndrome
Hyperaldosteronism

360
Q

When do you see a mixed picture ABG

A

Cardiac arrest

Resp failure

361
Q

pO2 in resp failure

362
Q

What are target sats in type 2 resp failure

A

88-92%
Loses hypoxic drive if given O2
Will retain more CO2

363
Q

Timeframe of metabolic compensation on ABG

A

Takes weeks to change (c/c condn) but CO2 compensation is v quick

364
Q

When is acute on chronic resp acidosis seen

A

Seen in exacerbations of COPD

365
Q

Features of acute on chronic acidosis on ABG

A

Low pH (acidotic)
Raised CO2
Extremely elevated bicarb

366
Q

When do we achieve 100% FiO2

A

15L of oxygen - max that can be given

367
Q

FiO2

A

Fraction of inspired oxygen

368
Q

Why would you given high flow O2 in an emergency despite type 2 resp failure

A

Hypoxia kills faster than hypercapnia

Redo ABG after

369
Q

Signs of hyperinflation on CXR

A

Flattened hemidiaphrgam
Thin heart
Increase in anterior ribs seen (5-7)

370
Q

Causes of stridor

A

Upper airway obstruction - croup, epiglottitis, inhalation of foreign body

371
Q

What pathological changes will occur if asthma is not treated

A

Thickening of basement membrane due to hypertrophy of smooth muscle
Mucous gland hyperplasia
Desquamation of epithelium

372
Q

Criteria for LTOT

A

Pt must be stable and on maximal therapy
PaO2 < 7.3
PaO2 7.3-7.8 w/ co-existing pulmonary disease

MBBS - Year 2 (20 decks)

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