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MBBS - Year 2 > Respiratory - Breathlessness: Restrictive Lung Disease > Flashcards

Respiratory - Breathlessness: Restrictive Lung Disease Flashcards

1
Q

Primary restrictive lung disease

A

Disease of lung parenchyma

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2
Q

Secondary restrictive lung disease

A

Chest wall and pleural disease

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3
Q

What does restrictive lung disease cause difficulty in

A

Inhaling

Reduced elasticity resulting in poor lung expansion

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4
Q

What are some mediators of infl

A

Leukocytes
Cytokine
Complement pathway proteins

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5
Q

The 5 R’s of infl & repair

A 
Recognition of the injurious agent 
Recruitment of the leukocytes 
Removal of the agents 
Regulation of the response 
Resolution/ repair
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6
Q

Why does lung fibrosis result in SOB

A

Pts will have dyspnoea, tachypnoea, fine end inspiratory crackles

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7
Q

A/c lung injuries

A

ARDS

Pneumonia

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8
Q

Mortality of ARDS

A

50%

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9
Q

ARDS

A

A/c Resp Distress Syndrome

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10
Q

What is ARDS

A

Primary resp failure characterised by refractory hypoxaemia and bilateral radiological evidence of alveolar collapse
No other attributable cause

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11
Q

What does ARDS end in

A

Vascular non-responsiveness

Leading to multiorgan failure due ton c/c hypoxia and effects of infl mediators

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12
Q

How can causes of ARDS be classified

A

Direct/ indirect lung injury

Common and uncommon

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13
Q

Common causes of ARDS - direct lung injury

A

Pneumonia

Aspiration of gastric contents

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14
Q

Uncommon causes of ARDS - direct lung injury

A

Pulmonary contusion
Inhalation injury
Fat emboli
Reperfusion injury

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15
Q

Common causes of ARDS - indirect lung injury

A

Sepsis

Severe trauma and shock

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16
Q

Uncommon causes of ARDS - indirect lung injury

A

Post-cardiac surgery
Pancreatitis
Drug overdose

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17
Q

Phases of ARDS

A

Exudative
Regernative
Repair

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18
Q

Exudative phase of ARDS

A

Necrosis of Type 1 pneumocytes then exposure and subsequent loss of the underlying basement membrane, fibrin release +/- haemorrhage, pulmonary collapse

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19
Q

How long does the exudative phase of ARDS last

A

~7/7

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20
Q

Regenerative phase of ARDS

A

Proliferation of pneumocytes and connective tissue

Infl

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21
Q

How long does the regenerative phase of ARDS last

A

1-2 weeks post injury

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22
Q

Repair stage of of ARDS

A

Infl, proliferating fibroblasts in the connective tissue produce granulation tissue (organising pneumonia) and/ or fibrous scar tissue

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23
Q

How long does the repair stage of ARDS last

A

2 weeks plus

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24
Q

Why is long intensive care required in ARDS

A

Pt have v high mortality weeks after initial event

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25
Q

Stages of pneumonia

A

A/c
Early resolving
Organising
From here there’ll either be complete resolution to normal or may go onto develop interstitial fibrosis

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26
Q

A/c stage of pneumonia

A

Neutrophil infiltrates into bronchi and alveoli

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27
Q

Early resolving stage of pneumonia

A

Fibrin, some neutrophils also macrophages, lymphocytes in air spaces

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28
Q

What can granulomatous responses in the lungs be caused by

A

Foreign bodies: inhaled exogenous substances e.g. beryllium
Infections: TB, fungi
Immune: hypersensitivity pneumonitis
unknown sarcoidosis

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29
Q

What is hypersensitivity pneumonitis

A

A c/c disease of the lungs resulting from inhalation of foreign substances showing both granulomatous and hypersensitivity reactions
Pathogen acts as a foreign antigen and triggers a local hypersensitivity reactions

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30
Q

What is hypersensitivity pneumonitis also known as

A

Extrinsic allergic alveolitis

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31
Q

Sources of exposure leading to hypersensitivity pneumonitis

A 
Mouldy hay - Farmer's lung
Mouldy grain - Grain handler's lung 
Pigeons, parakeets, fowl - Bird breeder's lungs 
Cheese mould - cheese worker's lung 
Paprika dust - Paprika splitter's lung 
Infested wheat - wheat weevil
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32
Q

C/c fibrosis ILD

A 
Pnuemoconiosis
Idiopathic pulmonary fibrosis/ UIP 
CTD 
Radiation 
Drugs

COP
NSIP

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33
Q

COP

A

Cryptogenic organising pneumonia

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34
Q

NSIP

A

Non-spp interstitial pneumonia

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35
Q

Pneumoconiosis

A

‘Dusty lung disease’
Permanent alteration of lung structures due to the inhalation of mineral dust and the tissue recitations of the lung to its presence

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36
Q

Commonest pneumoconiosis

A

Silicosis

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37
Q

Where does pneumoconiosis tend to be worse

A

In the upper lobes

This is due to more aeration of the lower lobes and better removal of particulate material

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38
Q

Pulmonary reactions seen in pneumoconiosis

A 
Macrophage accumulation w/ a little reticulin deposition 
Nodular or massive fibrosis
Diffuse fibrosis 
Epitheliod and giant cell granulomas
Alveolar lipoproteinosis 
Small-airway disease
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39
Q

Dust identification - pneumoconiosis

A

Clinical hx
Radiology - distribution of lung changes, upper, lower zones, nodule and fibrosis
Colour of the dust particles
Histology - refractory particles, crystal shape

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40
Q

What are asbestos related diseases

A

A family of pro-infl crystalline hydrated silicates
Crystals once phagocytosed activate an infl response which stimulates the release of proinfl factors and fibrogenic mediators
Macrophages attempt to phagocytose and digest fibres

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41
Q

What are asbestos related diseases associated with

A

Number of pulmonary and extra pulmonary diseases

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42
Q

Sequela of asbestos related diseases

A

Pleural plaques
Pleural effusions
Pulmonary fibrosis (asbestosis)
Malignancy - lung carcinoma, mesothelioma, extra pulmonary

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43
Q

Clinical findings of asbestosis

A

SOB
Dry cough
Finger clubbing

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44
Q

Macroscopic findings of asbestosis

A

Subpleural fibrosis particularly lower lobes

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45
Q

Microscopic findings of asbestosis

A

Intersititial fibrosis: peri bronchial and sub pleural ad the presence of ferruginous bodies

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46
Q

Resolution of asbestosis

A

The persistent c/c infl nature o d the disease is such that there is no disease resolution

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47
Q

What is idiopathic pulmonary fibrosis also known by

A

Its histological pattern: UIP

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48
Q

What is idiopathic pulmonary fibrosis

A

Progressive interstitial pulmonary fibrosis and reps failure caused by persistent epithelial injury and abnormal immune reaction

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49
Q

Cause of idiopathic pulmonary fibrosis

A

No known cause

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50
Q

Who do we see idiopathic pulmonary fibrosis in

A

Arises in genetically predisposed individuals who are prone to aberrant repair of recurrent alveolar injury

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51
Q

Secondary causes of lung fibrosis - Reactions to treatment

A

Drugs - various meds may cause a/c/ and c/c alteration in lung structure
Radiation pneumonitis

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52
Q

Types of radiation pneumonitis

A

A/c

C/c

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53
Q

A/c radiation pneumonitis

A

1/12 - 6/12 after treatment

May resolve completely w/ steroids or go on to a hypersensitivity pnuemoniti pattern

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54
Q

C/c radiation pneumonitis

A

Results in pulmonary fibrosis

Can also occur without a/c phase

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55
Q

Secondary causes of lung fibrosis - lung in systemic disease

A

Pulmonary - CTD

Extra-pulmonary - condns that limit MSK system or pleura e.g. scoliosis, and soon, neurodegenerative disease

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56
Q

Residual and functional volumes in obstructive disease

A

Increased

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57
Q

Inspiratory residual volume and inspiratory capacity in restrictive disease

A

Decreases

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58
Q

Examples of restrictive lung diseases

A

Fibrotic changes
Scoliosis
Muscular dystrophy
Ank spon

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59
Q

Atelectasis

A

Imperfect expansion off lungs
Specifically of failure of lungs to expand fully at birth
Congenital airway obstruction due to lack of surfactant in prematurity

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60
Q

Secondary atelectasis

A

Pulmonary collapse
Pressure changes and alveolar gas not replenished (absorption collapse) - obstruction prevents free entry of air into lungs

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61
Q

Epidemiology of sarcoidosis

A

2nd most common c/c reps disease in <40s

Bimodal distribution - 25-40 and 65+

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62
Q

Aetiology of sarcoidosis

A

Poorly understood - related to genetic predisposition plus exposure to antigen
Non-caeseating granulomas lead to organ damage and dysfunction

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63
Q

Which type of sarcoidosis manifestation has a better prognosis

A

A/c

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64
Q

What % of sarcoidosis develop c/c symptoms

A

1/3

Usually have non-spp, systemic symptoms

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65
Q

Pathophysiology of sarcoidosis

A

Antigen and host protein form a poorly soluble compound –. APCs activate macrophages & dendritic cells, producing cytokines –> Th1 help form epithelium granulomas

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66
Q

What does sarcoidosis chronicity depend on

A

Ability to clear antigen

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67
Q

Genetic causes of sarcoidosis

A

Multiple area of the HLA region BTNL2

ANXA11

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68
Q

Causes of sarcoidosis - exposures

A

Beryllium, silic, other dust
Mycobacterium tuberculosis and Propionibactera catalases
Moulds

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69
Q

How is sarcoidosis usually discovered

A

Incidental finding - no symptoms suggestive of sarcoidosis

Good prognosis

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70
Q

A/c presentation of sarcoidosis

A

Flu-like illnesses
Lofgren’s syndrome
Good prognosis - >605 in 2 yrs

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71
Q

Lofgren’s syndrome

A

Bilateral hilar lymphadenopathy
Erythema nodusum
Arthralgia

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72
Q

Who do we typically see Lofgren;s syndrome in

A

Northern Europeans/ caucasians

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73
Q

C/c presentation of sarcoidosis

A 
Progressive symptoms (e.g. dyspnoea, cough)
Associated extra-pulmonary disease and organ dysfunction
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74
Q

Eye involvement in sarcoidosis

A 
Uveitis 
Lacrimal gland involvement 
Optic nerve involvement 
Glaucoma 
Granulomatous tissue within orbit
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75
Q

Neurological involvement in sarcoidosis

A

Neuropathy
Meningitis
Raised ICP
Psychiatric problems

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76
Q

Resp tract involvement in sarcoidosis

A

Lymphadenopathy
ILD/ scarring
Airway obstruction and stenosis

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77
Q

Skin involvement in sarcoidosis

A

Erythema nodusum
S/c nodules
Lupus pernio

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78
Q

MSK involvement of sarcoidosis

A

Myositis
Arthralgia and arthritis
Entheistis

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79
Q

Cardiac involvement in sarcoidosis

A

Arrhythmia
Ventricular infiltration and failure
SCD

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80
Q

GI and GU involvement in sarcoidosis

A

Nephrocalcinosis
IBD mimic
Infertility
Obtruscive liver disease

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81
Q

What metabolic disturbance is seen in sarcoidosis

A

Hypercalcaemia

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82
Q

Eye symptoms in sarcoidosis

A

Eye pian
Visual disturbance
Vision loss

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83
Q

Resp symptoms seen in sarcoidosis

A

Breathlessness (exertional)
Cough
Wheeze

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84
Q

Neuro symtpoms seen in sarcoidosis

A

Seizures
Headaches
Cranial nerve palsies

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85
Q

GI and GU symptoms seen in sarcoidosis

A

Abdominal pain
Haematuria
Deranged LFTs
Change in bowel habits

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86
Q

Lymphadenopathy seen in pulmonary sarcoidosis

A

Mediastinal and hilar

bIlateral and symmetrical

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87
Q

Parenchymal disease seen in pulmonary sarcoidosis

A

Nodularity following bronchovacsular bindles and adjacent to tissues
Nodular disease (incl conglomerate masses)
Fibrosis

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88
Q

Airway disease in pulmonary sarcoidosis

A

Asthma-like symptoms/ bronchial hyper-reactivity (cough predominant)
Airway stenosis and occlusion

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89
Q

Which cardiac manifestations of sarcoidosis require mx

A 
Dyspnoea 
Collapse 
CM 
SCD/ arrythmias 
Pulmonary HTN
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90
Q

Which neurological manifestations of sarcoidosis require mx

A

Seizures
Aseptic meningitis
Cranial nerve palsies

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91
Q

Which metabolic manifestations of sarcoidosis require mx

A

Hypercalcaemia

Hypercalciura/ renal calculi

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92
Q

Which opthalmic manifestations of sarcoidosis require mx

A

Uveitis

Visual loss

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93
Q

Sarcoidosis mimics

A

C/c berylliosis - clinically identical but w/ clear exposure to beryllium
Granulomatous reactions to malignancy - context of known malignancy
Granulomatous - lymphocytic ILD (occurs in immune deficiency)
Drug reactions - anti-TNF monoclonal antibodies

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94
Q

Ix for sarcoidosis

A

Bloods
PFTs
CXR preceding tio CT chest
ECG (look for heart block)

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95
Q

Bloods for sarcoidosis

A

FBC - lymphopenia, anaemia
U&Es - renal dysfunction
LFTs - derangement (obstructive or hepatotoxic)
Serum ACE - elevated commonly but NOT spp
Ig - association w/ Ig defences esp IgA

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96
Q

Pulmonary function tests in sarcoidosis

A

Any pattern can occur (obstructive most common)

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97
Q

Radiology for sarcoidosis

A

Looking for subtle parenchymal changes in lungs or any asymmetry to suggest alternative pathologies

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98
Q

CXR staging for sarcoidosis

A

Stage I to IV

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99
Q

Stage I sarcoidosis - radiological

A

Bilateral hilar lymphadenopathy

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100
Q

Stage I sarcoidosis - radiological

A

Bilateral hilar lymphadenopathy

Increased paratracheal stripe

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101
Q

Stage II sarcoidosis - radiological

A

BHL and pulmonary infiltrates

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102
Q

Stage III sarcoidosis - radiological

A

Pulmonary infiltrates without BHL

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103
Q

Stage IV sarcoidosis - radiological

A

Advanced pulmonary fibrosis
Loss of lung volume
Apical fibrotic change

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104
Q

Which stage of sarcoidosis is most pts in

A

Stage I

Reolustion of 60-90%

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104
Q

Which stage of sarcoidosis is most pts in

A

Stage I

Reolustion of 60-90%

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104
Q

Which stage of sarcoidosis is most pts in

A

Stage I

Resolution of 60-90%

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105
Q

CT findings for sarcoidosis

A

Hilar and mediastinal nodes - symmetrical, bilayer enlargement
Nodules
Fibrotic changes

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106
Q

Bronchoscopy for pulmonary sarcoidosis

A

Pts are likely to require biopsy from lungs

Done at same time

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107
Q

Possible targets for lung biopsies - pulmonary sarcoidosis

A

Endobronchial lesions – cobble stoning
Transbronchial biopsies – more risky
EBUS-TBNA – biopsy of lymph nodes, helps rule out metastaic malignancy

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108
Q

Treatment for pulmonary sarcoidosis

A

Majority of pts will not require immediate treatment; raise w/ more severe disease require early mx

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109
Q

Reasons to initiate treatment in sarcoidosis

A

Wells Law
Danger of damage of organs (incl preventing mortality)
Improve QoL

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110
Q

Reasons to initiate treatment in sarcoidosis

A

Wells Law
Danger of damage of organs (incl preventing mortality)
Improve QoL

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111
Q

1st line drug of sarcoidosis

A

40-60mg Prednisolone - weaned over 6-18 months

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112
Q

1st line drug of sarcoidosis

A

40-60mg Prednisolone - weaned over 6-18 months

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113
Q

2nd line drugs for sarcoidosis

A

MTX - 10-15mg once weekly

Azathioprine - 1-3mg/kg - good for neuro-sarcoid

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114
Q

SE of MTX

A

Cytopenias
GI side-effects
Pneumonitis

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115
Q

SE of azathioprine

A

Cytopenias
GI side effects
LFT derangement

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116
Q

3rd line drugs for sarcoidosis

A

Mycophenolate Mofetil
Hydroxychloroquine
Anti-TNF

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117
Q

Mycophenolate

A

Cytopenias
GI side effects
LFTs derangement

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118
Q

SE of hydroxychloroquine

A

Optic neuritis

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119
Q

Follow up for Lofgren’s syndrome (Stage I CXR)

A

6 monthly for 2 yrs

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120
Q

Follow up for Stage II - IV sarcoidosis CXR

A

3-6 monthly or annually
Depending on clinical suspicion of a change in disease behaviour
No discharge

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121
Q

Follow up of pulmonary sarcoidosis pts who’ve been withdrawed from steroid therapy

A

2-3 monthly or 3-6 monthly
Minimum 3 years after cessation
No discharge

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122
Q

Mortality and sarcoidosis

A

Mortality attributable to sarcoidosis in pts w/ significant disease manifestations are more like 25%

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123
Q

Diffuse Parenchymal Lung diseases (DPLD)

A

Vast majority cause restrictive PFTs
Gradual onset breathlessness
Frequently cause cough
Will hear inspiratory carpitations

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124
Q

Causes of DPLD

A

Idiopathic interstitial pneumonia
Spp cause - drugs, hypersensitivity pneumonitis, CTD
Granulomatous - sarcoidosis

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125
Q

What is seen in the interstitium

A

ECM

Fibroblasts

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126
Q

Aetiology of DPLD

A

Drugs, therapies, iatrogenic - bleomycin, amiodarone
Inhalation of dusts (occupation, environment)
CTD (collagen diseases)
Unknown (idiopathic)

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127
Q

Idiopathic Interstitial Pneumonia

A 
IDO 
NSIP 
COP 
Resp bronchiolitis ILD (R-BILD)
Desquamative Interstitial Pneumonia (DIP)
A/c interstitial pneumonia
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128
Q

CT of UIP

A

Honeycombing +/- traction bronchiectasis

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129
Q

Epidemiology of NSIP

A

40-50yrs
M>F

Better prognosis than IPF
May be associated w/ CTD

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130
Q

CT of NSIP

A

Ground glass

Reticular shadowing

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131
Q

CT of COP

A

Consolidation or nodules

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132
Q

R BILD

A

Exaggerated bronchiolitis response to smoking

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133
Q

CT of R BILD

A

Patchy ground glass
Centrilolobular micro nodules
Regional attenuation

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134
Q

Who do we see DIP in

A

Heavy smokers

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135
Q

CT of DIP

A

Ground glass opacities

Bronchial thickening

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136
Q

CT of a/c interstitial pneumonia

A

Consolidation

Ground glass

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137
Q

What type of hypersensitivity reaction causes hypersensitivity pneumonitis

A

Type III or Type IV

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138
Q

Mx of hypersensitivity pneumonitis

A

Removal from antigen

Steroids

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139
Q

Examination finding in pts w/ restrictive lung disease

A

Fibrosis - fine end inspiratory crackles/ crepitation
Sarcoidosis - normal
Hypersensitivity pneumonitis - crackles, wheeze, squeaks

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140
Q

Main ix for restrictive lung disease

A

Pulmonary function tests
Bloods
Radiology

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141
Q

Blood for restrictive lung disease

A

FBC (eos)
U&ES
LFT
Serological - ANA,, RhF, anti-CCP, spp IgG’s

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142
Q

Other tests for restrictive lung disease

A

ECG
Echo
Radiology - CXR

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143
Q

HRCT of chest in restrictive lung disease

A 
Ground glass - non spp 
Consolidation 
Reticular shadowing*
Traction bronchiectasis* 
Honeycombing*
  • signs of fibrosis
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144
Q

Ground glass appearance on HRCT

A

Hazy Opoacity that doesn’t obscure the associated pulmonary vessels

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145
Q

What causes a ground glass appearance

A

Parenchymal abnormalities - infl or fibrosis

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146
Q

MDT for restrictive lung disease

A

Physician
Radiologist
Pathologist

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147
Q

Treating fibrosis in restrictive lung disease

A

Anti-fibrosis

Only for IPF (progressive fibrosis on named pt basis)

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148
Q

Treatment for infl in restrictive lung disease

A

Corticosteroids
MTX/ hydroxychloroquine
Azathioprine/ mycophenolate
Cyclophosphamide

149
Q

Non Pharma treatment for restrictive lung disease

A 
Education 
Pt support group 
Pulmonary rehab 
Oxygen therapy 
Palliative care - early referral provides better outcomes
150
Q

Pathophyisology of idiopathic pulmonary fibrosis

A

Epithelial-Fibroblast Pathway (fibroblastic foci) —> interstitial infl —> fibrosis (collagen)

151
Q

Main diagnostic tool for restrictive lung disease

152
Q

Prognosis of restrictive lung disease

A

No biomarkers can predict prognosis, only clinical

Scoring calculators - GAP score

153
Q

Mx for restrictive lung disease

A 
Oxygen 
Lung transplant 
Pirfenidone 
Nintedanib 
Pulmonary rehab
154
Q

When would anti-fibrotics be given

A

When FVC 50-80% predicted

155
Q

Anti-fibrotics given for restrictive lung disease

A

Pirfenidone

Nintedanib

156
Q

Pirfenidone action

A

Reduced fibroblast proliferation

Inhibits production of TGF-beta production and collagen stimulation

157
Q

SE of pirfenidone

A

Nausea

Photosensitivity rash

158
Q

Nintedanib

A

Triple growth-factor receptor inhibitor

Platelet derived, fibroblast and vascular endothelial growth factor receptor (PDGF, FGF, VEGF)

159
Q

SE of Nintedanib

160
Q

Symptoms seen in a/c exposure causing HS pneumonitis

A

Fever
SOB
Cough

161
Q

What is seen in c/c exposure causing HS pneumonitis

A

Progressive fibrosis

162
Q

Type 1 resp fialure

A

Hypoxia W/OUT hypercapnia

163
Q

Type 2 resp failure

A

Hypoxia and hypercapnia

Can be a sign of lfe-threatening asthma attack

164
Q

Common occupational lung diseases

A

Asbestos related diseases
Asthma (occupational)
Pneumoconiosis
Beryllium disease

165
Q

Susceptible trades and industries for occupational lung diseases

A 
Construction 
Engineering 
Welding 
Foundries/ quarries and potteries 
Motor vehicle repair 
Stonemasons 
Farmers
166
Q

When were asbestos fully banned

167
Q

Asbestos

A

Cheap, strong, fire and heat resistant fibres used in building

168
Q

Why are asbestos dangerous

A

Fibres <3 microns diameter ca reach alveoli

169
Q

When do symptoms of mesothelioma appear

A

Until 20 to 50+ years after exposure

170
Q

Manifestations of asbestos exposure

A 
Pleural plaques 
Diffuse pleural thickening 
Malignant mesothelioma 
Asbestosis 
Lung cancer 
Laryngeal cancer
171
Q

Inhalation of asbestos fibres

A

Particles <10um may penetrate alveoli
Long straight fibres can reach alveoli despite length \
Longer fibres more resistant to clearance by phagocytosis

172
Q

What is asbestosis

A

Form of pneumoconiosis caused by inhalation of asbestos fibres which is characterised by scarring and infl of lung tissue

173
Q

Is asbestosis reversible

A

No
A c/c and irreversible condn which symptoms develop several decades following exposure
Symptoms may seriously progress –> affecting ADL –> fatal complications

174
Q

Clinical features seen in asbestosis

A 
Dyspnoea 
Non-productive cough 
Wt loss 
Fine end inspiratory crackles 
Finger clubbing 
Susceptibility & deterioration associated w/ smoking
175
Q

Ix for asbestosis

A 
Spirometry 
CXR 
HRCT
Lung biopsy 
Transfer factor
176
Q

Spirometry in asbestosis

A

Usually restrictive

177
Q

Transfer factor seen in asbestosis

178
Q

CXR in asbestosis

A

Fine nodular shadoiwng

179
Q

HRCT for asbestosis

A

More sensitive than CXR at showing fibrosis

180
Q

Lung biopsy for asbestosis

A

Interstitial fibrosis and asbestos bodies

181
Q

Asbestos exposure mx

A

Supportive

Stop smoking

182
Q

Malignant mesothelioma

A

Form of cancer that principally affects the pleura and peritoneum
Strong association w/ exposure to asbestos

183
Q

Why are most cases of malignant mesothelioma diagnosed at an advanced stage

A

As symptoms are non-spp and appear late

184
Q

Symptoms of malignant mesothelioma

A

Chest pain
SOB
Pleural effusion

185
Q

Industrial injuries disablement benefit

A 
Asbestosis 
Mesothelioma 
Primary carcinoma lung 
Diffuse pleural thickening 
Non pleural plaques
186
Q

How can work aggravate asthma

A

Provokes symptoms of pre-existing asthma

A/c transient airway narrow after exposure to resp irritant such as dust, smoke, DO2, cold, exercise

187
Q

Irritant induced occupational asthma

A

Single exposure to high level of irritant e.g. NH3, Cl2 (RADS)
C/c moderate level exposure - more delayed onset of symptoms

188
Q

RADS

A

Respective Airways Dysfunction Syndrome

189
Q

Sensitiser induced occupational asthma

A

Asthma caused by immunological sensitisation to agents in the agents in the workplace (Type 1 HS)
Latency between weeks and yrs

190
Q

What % of adult asthma is occupational

191
Q

Is occupational asthma a ‘prescribed diseases’

A

Yes

Pt may be eligible to industrial injuries disablement benefits

192
Q

Initial px of occupational asthma

A

Initially symptoms of wheeze, dyspnoea and chest tightness at work or after work, improving over weekends & holidays
Over time this pattern can be lost

193
Q

Occupations that might cause asthma

A 
Paint spraying 
Cleaners 
Bakers 
Lab workers 
Carpentry
194
Q

Dx of occupational asthma

A 
Hx 
Serial peak flow looking for >20% variation across shift and Lowe/ more variable peak flow on workdays 
RAST (spp IgE), skin prick 
Spp inhalation challenge 
Workplace challenge
195
Q

Mx of occupational asthma

A

Treatment as per BTS guideline

Symptoms usually resolve if exposure in eliminated

196
Q

Hierarchy of control measures for occupational asthma

A

Elimination or substitution
Engineering controls e.g. enclose work process
Admin controls e.g. relocation to a diff job/ work area
PPE

197
Q

What % of people w/ occupational asthma remain in same job

A

25%

25% remain w/ same employer in an alternative job

198
Q

Long term changes caused by localised infl response in pneumoconiosis

A

Fibrosis
Necrosis
Cavitation
Coalescence into larger masses

199
Q

Mechanisms protecting lungs from inhaled particles

A

Particles >20um trapped in nasal cavity
10-20um trapped in upper branches of resp tract, cleared by mucocilliary escalator
Particles may also be transported to lymphatics
The mechanisms can be overwhelmed by large amounts of particulate matter

200
Q

Coal Workers Pneumoconiosis

A

Tissue reaction to dust in the lung parenchyma
Often asymptomatic
Usually (but not always) non-progressive if removed from exposure

201
Q

IX for simple CWP

A

Spiro - obstructive (emphysemna) or restrictive (fibrosis)

CXR - nodular opacities

202
Q

PMF (progressive massive fibrosis)

A

Fibrotic masses in upper or middle zones, 3-10cm diameter, can cavitate
Lung function loss mainly obstructive

203
Q

Symptoms seen in PMH

A 
Dyspnoea 
Productive cough (black sputum)
204
Q

A/c silicosis

A

Heavy exposure to dust respirable crystalline silica (silicon dioxide)
Direct cytotoxicity causing alveolitis
Progressive & often fatal over few months

205
Q

Symptoms in a/c silicosis

A

Progressive dyspnoea & cough

206
Q

CXR for a/c silicosis

A

Pulmonary oedema

207
Q

Mx of silicosis

A

No spp treatment

208
Q

Nodular/ c/c silicosis

A

10-15 yrs of lower level exposure
Cough & dyspnoea
May see silico-TB

209
Q

Sources of exposure of silicon dioxide

A

Mining
Constrcution
Stone working
Abrasive blasting

210
Q

Silicosis CWP

A

Opacities larger than in CWP
More marked in upper lobes
May see pleural thickening
‘Egg shell” calcification hilar lymph nodes

211
Q

When does COPD become a prescribed disease

A

If coal miner > 20 yrs

212
Q

Occupational resp infections

A

Viral resp tract infections
TB
Legionnaires
Psittacosis (Chlamydia psittaci)

213
Q

IPF lungs

A

Irreversibly enlarged, damaged bronchioles and distorted alveoli
Honeycombing - clustered cystic air spaces
Fibrosis between alveoli greatly decreases gas exchange

214
Q

UIP fibrosis on HRCT

A 
Sub -pleural 
Basal predominance 
Reticular shawoing 
Honeycombing 
Traction bronchiectasis
215
Q

MDT team for ILD

A 
ILD consultant 
ILD CNS 
Radiologist 
Thoracies 
Pathologist
216
Q

Pulmonary involvements in CTD

A

Pleural diseases - thickening, effusion
Airway complications
ILD
Pulmonary Vascular disease - pulmonary HTN
Opportunistic infections due to immunosuppression
Drug toxicity - MTX

217
Q

Median survival of IPF/ UIP

A

2.5 yrs - 3.5 yrs

218
Q

How long is steroid. treatment required for COP

219
Q

AIP

A

A/c interstitial pneumonia
Rapid onset of symptoms, dramatic clinical deterioration
Hypoxaemia, resp failure

220
Q

CTD associated w/ ILD

A 
RhA 
SScl 
SLE 
Dermatomyositis 
Sjorgen's syndorme 
Mixed CTD
221
Q

Epidemiology of IILD - RhA

A

More common in males

222
Q

Prognosis for ILD - RhA

A

Prognosis varies depending on subtype of ILD and degree of fibrosis
Progressive symptoms of breathlessness is a strong predictor of poor prognosis

223
Q

Ix for ILD - RhA

A

Lung volume of CXR
Extent of fibrosis on HRCT
Serial FVC on lung function

224
Q

Relation between RhA symptoms and ILD

A

No relation between control of joint symptoms and course of ILD
Progressive ILD can precedent synovitis or occur before onset of joint disease

225
Q

ILD - RhA mx

A

Anti-TNF alpha

Corticosteroids - good response in pts w/ COP subtype

226
Q

Which subtype of SScl is more frequently associated w/ ILD

A

DcSScl

Patients w/ dcSSc and lung involvement have 5-year survival < 50%

227
Q

Relation between SScl symptoms and ILD

A

Extent of skin evolvement doesn’t correlate w/ severity of lung disease
Resp symtoms rarely preced
Majority of pts have progressive symptoms

228
Q

Mx of ILD - SScl

A

Directed at detecting ILD early
Various immunosuppressive agents e.g. steroids, colchicine, D-pencillamine
Cyclophosphamide is most effective

229
Q

Manifestations of ILD in SLE

A

Usually a.c - a/c lupus pneumonitis w/ alveolar haemorrhage is well known
Repeated episodes may cause residual and c/c fibrosis

230
Q

Mx of lupus pneumonitis

A

Heavy immunosuppression and plasmapheresis - corticosteroids and azathioprine/ cyclophosphamide
Mortality as high as 50%

231
Q

Relation between Dermatomyositis symptoms and ILD

A

ILD preceded skin or muscle manifestation in about 1/3 of pts

232
Q

How may ILD in dermatomyositis present

A

Rapidly progressive AIP
Slowly progressiveing symptoms (UIP) or COP
Abnormal imaging/ PFT but no resp symptoms

233
Q

Why might dermatomyositis pts have SOB

A

Due to ILD or 2’ to pulm HTN, cardiac involvement or muscle weakness

234
Q

When are corticosteroids useful in ILD- DM

A

Those w/ a/c onset illness

235
Q

Poor prognostic features of ILD-DM

A

Older age group
Short hx
Dysphagia
Inadequate response to treatment

236
Q

Subtypes of ILD seen in Sjogrens

A

UIP/ IPF – worst prognosis
NISP
COP

237
Q

Resp symtoms seen in Sjorgrens

A

Cough
Breathlessness
Will hear fine ends inspiratory crackles

238
Q

Usual mx for ILD -sjorgrens

A

Corticosteroids and azathioprine & cyclophosphamide

239
Q

ILD in MCTD

A

ILD spectrum similar to that seen in SScl

Degree of ;lung forbrosis more severe in pts w/ SScl features

240
Q

Common symptoms in MTX lung injury

A

Cough
Dyspnoea
Fever

241
Q

Pulmonary function tests in MTX lung injury

A

Restrictive defects

Low diffusion capacity

242
Q

CXR for MTX lung injury

A

Alveolar infiltrates
Reticonodular shadowing
Predominantly diffuse or lower lobe involvement

243
Q

HRCT for MTX lung injury

A

Patchy ground glass shadowing

244
Q

Mx of MTX lung injury

A

Discontinuation of therapy or corticosteroids (for breathlessness)
Majority recover well and 25% experience reoccurrence once MTX in reintroduced (worse on high doses)

245
Q

Which pts have the lowest incidence of MTX lung injury

A

Pts on low dose MTX

246
Q

Anti-TNF treatment and ILD

A

Fatal exacerbations in pts w/ pre-existing ILD w. infliximab

247
Q

Assessment of iLDN in CTD pts

A

High clinical suspicion w/ good hx taking
Examination - fine end inspiatry crackles
CXR, PFT and HRCT
Biopsy

248
Q

If there’s rapid deterioration in pts on immunosupression, what should come come to mind

A

Pneumocystis jiroveci pneumonia

249
Q

What approach should be taken to mx CTD pts w/ ILD

250
Q

Where does the nasal cavity extend from

A

Anterior nares to nasopharynx

251
Q

unction of nasal cavity

A

Warm, filer and humidify air

252
Q

Medial wall of nasal cavity

A

Septal cartilage
Perendicular plates of ethmoid & vomer
Some palatine, maxillary and sphenoid

253
Q

Floor of nasal cavity

A

Roof of oral cavity
Palatine process of maxilla
Horizontal part palatine bones

254
Q

Roof of nasal cavity

A

Nasal cartilages

Nasal and frontal bones

255
Q

Lateral walls os nasal cavity

A

3 turbinates (conchae)

256
Q

Space below each turbinate

257
Q

Space above each turbinate

A

Sphene-ethmoidal recess

258
Q

Paranasla sinuses

A

Group of air filled spaces that lie in bones of skull and drain into nasal cavity

259
Q

Paired air sinuses

A

Frontal
Maxillary
Sphenoid
Ethmoid

260
Q

Floor of oral cavity

A

Tongue

Sub-lingual gland

261
Q

Roof of oral cavity

A

Palate (hard, soft, uvula)

262
Q

Dentition in oral cavity

A

Adult - permanent 32

Child- deciduous 20

263
Q

Components of oral cavity

A 
Floor 
Roof 
Dentition 
Cheeks and lips 
Tonsils
264
Q

Where is the pharynx found

A

Base of skull to C6

265
Q

How many paired constrictors does the pharynx have

A

3 - superior, middle and inferior

266
Q

What does the lining of the pharynx reflect

A

Where it is

Rest epithelium in nasopharynx and stratified squamous epithelium in oro- and laryngopharynx

267
Q

Innervation of pharynx

A

Pharyngeal plexus - vagus and glossopharyngeal nerves

268
Q

Whatcare the skeletal elements of the larynx joined bu

A

Thyrohyoid membran
Cricothyroid membrane
Aryepiglottic membrane

269
Q

Where is the vocal cord found

A

Fold between thyroid and arytenoid

270
Q

What is the space between false and true cords called

A

Sinus (ventricle of larynx)

271
Q

Mucosal innervation of larynx

A

Above vocal cord - internal laryngeal

Cord level and below - recurrent laryngeal nerve

272
Q

Extrinsic muscles of the larynx and hyoid bone

A

Suprahyoid and stylopharyngess - elevate hyoid and larynx as a whole
Infra hyoid - depress the hyoid and larynx as a whole

273
Q

Intrinsic muscles of the larynx

A 
Cricothyroid 
Tyro-arytenoid 
Posterior cricoid-arytenoid 
Lateral rico-arytenoid 
Transverse and oblique arytenoids 
Vocalise
274
Q

Action of the cricothyroid

A

Covers anterior cricoid superiorly and inferiorly stretches and covers vocal ligaments

275
Q

Action of thyro-arytenoid

A

Relaxes vocal ligament

276
Q

Action of posterior crico-arytenoid

A

Adducts vocal fold

As well as lateral crico-arytenoid

277
Q

Action of transverse and oblique arytenoids

A

Adduct arytenoids closing posterior rim of glottis

278
Q

Action of vocalist

A

Relaxes posterior vocal ligament while maintaining tension of anterior part

279
Q

Cricothyroid innervation

A

External laryngeal nerve (branch of CNX)

280
Q

Innervation of intrinsic muscles of larynx (expert cricothyroid)

A

Recurrent laryngeal nerve (branches of CNX) also called inferior laryngeal nerve - the terminal branches of recurrent laryngeal

281
Q

Where are intercostal muscles found

A

Between each rib

282
Q

Function of iC muscles

A

Bridge gaps between ribs and stop any air or pressure transfer

283
Q

Layers of IC muscles

A

External Ix are found outside then internal IC

Transverse thoracic muscles are innermost

284
Q

What is in the IC neuromuscular bundle

A

IC vein, artery and nerve (superior –> inferior)

Sits between internal IC and innermost IC

285
Q

How does the structure of the external IC change

A

Gets thinner laterally

286
Q

Muscle attachment of SCM

A

Runs obliquely from mastoid process down to sternum

Attaches to manubrium and clavicle (lateral boundary of triangle)

287
Q

SCM

A

Sternocleoimastoid

288
Q

Inferior border of anterior triangle of neck

A

Manubrial notch

289
Q

Superior border of anterior triangle of neck

A

Lower border of mandible

290
Q

Midline of anterior triangle of neck

A

Midline of neck separates R and L

291
Q

Where are the infrahyoid muscles found

A

Deep to SCM - run from hyoid bone to clavicle of scapula

292
Q

What does the contraction of suprahyoid muscles cause

A

The hyoid bone to be pulled up

293
Q

What does the contraction of the infrahyoid muscles cause

A

Hyoid bone to be pulled down

294
Q

What is the laryngeal prominence attach dto

A

Thyroid cartilage

295
Q

What is under the laryngeal prominence

A

Cricoid cartilage

296
Q

Where do the vocal cords lie

A

Deep in thyroid cartilage

297
Q

Where is the cricothyroid membrane found

A

In between thyroid and cricoid cartilage

298
Q

What structures lie deep to SCM

A

Anterior jugular veins

Common carotids, internal jugular and vagus nerve - carotid sheath

299
Q

What does the parietal pleura line

A

Internal surface of thoracic cavity, diaphragm and mediastinum

300
Q

What does the visceral pleura cover

A

Surface of lungs

301
Q

Cervical pleura

A

Parietal pleura in cervical region

302
Q

Costal pleura

A

Parietal pleura in thoracic region

303
Q

Diaphragmatic pleura

A

Parietal pleura covering diaphragm

304
Q

Mediastinal pleura

A

Parietal pleura covering mediastinum

305
Q

What is the diaphragmatic pleura innervated by

A

Phrenic nerves

306
Q

What is the costal pleura innervated by

307
Q

What is the cervical pleura innervated by

A

Upper IC nerve and cervical plexus

308
Q

What is the mediastinal pleura innervated by

A

Phrenic nerves

309
Q

Why is the pain from the visceral pleura dull

A

Visceral is innervated autonomically not somatically

310
Q

What type of pleura causes radiating pain

A

Dipahragmatic or mediastinal - referred pain at shoulder

Costal pain is v localised

311
Q

Where do the phrenic nerves pass from

A

C3,4 & 5, pass through neck, over anterior scalene and descend on R and L side of mediastinum.

312
Q

Why is the diaphragm higher on the R side

A

Due to liver

313
Q

If there is a build up of fluid in the thoracic cavity, where will fill up

A

Costa-diaphragmatic recess - visible on CXR

314
Q

Anterior attachment of diaphragm

A

Posterior aspect of diploid process

315
Q

Lateral attachment of diaphragm

A

Costal cartilages of lower ribs (T7-T10)

316
Q

Posterior attachment of diaphragm

A

Arcuate ligament and lumbar vertebrae via crura

317
Q

Mpvemen of diaphragm in breathing

A

Up in inspiration and down in expiration

318
Q

What can agitation to diaphragm result in

A

Referred pain - shoulder or jaw pain

319
Q

How long do you have to use ICS to see results

A

8-10 days of continued use

320
Q

What is the peak flow variability threshold

321
Q

What is the peak flow reversibility threshold

322
Q

3 main causes of COPD

A

Rhinitis/ PND
Asthma
GORD

323
Q

Taking spirometry measurements

A

Ask pt to sit up, legs uncrossed
Need to do 3 relaxed blows and 3 forceful
For the relaxed blows, the pt needs to hold their nose
There needs to be a proper seal around mouthpiece

324
Q

How should inhalers be taken

A

Puff needs to be coordinated w/ inspiration

325
Q

Examples of MART drugs

A

LABA/ICS inhaler:
Duoresp
Fostair
Symbicort

326
Q

How often is COPD reviewed

327
Q

Normal spirometer readings

A

FEV1 > 80%
FVC > 80%
Ratio > 0.7

328
Q

Obstructive spirometer readings

A

FEV1 < 80%
FVC <80% or >80%
Ratio < 0.7

329
Q

Restrictive spirometer readings

A

FEV1 < 80%
FVC < 80%
Ratio > 0.7 (both reduced)

330
Q

On which side would you see a gastric air bubble on a CXR

A

L - stomach

331
Q

What are signs of a raised diaphragm on a CXR

A

<6 ribs visible anteriorly

332
Q

Sign of hyperinflation on CXR

A

If >8 ribs visible

333
Q

When might you see surgical emphysema

A

During a PTX drain - air travels elsewhere
Stab wounds

Airbubble on CXR

334
Q

Percussion in pneumonia pts

335
Q

Auscultation in pneumonia pts

A

Crackles
Bronchial breathing
Increased vocal resonance

336
Q

Percussion in pleural effusion

A

Stony dullness

337
Q

Auscultation in pleural effusion pas

A

Decreased vocal resonance

Decreased breath sounds

338
Q

Percussion in PTX pts

A

Hyper resonant

339
Q

Auscultation in PTX pts

A

Absent breath sounds

Decreased breath sounds

340
Q

Percussion in lung collapse pts

341
Q

Auscultation in lung collapse pts

A

Decreased breath sounds

Decreased VR

342
Q

In which lobes is collapse most common

343
Q

What should you suspect if you see hypercalcaemia in resp pts

A

Sarcoidosis or cancer

344
Q

What condition is V/Q scan most indicated in

345
Q

What is lymphoma associated with on a CXR

A

Mediastinal node enlargement

346
Q

Types of causes of fibrotic lung disease

A 
Lung damage: infarction, pneumonia, TB
Irritants: Coal dust, silica
DPLD: IPF, HS pneumonitis 
CTD: RhA, SLE, SScl
Meds - amiodarone, nitrafurantoin
347
Q

What kind of granuloma is seen in sarcoidosis

A 
Non caeseating (non necrotising)
Also seen in HS pneumonitis
348
Q

Pathophysiology of resp failure

A

Perfusion of a part of the lung is subjected to impaired ventilation causing hypoxic and CO2 containing blood entering the pulmonary vein

349
Q

Causes of Type 1 a/c resp failure

A 
A/c asthma 
Pulmonary oedema 
Pneumonia
Lobar collapse 
PTX 
PE 
ARDS
350
Q

Causes of Type II a/c resp failure

A 
A/c severe asthma
A/c exacerbation of COPD
Upper airway obstruction 
Central depression 
Muscle weakness
351
Q

Ix for a/c resp fsilure

A 
ECG 
CXR
Bloods 
Dipstick 
ABGs
352
Q

Mx of a/c resp failure - Type 1

A

High conc of oxygen (40-60%) by mask
Mechanical ventilation will be needed to relieve hypoxia
Oxygen given should be humidified

353
Q

Mx of Type II a/c resp failure

A

Emergency - immediate intubation or tracheostomy
Treat cause
Supported ventilation may be needed IF responsive

354
Q

Most common cause of ‘a/c on c/c’ type II resp failure

A

Severe COPD - exacerbations

355
Q

In which zone is asbestosis usually found

A

Lower zones

356
Q

UIP pattern

A

Fibroblastic infiltrates
Mature fibrosis
Honey combing - end stage fibrosis

Histological + radiological pattern, not separate disease

357
Q

What zone does HS pneumonitis usually affect

358
Q

When do we see BHL on a CXR

A

Sarcoidosis
TB
Lymphoma

359
Q

When do we see reticular shadowing on a CXR

A

Infection
Cancer
ILD

360
Q

Why does hypercapnia cause resp acidosis

A

Formation of carbonic acid

361
Q

Compensation of resp acidosis cased by increased pCO2

A

Increase in HCO3-

362
Q

Compensation for metabolic acidosis caused by decreased HCO3-

A

Decreased CO2

363
Q

Stages of treatment for Type 2 resp failure;ure

A

Reduce oxygen and recheck ABG (if over oxygenated)
NIV if still in resp failure
Invasive mechanical ventilation
Palliate - respect form

364
Q

What causes finger nail clubbing

A

C/c hypoxaemia

365
Q

Honeycombing vs ground glass appearance

A

Honeycombing is spp for end stage ILD

Ground glass is more mild and not spp

366
Q

Appearance description of UIP on CT

A

Honeycombing

Traction bronchiectasis

367
Q

Appearance description of NSIP

A

Ground glass

368
Q

When is UIP pattern seen the most

A

IPF or RhA

369
Q

When is NSIP pattern on CT seen most commonly in

A

CTD - ILD

Except RhA

370
Q

What pathologies will cause a multiple ill-defined opacities in the lungs

A 
Pulmonary infarcts
Pulmonary metastases
RhA
Granulomatosis w/ polyangitiis
Septic emboli
371
Q

Why do we see bilateral parotid swelling in sarcoidosis

A

Lymphomatous infiltration

372
Q

Causes of respiratory alkalosis

A 
CNS infection 
SAH
Panic attack 
Aspirin overdose 
PE (reflex hyperventilating)
Anaemia

MBBS - Year 2 (20 decks)

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