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Respiratory > Interstitial Lung Disease > Flashcards

Interstitial Lung Disease Flashcards

1
Q

what is interstitial lung disease

A

Generic term to describe a number of conditions that affect the lung parenchyma in a diffuse manner
Characterised by chronic inflammation and/or progressive interstitial fibrosis and share a number of clinical and pathological features

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2
Q

what are the different types of ILD with known cause

A

Occupational/environmental e.g. asbestosis, berylliosis, silicosis, cotton workers lung (pneumoconiosis)
 Drugs – nitrofurantoin, bleomycin, amiodarone, sulfasalazine, busulfan
 Hypersensitivity reactions – extrinsic allergic alveolitis
 Infections
 GORD

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3
Q

what are the different types of ILD associated with systemic disorders

A

 Sarcoidosis
 RA
 SLE, systemic sclerosis, mixed connective tissue disease, Sjogren’s syndrome
 UC, renal tubular acidosis, autoimmune thyroid disease

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4
Q

what are the different idiopathic ILDs?

A

 Idiopathic pulmonary fibrosis
 Cryptogenic organising pneumonia
 Lymphocytic interstitial pneumonia

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5
Q

what are the shared clinical features of ILDs?

A

Dry cough
Dyspnoea
Digital Clubbing
Diffuse Inspiratory crackles

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6
Q

what is the most common ILD?

A

idiopathic pulmonary fibrosis

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7
Q

what are the causes of idiopathic pulmonary fibrosis?

A

Unknown
Environmental factors
RA, SLE, Systemic sclerosis
Drugs – amiodarone
Risk Factors – smoking, occupation, viruses, GORD, male, age
Familial – pulmonary surfactant mutations

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8
Q

what are the clinical features of idiopathic pulmonary fibrosis?

A
  • Worsen over time
  • Dry Coughing
  • Progressive SOB
  • Cyanosis
  • Digital clubbing
  • Fine inspiratory crackles
  • Over time – significant respiratory failure
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9
Q

what investigations can be done for IPF?

A

chest imaging

PFT

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10
Q

what features will be present in the imaging of IPF?

A

o Xray – shadowing at bottom + periphery

o CT – honeycombing + bilateral infiltrates

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11
Q

what is PFT of IPF?

A

Restrictive pattern

Restricted lung expansion = restrictive lung disease = decreased TLC, decreased FVC, decreased FEV1

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12
Q

what is the treatment of IPF?

A
  • Supportive – Oxygen, rehab, opiates
  • Antifibrotic (slow rather than stopping)
  • Only definitive treatment is Lung transplant
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13
Q

what is the normal process of alveolar lining repair?

A

When alveolar lining is damaged, Type 1 pneumocytes release TGB1
TGB1 stimulates Type 2 to stimulate fibroblasts to proliferate and develop into myofibroblasts
Myofibroblasts secrete reticular fibres and elastic fibres
Normally myofibroblasts undergo then undergo apoptosis

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14
Q

what is the inflammatory mechanism causing IPF?

A

Type 2 over proliferate in repair process and myofibroblasts don’t undergo apoptosis = too much collagen
• Collagen accumulates and thickens interstitial layer – problems with ventilation
• Also causes lungs to become stiff – air struggles to flow in and out
= Restricted lung expansion and loss of alveoli (fluid cysts)

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15
Q

what are the common causes of occupational/environmental pneumoconiosis and who are at risk of those?

A
  • Asbestosis – plumbers, roofers, mechanics, shipyard workers
  • Silcosis – miners, sandblasters, stonemasons
  • Coal workers lung – inhaled dust
  • Berylliosis
  • Caplans (RA) – if pneumoconiosis occurs with RA
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16
Q

what are the clinical features of simple occupational pneumoconiosis?

A

few symptoms, slight xray abnormality

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17
Q

symptoms of complicated occupational pneumoconiosis

A 
o	Shortness of breath (exacerbated by exercise)
o	Cough – dry + severe
o	Fatigue
o	Tachypnoea
o	Loss of appetite + weight loss
o	Chest pain
o	Fever
o	Finger clubbing
o	Silcolosis (blue skin)
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18
Q

what is the underlying pathophysiology of occupational pneumoconiosis?

A
  • If some particles are very small, travel and get trapped in alveolar ducts and bifurcations
  • Attract pulmonary alveolar macrophages – activate inflammation and induce IL-1
  • Initiate fibroblasts and collagen production = Scarring
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19
Q

what are the differentials of occupational pneumoconiosis?

A

COPD
HF
Cardiomyopathy

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20
Q

what investigations can be used for occupational pneumoconiosis?

A

xray

spirometry

21
Q

what features will be present in an xray of someone with occupational pneumoconiosis?

A

o Asbestosis = pleural plaques
o Silicosis = egg shell calcification, fibrotic nodules
o Upper zones affected

22
Q

what will the PFT of occupational pneumoconiosis?

A

Restrictive

23
Q

what is the treatment of occupational pneumoconiosis?

A 
no cure
avoidance
o	Pulmonary rehabilitation
o	Inhaled corticosteroids
o	Inhaled bronchodilators
o	O2 if sats / symptoms indicate it is required
o	Smoking cessation
Lung transplant
24
Q

Features of Asbestosis

A
  • Straight fibres (white, blue – most fibrogenic, brown)
  • Disease correlated to level of exposure but disease can take up to 10-60 years to develop
  • Linked to mesothelioma
25
Q

Features of chronic silicosis

A

o Caused by long periods of low level exposure
o Multiple nodules throughout the lungs
o Mild symptoms (sometimes none)

26
Q

features of acute silicosis

A

o Large exposure over a short period of time

o Rapidly advancing silicosis – often results death

27
Q

features of progressive massive fibrosis (PMF)

A

o Develops from chronic simple silicosis
o The nodules enlarge and coalesce into large masses
o Severe respiratory symptoms

28
Q

features of coal causing occupational pneumoconiosis

A
  • Often co -exists with silicosis
  • 10 years from exposure
  • Similar disease pattern to silicosis – most cases are chronic simple pneumoconiosis
29
Q

what is the source of exposure and antigen of farmers lung

A

mouldy hay, Saccharopolyspora rectivigula

30
Q

what is the source of exposure and antigen of Bagassosis

A

Mouldy sugar cane

Thermoactinomyces sacchar

31
Q

what is the source of exposure and antigen of Grain handlers lung

A

Mouldy grain

S retivigula, T rectivgula

32
Q

what is the source of exposure and antigen of humidifier/air conditioner

A

Contaminated force-air system

S rectivigula, T rectivigula

33
Q

what is the source of exposure and antigen of Bird Breeders Lung

A

Pigeons, parakeets

Avian or animal proteins

34
Q

what is the source of exposure and antigen of cheese worker

A

Cheese mould

Penicillin casei

35
Q

what is the source of exposure and antigen of malt worker

A

Mouldy malt

Aspergillus clavatus

36
Q

what is the source of exposure and antigen of wheat wheevil

A

Infused wheat

Sitophilus granaries

37
Q

what is the source of exposure and antigen of mollusc shell

A

Shell dust

Sea snail shells

38
Q

what is the source of exposure and antigen of paprika splitter

A

Paprika dust

Mucor stdonifer

39
Q

what type of hypersensitivity reaction is Extrinsic Allergic Alveolitis

A

Type III - immune complexes present

40
Q

Extrinsic Allergic Alveolitis can be split into:

A

acute and chronic

41
Q

what is the inflammatory process of acute EAA

A

alveoli infiltrated with acute inflame cell

42
Q

what is the inflammatory process of acute EAA

A

granuloma formation and obliterate bronchioles

43
Q

what are the clinical features of acute EAA

A

o Symptoms start 4-6hrs post exposure
o Cough, breathlessness, fever, myalgia
o +/- pyrexia crackles (no wheeze) hypoxia

44
Q

what are the clinical features of chronic EAA

A

o Increasing dyspnoea, reduced weight, exertional dyspnoea
o Type 1 respiratory failure
o Cor pulmonale

45
Q

what is the diagnosis of acute EAA

A

o FBC, ESR↑, ABGs
o CXR – upper zone (+mid), mottling/consolidation, hilar, lymphadenopathy
o Lung Function – reversible reduced

46
Q

what is the diagnosis of chronic EAA

A

o Blood tests – positive serum precipitations = IgG (no eosinophilia)
o CXR – upper zone fibrosis/honeycombing
o Lung function = RESTRICTIVE

47
Q

what is the treatment of acute EAA

A

Oxygen, Oral prednisolone, Antigen avoidance

48
Q

what is the treatment of chronic EAA

A

Antigen avoidance (PPE), Long term steroids, Compensation

49
Q

what is important to ask in the history of EAA

A

Pets and occupation

Respiratory (12 decks)

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