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Cardiorespiratory 2 > Restrictive lung disease > Flashcards

Restrictive lung disease Flashcards

1
Q

what is a restrictive lung disease

A

Restrictive lung disease is when there is reduced lung volume and thus reduced TLC

  • Lung parenchyma
  • Pleura, chest wall or neuromuscular apparatus
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2
Q

what are the two major categories of restrictive lung disease

A
  • Intrinsic

- Extrsinic

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3
Q

what is the

  • pathology
  • outcome
  • disease for intrinsic restrictive lung disease
A
  • Pathology – lung parenchyma inflammation and lung scarring
  • Outcome – decrease in alveolar; arterial gas transfer, exudate and debris (pneumonitis)
  • Disease – interstitial lung disease
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4
Q

what is the

  • pathology
  • outcome
  • disease for extrinsic restrictive lung disease
A
  • Pathology – abnormal function of chest wall, pleura, and neuromuscular apparatus
  • Outcome – impaired ventilator function, respiratory failure
  • Disease - Myasthenia Gravis, Obesity
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5
Q

Name 3 major interstitial lung diseases

A
  • Idiopathic Pulmonary Fibrosis
  • Sarcoidosis -
  • pneumoconiosis
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6
Q

what is the survival rate for idiopathic pulmonary fibrosis

A
  • 1 in 3 expected to die within next 12 months

- 50% die within 2 to 3 years after diagnosis

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7
Q

what are some risk factors for idiopathic pulmonary fibrosis

A
  • Smoking
  • Environment exposures
  • Chronic virla infections
  • Abnormal acid reflux
  • Family history
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8
Q

what is the result of idiopathic pulmonary fibrosis

A
  • Scarring and honeycombing in the lung restricts breathing and oxygen exchange
    Airway remodelling
    – leads to impaired oxygenation, it is progressive and incurable
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9
Q

what are the pathophysiology proposed for idiopathic pulmonary fibrosis

A
  • Genetic susceptibility – ageing, telomere attrition, mitochondrial dysfunction, genetic instability, environmental factors
  • Epigenetic reprogramming
  • These lead to repetitive micro injuries
  • These lead to fibroblast migration and proliferation
  • These lead to the scarring and are like roadblocks
  • As you breath in and out the airways collapse and expand
  • Ability to expand is reduced
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10
Q

what are the environmental factors that lead to idiopathic pulmonary fibrosis

A
  • Decreased epithelia cell integrity
  • Accelerated ageing associated changes
  • Exaggerated fibroblast expansion
  • There is dilation of the bronchi
  • Alveolar remodelling
  • Parenchymal fibrosis – laying down of fibroblast that act as road blocks
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11
Q

what are the symptoms of idiopathic pulmonary fibrosis

A
    • difficult to distinguish
  • Extertional dyspneoa
  • Clubbing
  • Dry cough
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12
Q

how do you diagnose idiopathic pulmonary fibrosis

A
  • Medical history
  • Physical examination – fine, high pitched bibasilar inspiratory crackles (Velcro like sounds)
  • The volume is significantly less
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13
Q

how do you work out the DLCO and what is it

A

Lung surface area available for gas exchange (Va) X rate of capillary blood CO uptake (kco)

  • Quantity of carbon monoxide transferred per minute form alveolar gas to red blood cells (ml/min/mmHg)
    mil of CO transferred per minute for each mmHg of pressure difference across the total available functioning lung gas exchange surface
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14
Q

what does DLCO stand for

A

Diffusing capacity of the lungs for carbon monoxide

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15
Q

why does the DLCO decrease in interstitial lung disease

A

↓DLCO primarily due to ↓Kco

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16
Q

what is the DLCO used for

A

Useful for early stage ILD detection before substantial reduction in lung volumes

17
Q

what are the concerns for using the DLCO

A
  • Falsely reduced in individuals who fail to inspire to TLC(total lung capacity)
  • Significant variation
18
Q

how do you treat idiopathic pulmonary fibrosis

A
  • Pirfenidone
  • Nintedanib
  • Antacid therapy
19
Q

how do you treat idiopathic pulmonary fibrosis non pharmacologically

A
  • Pulmonary rehab increases physical and psychological, increase walk distance, increase QoL
  • Long term oxygen – patients with hypoxemia at rest, short burst oxygen therapy; exertional hypoxemia
  • Lung transplant – moderate severe disease
20
Q

how does pirfendione work

A
  • Anti-fibrotic agent
  • Mechanism of action unclear
  • ↓Physiological deterioration
  • ↑Progression-free survival
  • AEs = GI, photosensitivity, anorexia, skin rash & liver toxicity
21
Q

How does nintedanib work

A

Tyrosine kinase inhibitor
• ↓FVC decline
• AEs: diarrhoea, weight loss & liver toxicity

22
Q

how does antacid therpay work

A
  • IPF with gastro-oesophageal reflux

* AEs (long-term): Infection, cognitive function & MI

23
Q

What is sarcoidosis

A

Sarcoidosis is a disease involving abnormal collections of inflammatory cells that form lumps known as granulomas

  • these granulomas can infiltrate and invade any part of the organism
  • it is usually acute and self-limiting
24
Q

what are the symptoms in sarcoidosis

A
  • Eye – dry eyes, blurry vision
  • Lymph nodes – enlarged
  • Lungs – hacking cough, cough up blood
  • Heart – complciations
  • -liver and spleen – enlargement
  • Joints – pain, arthritis, swelling of the knees
  • Skin – rashes, lupus pernio, erythema nodosum, skin lesions on back, subcutaneous nodules
25
Q

what can cause sarcoidosis

A
  • Antigen (bacteria?) phagocytosed by antigen-presenting cells
  • Presentation of antigen to T cells by HLA class II molecules, CD4 positive Cells, leas to activation of TNF leaves to alveolitis – inflammation and clumping around the alveoli region
  • Formation of sarcoid granuloma
26
Q

how to you diagnose sarcoidosis

A
  • Info from the patient and
    Clinicoradiographic data:
  • Bilateral hilar adenopathy on the chest radiograph
  • Lofgren syndrome (erythema nodosum skin rash + bilateral hilar adenopathy on chest radiograph +/- fever and arthritis)
  • Diagnosis possible versus idiopathic granulomas – for example one organ has granulomas if there is more than one granuloma then diagnosis is more likely
27
Q

describe how the chest x ray stage of sacoidosis works

A

stage 0/1

  • no symptoms
  • no systemic therpay

stage 2-4

  • symptomatic
  • treat with corticosteroids

steroid sparing alternatives for chronic pulmonary sarcoidosis

  • methotrexate
  • folic acid
  • azathioprine
  • leflunomide
  • mycophenolate

treatment of refractory sarcoidosis
- infliximab

28
Q

how do corticosteroids work

A
  • CS binds to GR when bound
  • Translates into the nucleus
  • Increases gene expression of anti-inflammatory genes
  • Or it may recruit genetic machinery that dampens pro-inflammatory genes

Cardiorespiratory 2 (43 decks)

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