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103: Theme 4 - 304 - Respiratory > Restrictive lung disease and combo diseases > Flashcards

Restrictive lung disease and combo diseases Flashcards

1
Q

What defines Lung restriction?

A

results in a reduction in:

  • RV: Residual volume
  • FRC: Functional residual capacity
  • TLC: Total Lung capacity
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2
Q

lung function tests

What is the difference between restrive and obstructive lung function?

A
  • there is also a reduced TLCO (the diffusion capacity of CO from capillaries to alveoli)
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3
Q

What causes skeletal and connective tissue restrictions?

A
  • extensive burns affecting the chest wall
  • obesity
  • Kyphoscoliosis: the curvature of the spine characterised by abnormal vertebral curving
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4
Q

Give examples of Neuromuscular chest wall disorders

A
  • Guillain-Barre: auto-immune syndrome, the immune system attacks your nerves
  • Degenerative spinal diseases
  • Motor neurone disease: gradual degradation of the nerves system
  • Poliomyelitis (Polio): a viral illness, that can cause nerve injury leading to paralysis, difficulty breathing and potentially death
  • Myasthenia gravis: weakness and rapid fatigue of voluntary muscles
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5
Q

What is pleural effusion?

A
  • the abnormal accumulation of serous fluid in the pleural space/cavity

> 25 mL

  • there is usually a net filtration of transudative (protein poor) fluid into the pleural space that is balanced with reabsorption from the parietal lymphatic
  • when there is pleural effusion this doesn’t occur, as either too much fluid is produced or not enough is being taken away
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6
Q

What are some presenting symptoms of Pleural effusion?

A
  • pleuritic chest pain
  • dull aching pain
  • the fullness of the chest (heavy)
  • dyspnoea
  • or asymptomatic
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7
Q

What are clinical signs of the effusion?

A
  • decreased chest expansion
  • absent breath sounds
  • dullness to percussion
  • compressive atelectasis (partial lung collapse) may cause bronchial breath sounds
  • Tracheal deviation and a mediastinal shift is massive effusion
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8
Q

What would be seen in a chest x-ray of bilateral pleural effusion

A
  • > 300 mls visible in the cxr
  • blunted costophrenic angle
  • Homogenous opacification
  • loss of diaphragmatic and mediastinal borders
  • meniscus
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9
Q

Explain Transudative Effusion

A
  • due to an imbalance in Starlings forces across the pleural membrane
  • have protein poor fluid
  • often bilateral
  • not associated with a fever, pleuritic pain, or tenderness on palpation
  • the most common cause is congestive heart failure
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10
Q

Explain Exudative Effusion

A
  • implies disease of the pleura or the adjacent lung
  • increased protein, lactate dehydrogenase (LDH), cholesterol or WBC
  • Measurement of all the above including pleural aspirate count, pH and glucose should be taken
  • needs to be drained: tube thoracostomy or needle aspiration
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11
Q

What are the causes of Transudative Effusion?

A

Increased venous pressure

  • Congestive heart failure
  • fluid overload
  • constrictive pericarditis

Low protein (decreased oncotic pressure)

  • nephrotic disease
  • Cirrhosis Hepatic hydrothorax (liver failure)
  • Hypothyroidism
  • Meia’s syndrome: benign ovarian fibroma
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12
Q

What are the causes of Exudative Effusion?

A

Infection

  • acute bacterial infection,
  • parapheumonic,
  • empyema,
  • TB
  • PE: causing a pulmonary infarct
  • Malignant cancer
  • Inflammatory: rheumatoid arthritis
  • Pancreatitis
  • Dressler’s syndrome: 2-10 weeks post-MI
  • Chylothorax
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13
Q

what will it show?

What Fluid studies can be carried out?

A
  • pH: <7.2 indicates the need for tube drainage
  • Cell counts: lymphocytosis suggests heart failure, malignancy TB
  • Microscopy, Culture & Sensitivity (MC&S): infection
  • Cytopathology: cancer cells
  • Protein, glucose, LDH: Light’s criteria
  • +/- triglyceride levels if chylothorax suspected
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14
Q

Lactate dehydrogenase

What is Light’s criteria for determining exudative effusion?

A
  • when Protein pleural level/level in serum > 0.5
  • LDH pleural level/level in serum >0.6
  • LDH pleural level > 2/3 the upper limit of the normal level in the serum
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15
Q

How would you recognise a parapneumonic effusion?

A
  • sterile inflammation
  • pH > 7.2
  • small/ free flowing
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16
Q

How would you recognise Empyema?

A
  • infected pleural space
  • pus cells present
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17
Q

Hct = Hematocrit

How would you recognise Haemothorax?

A
  • pleural fluid Hct > 50% pf blood Hct
18
Q

How would you recognise Hepatic hydrothorax?

A
  • cirrhotic fluid transverses the diaphragm into the pleural space
19
Q

How would you recognise Chylothorax?

A
  • Triglycerides > 110mg/dL
  • fluid looks milky
20
Q

How does an effusion cause restriction?

A
  • Compressive atelectasis
21
Q

What happens if effusions are not drained?

A
  • Parapneumonic effusions should heal as the pneumonia infection resolves (unless pH<7.2)
  • Haemothorax and empyema require complete evacuation to prevent the development of fibrous visceral pleural peel -> trapped lung (unexpandable lung)
22
Q

What occurs during spontaneous pneumothorax and what are the risk factors?

A
  • rupture of the pleural blebs
  • changes in intrapleural pressure
  • often occur at rest

Risk Factors

  • tall, thin, male, smoker
23
Q

Describe the Intersitrium of the lung

A

- Intralobular Septa: this surrounds the alveoli, where the capillaries are found

- Interlobular Septa: outline the secondary lobules, this is where the lymphatics and veins of the lungs are

  • these interstitial structures can be affected by inflammation or fibrosis (scarring)
24
Q

ILD= Interstitial Lung Disease

What are the origins of Interstitial lung diseases

A
  • IDF: Idiopathic pulmonary fibrosis

Inflammatory Diseases

  • Sarcoidosis
  • Autoimmune ILD
  • Organic exposure leads to Hypersensitivity pneumonitis

Inorganic Exposure

  • Silicosis
  • Coal miners lung
  • Asbestosis
25
Q

What can be seen in Pneumoconiosis chest images, and what are the causes?

A
  • nodular diseases common in silica and coal dust exposure
  • arrows in the MRI point to progressive massive fibrosis
  • arrows in the CT point to pleural plaques, caused by asbestos
  • asbestos exposure can also lead to fibrosis
26
Q

Explain the different levels of hypersensitivity Pneumonitis

A

Diffuse inflammation of parenchyma in response to inhaled antigen

•bird-fanciers, farmers, aspergillus (ubiquitous fungus),

Acute

  • SOB, cough, fever, malaise, crackles within 4-6 hours of heavy exposure ]
  • Often misdiagnosed as an infection

Subacute

•Gradual onset of symptoms, weight loss common

Chronic

  • Insidious onset, history of acute episodes may be absent
  • Incomplete resolution with the removal antigen
  • May lead to irreversible fibrosis
27
Q

What can be used to diagnose Hypersensitivity Pneumonitis?

A
  • the precipitins test using Serum precipitins: circulating IGG antibody-antigen complexes
  • negative results do not exclude HP
  • usually steroid-responsive in early disease
  • may progress to irreversible fibrosis
28
Q

Explain Idiopathic Pulmonary Fibrosis

A

Progressive incurable restrictive lung disease, median survival 2-3 years

  • disease of older age
  • most patients have smoked
  • mostly affects the lower & peripheral aspects of the lungs
  • presents in imaging as fine peripheral lines & honeycomb cysts
  • lots of fibroblast cells: thee make collagen
  • there is minimal inflammation
29
Q

What is the clinical presentation of Idiopathic Pulmonary Fibrosis?

A

symptoms and clinical signs appear gradually

  • slowly progressing exertional dyspnoea: ultimately leads to dyspnoea at rest
  • Non-productive cough
  • Dry, inspiratory bibasal, velcro crackles
  • Clubbing fingers
  • abnormal pulmonary function test results: evidence of restriction and impaired gas exchange
30
Q

What is the pathophysiology of Sarcoidosis?

How is it diagnosed?

A
  • An (antigen) particle is inhaled
  • In the lung it is loaded onto an MHC-II complex (of an antigen-presenting cell, aka APC). The lung is full of APCs, such as dendritic cells, on surveillance for microbes.
  • Receptors on CD4+ T cells bind to the antigen
  • APCs and antigen-bound T cells release cytokines
  • These activate macrophages which organize into granulomas
  • Granulomas also occur in TB and fungal infections, but in sarcoidosis they are sterile.

A biopsy demonstrating granulomas is needed to diagnose sarcoidosis.

31
Q

What ways can Sarcoidosis manifest itself?

A
  • Bilateral hilar lymphadenopathy
  • Diffuse small nodules
  • Nervous system disease; small fibre neuropathy from peripheral nerve damage
  • sarcoidosis in the heart can lead to: heart block, arrhythmias, heart failure
  • nodules and or violaceous plaques on the skin: (lupus pernio when it’s around the nose)
  • Eyes and glands: uveitis, parotitis
  • Systemic reaction: erythema nodosum
32
Q

What are some symptoms of sarcoidosis?

A
  • sometimes asymptomatic: especially in isolated lymphadenopathy
  • organ-based symptoms: in the pulmonary sarcoidosis: cough, dyspnea with exertion, chest tightness
  • systemic symptoms: fatigue, sweats, weight loss, fevers, generalized machines occur in many patients
33
Q

What disease does this lung image show?

What would a PFT reveal in this case?

A

Lymphadenopathy: with essentially normal lung tissue

  • decreased FEV1/FVC ratio
34
Q

What disease does this lung image show?

What would a PFT reveal in this case?

A

Inflammatory sarcoidosis affecting lung

  • lower spirometry and diffuse capacity function
35
Q

What disease does this lung image show?

What would a PFT reveal in this case?

A

Fibrotic sarcoidosis

  • sever restriction in PFT: inspiration and expiration reduced
36
Q

What is the clinical management of sarcoidosis?

A
  • Medication treatment if needed for symptoms or declining lung function: systemic corticosteroids (eg. prednisolone), +/- other immunosuppressant medications
  • Screen for multi-organ disease: eye exam, EKG, blood tests for blood cell counts/liver function/kidney function/calcium
37
Q

How is Cystic Fibrosis diagnosed?

A

- Genetic screening

  • CFTR protein = 1480 amino acids
  • Many gene alterations identified in CF
  • ΔF508 (loss of phenylalanine at amino acid position 508) = most common
  • ΔF508: CFTR protein doesn’t fold properly –> gets degraded

- Sweat Test: salty sweat levels of Cl- >60 mEq

38
Q

What are the symptoms and lung features are seen in Cystic Fibrosis?

A

SYMPTOMS:

  • Excessive mucous, difficult to mobilize
  • Dyspnoea

EXAM FINDINGS:

  • Wheezing
  • Rhonchi

IMAGING FINDINGS:

  • Bronchiectasis
  • Mucous plugging
  • Hyperinflation young age –> shrunken, fibrotic lungs later
39
Q

What are infectious pulmonary complications of Cystic Fibrosis?

A

Acute infections

  • Gram-positive common in young age –> both gram-positive and gram negatives in older age
  • Resistance is a common and BIG problem: MRSA and pseudomonas aeruginosa

•

Chronic infection

  • Pseudomonas and Burkholderia cepacia
  • Allergic bronchopulmonary aspergillosis (ABPA) from aspergillus growing in the airways
40
Q

What other pulmonary complications are there in Cystic fibrosis?

A
  • Haemoptysis
  • Respiratory failure
41
Q

What treatments are there for cystic fibrosis?

A
  • Airway clearance
    • postural drainage
    • chest physical therapy
    • percussion chest
  • Inhaled bronchodilators
  • Mucus thinners
    • Hypertonic nebulizer treatments
  • Others
    • Corticosteroids, inhaled is better than systemic
    • Antibiotics
    • CFTR potentiators: Ivacaftor
    • Lung transplant
    • Pancreatic enzyme replacement: lipase, protease, amylase
42
Q

What other multi-system diseases are caused by Cystic fibrosis?

A
  • Meconium ileus: bowel obstruction due to meconium in the child’s intestine being thicker and stickier than normal meconium
  • Pancreatic insufficiency: thick mucus blocks pancreatic enzymes from entering the small intestine
  • Malnourishment
  • Osteoporosis
  • Male infertility: blockage or absence of the sperm canal

103: Theme 4 - 304 - Respiratory (12 decks)

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