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Jess Resp > First Aid: Obstructive and restrictive lung disease > Flashcards

First Aid: Obstructive and restrictive lung disease Flashcards

1
Q

What happens to the following lung volumes in obstructive and restrictive lung disease?

a) RV
b) FRC
c) TLC
d) FEV1
e) FVC
f) FEV1/FVC

A

Obstructive:
Increased: RV, FRC and TLC
Decreased: FEV1 (very decreased), FVC and FEV1/FVC

Restrictive:
Decreased: RV, FRC, TLC, FEV1, FVC
Increased or normal: FEV1/FVC as the FEV 1 has decreased proportionately with the FVC

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2
Q

How is the flow-volume loop changed in obstructive and restrictive lung disease?

A

Obstructive: shifts left
Restrictive: Shifts right (R-R)

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3
Q

What two diseases comprise COPD?

A

Chronic bronchitis and emphysema

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4
Q

What is the pathology of obstructive lung disease?

A

Obstructed airflow leads to increased trapping of air in the lungs. Airways close prematurely at high lung volumes, leading to further trapping

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5
Q

What can chronic hypoxic pulmonary vasoconstriction lead to?

A

Cor pulmonale

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6
Q

How does chronic bronchitis commonly present?

A

Blue Bloater: WCPCDC

Wheezing, cyanosis, can cause secondary polycythemia, CO2 retention, dyspnea, crackles

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7
Q

How does chronic bronchitis cause secondary polycythemia?

A

As it leads to chronic hypoxemia which triggers increased EPO from the kidneys

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8
Q

What is the pathology of chronic bronchitis?

A

Hyperplasia and hypertrophy of the mucus-secreting glands

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9
Q

What is the Reid index and what would it indicate in chronic bronchitis?

A

Pathological measurement of the ratio between the thickness of submucosal mucus-secreting glands and the thickness between the cartilage and epithelia that line the bronchi, in chronic bronchitis this would be >50%

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10
Q

What is the diagnostic criteria for chronic bronchitis?

A

Productive cough for >3 months in a year, for two consecutive years

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11
Q

How does emphysema commonly present?

A

Barrel chest and pursed lips on expiration (to increase airway pressure and prevent airway collapse)

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12
Q

Describe the two pathological patterns of emphysema, what they’re associated with and the lobes involved

A

Centriacinar: affects the upper lobes, respiratory bronchioles and proximal alveoli (with sparing of the distal alveoli). Associated with smokers

Panacinar: affects the whole lung but more commonly the lung base, (including respiratory bronchioles -> distal alveoli), associated with alpha1 antitrypsin deficiency

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13
Q

Why is there an increase in lung compliance in emphysema?

A

An imbalance of proteases and antiproteases leads to increased elastase, this decreases the elastic recoil fibres and increases lung compliance

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14
Q

What happens as a result of the enlargement of air spaces in emphysema?

A

Decreased: recoil, DLCO (from the destruction of alveolar walls) and blood volume in the pulmonary capillaries

Increased: compliance

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15
Q

What is found on a CXR in emphysema?

A
  1. Increased AP diameter
  2. Increased lung field lucency
  3. flattened diaphragm
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16
Q

What are the clinical findings of asthma?

A

DWCTHIMP: dyspnea, wheeze, cough, tachypnea, hypoxemia, decreased inspiratory/expiratory ratio, mucus plugging, pulsus paradoxus

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17
Q

What are the triggers for asthma?

A

Viral URIs, allergens and stress

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18
Q

What is pulsus paradoxus and what causes it?

A

A significant drop in BP during inspiration (>10 mmHg)

RILE: increased bloodflow to R heart on inspiration and increased bloodflow to L heart on expiration. When the patient inspires the increase in blood in the R heart pushes on the septum, decreasing the space for blood to fill the L heart -> resulting in a decreased CO and BP

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19
Q

Describe the pathology of asthma (including the two microscopic findings)

A
  1. Hyper responsive bronchi leading to reversible bronchoconstriction
  2. Hyperplasia and hypertrophy of the smooth muscle cells

Microscopic findings:

  1. Curschmann spirals: mucus spiral plugs from subepithelial mucus gland ducts of bronchi
  2. Charcot-Leyden crystals: hexagonal, double-pointed eosinophilic crystals formed via eosinophilic degradation in the sputum
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20
Q

What type of hypersensitivity reaction occurs in asthma?

A

Type 1

21
Q

What supports the diagnosis of asthma?

A

Spirometry and the methacholine challenge

22
Q

What makes up NSAID exacerbated respiratory disease?

A

COX inhibitors (inhibit cyclooxygenase (COX) which helps produce prostaglandins from arachidonic acid, with this inhibited arachidonic acid forms leukotrienes (which are released from mast cells during an asthma attack) and cause bronchoconstriction

Chronic sinusitis w nasal polyps (a result of chronic inflammation)

Asthma symptoms

23
Q

What are the clinical findings in bronchiectasis?

A

PPHD: purulent sputum, recurrent infections (most commonly P. aeruginosa), hemoptysis and digital clubbing

24
Q

What happens pathologically in bronchiectasis and why?

A

Permanently dilated airways due to chronic necrotizing infection of the bronchi or obstruction

25
Q

What is bronchiectasis associated with?

A

ABCC
1. Allergic bronchopulmonary aspergillosis

  1. Bronchial obstruction
  2. CF
  3. Impairment of mucociliary escalator: i.e due to smoking or kartagener syndrome (rare autosomal recessive ciliary disorder)
26
Q

What are some associated conditions when there is poor breathing mechanics in restrictive lung disease?

Is it extrapulmonary or pulmonary, and how does it affect the DLCO and A-a gradient?

A
  1. Poor muscular effort: polio, MS, Guillain barre
  2. Poor structural apparatus: scoliosis, morbid obesity

Extrapulmonary, normal DLCO and A-a gradient

27
Q

What are some associated conditions when there is ‘interstitial disease’ in restrictive lung disease?

Is it extrapulmonary or pulmonary, and how does it affect the DLCO and A-a gradient?

A

GLISPHD

  1. Granulomatosis with polyangiitis (Wegener’s granulomatosis)
  2. Pulmonary Langerhans cell histiocytosis (eosinophilic granuloma)
  3. Idiopathic pulmonary fibrosis
  4. Sarcoidosis
  5. Pneumoconioses (i.e coal workers pneumoconiosis, silicosis, asbestosis)
  6. Hypersensitivity pneumonitis
  7. Drug toxicity (i.e methotrexate, bleomycin, busulfan, amiodarone)

Pulmonary, decreased DLCO and increased A-a gradient

28
Q

What happens in idiopathic pulmonary fibrosis? How does the lung appear?

A

When there are repeated cycles of lung injury and wound healing with increased collagen deposition, the lung has a “honeycomb” appearance

29
Q

What is hypersensitivity pneumonitis? What symptoms can it cause, and where is it commonly seen? Is it reversible?

A

A mixed type 3/4 hypersensitivity reaction to an environmental antigen, can cause: dyspnea, cough, chest tightness, fever and headache

Commonly seen in farmers and those exposed to birds and is reversible in early stages if the stimulus is avoided

30
Q

What is sarcoidosis characterized by? Describe what you would find in the serum levels, bronchoalveolar lavage fluid, on a CXR and a CT scan

A

Characterized by immune-mediated widespread noncaseating granulomas

Serum: elevated ACE and Ca2+ (hypercalcemia is due to the increase in 1alpha hydroxylase-mediated vitamin D activation in macrophages)

Bronchoalveolar lavage fluid: elevated CD4/CD8 ratio

CXR: bilateral adenopathy and coarse reticular opacities

CT: better demonstrates the extensive hilar and mediastinal adenopathy

31
Q

What population is most commonly affected by sarcoidosis? Is it symptomatic?

A

African American females, often asymptomatic other than enlarged lymph nodes

32
Q

What conditions are associated with sarcoidosis?

A

A facial droop is UGLIER (neurosarcoidosis can cause sudden facial weakness)

U: Uveitis
G: granulomas (noncaseating epithelioid, containing microscopic Schaumann and asteroid bodies)
L: Lupus pernio (skin lesions on face resembling lupus; hard and purplish)
I: Interstitial fibrosis
E: erythema nodosum
R: rheumatoid arthritis-like arthropathy

33
Q

How is sarcoidosis treated?

A

With steroids, if it’s symptomatic

34
Q

What causes inhalation injury and sequelae and what does it result in?

A

Inhalation of noxious stimuli (i.e smoke), caused by heat, particulates or irritants (i.e NH3) which leads to chemical tracheobronchitis, edema, pneumonia and ARDS

35
Q

How do many patients present with inhalation injury and sequelae? What might be observed on examination?

A

Secondary burns, CO inhalation, cyanide poisoning or arsenic poisoning.

Singed nasal hairs or soot in the oropharynx are common on examination

36
Q

What might be noted on a bronchoscopy in inhalation injury and sequelae?

A

Severe edema, congestion of the bronchus and soot deposition

37
Q

What parts of the lungs do asbestos and silica affect?

A

Asbestos: base/lower lobes
“Is from the roof but affects the base”

Silica: Upper lobes
“Is from the base (earth) but affects the roof”

38
Q

What increases your risk of getting asbestosis?

A

shipbuilding, roofing, plumbing

39
Q

What is pathognomonic of asbestosis?

A

“Ivory white” calcified supradiaphragmatic and pleural plaques

40
Q

What does asbestosis increase your risk of?

A
  1. bronchogenic carcinoma (> mesothelioma)
  2. Caplan syndrome (rheumatoid pneumoconiosis)
  3. Pleural effusions
41
Q

How do asbestos particles appear histologically? Where and how can they be visualized and obtained?

A

Golden-brown fusiform rods, visualized in alveolar sputum using Prussian blue stain - and are often obtained via bronchoalveolar lavage

42
Q

What increases your risk of getting berylliosis? How does it appear histologically and how can it be treated?

A

Exposure to beryllium in aerospace and manufacturing industries. Noncaseating granulomas on histology and so is occasionally responsive to steroids

43
Q

Which part of the lung is affected by berylliosis and what can it increase your risk of?

A

The upper lobes, increased risk of cancer and cor pulmonale

44
Q

Describe the pathology of coal worker’s pneumoconiosis, what can it increase your risk of?

A

Prolonged coal dust exposure -> leads to macrophages laden with carbon -> inflammation and fibrosis

Increased risk of Caplan syndrome

45
Q

Which part of the lung is affected by coal worker’s pneumoconiosis? How does it appear on imaging

A

Upper lobes, small rounded nodular opacities are seen on imaging

46
Q

What term is used to describe the asymptomatic nature of pneumoconiosis found in many urban dwellers exposed to sooty air

A

Arthracosis

47
Q

What increases your risk of getting silicosis? How does it appear on a CXR?

A

The Silly Egg sandwich I found is mine!

Increased risk of getting it when: SANDblasting, FOUNDries, MINEs

CXR: “EGGshell” calcifications of hilar lymph nodes

48
Q

How do macrophages respond to silica and what happens as a result of this?

A

They release fibrogenic factors leading to fibrosis

49
Q

What does silicosis increase your risk of?

A

Silica may also disrupt phagolysosomes and impair macrophages - increasing susceptibility to TB

3 Cs: Cancer, cor pulmonale, Caplan’s syndrome

Jess Resp (20 decks)

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