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Bateman - Phase 2a COPY > Lung Pathology > Flashcards

Lung Pathology Flashcards

1
Q

How common are occupational lung disorders?

A

Extremely.

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2
Q

What are the different modes for OLD to get?

A

Vapour.

Gases.

Dusts.

Fume.

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3
Q

What is vapour or gases?

A

Liquid or solid substance suspended in air.

Including mists.

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4
Q

What is dust?

A

Aerosolised solid particles. Size from 1 to less than 100 nanometers.

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5
Q

What is a fume?

A

Normally vapour or gas.

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6
Q

When do most occupational lung disorders occur?

A

After a period of latent (asymptomatic) exposure.

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7
Q

What is the current exposure factors for OLD?

A

Earlier recognition

Identify and cease exposure

Improve prognosis

Health versus income

Loss of employment

Eg allergic OA

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8
Q

What is the historical exposure factors for OLD?

A

Recognised years later

Not normally exposed

Supportive measures

Little/no impact on prognosis

Benefits advice

Eg asbestosis

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9
Q

What factors do you have to think about when looking at OLDs?

A

Susceptibility

-Genetic/individual vs population

Severity

-No sx vs disability/death

Reversibility

-Reversible vs irreversible

Employment

-Working vs employed

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10
Q

What are the most common OLDs?

A

Asthma.

Allergic alveoli’s.

Bronchitis/empyhsema.

Non-malignant pleural disease.

Mesothelioma.

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11
Q

How can occupational asthma be caused?

A

90% Asthma induced by sensitisation (allergy) to an agent inhaled at work.

10% Asthma induced by massive accidental irritant exposure at work (direct airway injury).

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12
Q

How much of adult onset asthma does occupational asthma take up?

A

9-15%.

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13
Q

What happens with occupational asthma prolonged exposure?

A

Ongoing exposure worse prognosis

Early identification important

Treat or even cure

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14
Q

What would a case study of occupational asthma show?

A

Normal spirometry.

Work-effect confirmed by seal PEF.

Positive IgE to wheat flour.

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15
Q

What is an example of allergic sensitisation?

A

Extrinsic allergic alveolitis.

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16
Q

How can extrinsic allergic alveolitis be caused?

A

Occupational or environmental.

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17
Q

What is extrinsic allergic alveolitis?

A

An interstital lung disease

Upper lobe predominant, gas trapping, ground glass, progresses to fibrosis.

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18
Q

How is extrinsic allergic alveolitis classed?

A

Duration.

Acute (may be self-limiting).

Subacute.

Chronic (scarring).

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19
Q

What are the different occupational hazards for extrinsic allergic alveolitis?

A

Microorganisms.

Animals.

Vegetation.

Chemcials.

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20
Q

What are the different microorganisms causing for EAA?

A

FARMERS!

wood pulp workers, sewage workers, maple bark strippers, cheese washers, metalworking engineers, mushroom workers, suberosis, bagassosis

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21
Q

What animals, vegetation and chemicals can cause EAA?

A

•Animals

–Birds, wheat weevil, fish meal, rodent handlers

•Vegetation

–Coffee, wood

•Chemicals

–Vineyard sprayers, insecticide, isocyanates, anhydrides, plastics

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22
Q

What does prognosis of EEA depend on?

A

Early recognition and avoiding exposure.

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23
Q

What percentage of COPD happens within occupational exposure?

A

10-15%.

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24
Q

What historic VGDF cause COPD?

A

Coal, silica, grain

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25
Q

What is an occupational hazard that can cause COPD?

A

Dust exposure.

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26
Q

What deficiency makes a person more likely to develop COPD?

A

Alpha-1 antitrypsin deficiency.

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27
Q

What are some asbestos-related lung diseases?

A

Pleural plaques

Diffuse pleural thickening.

Asbestosis.

Lung cancer.

Mesothelioma

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28
Q

What is asbestos?

A
  • Naturally occurring mineral fibre
  • Used for millenia

–Insulating, fire-retardant, tensile strengh

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29
Q

What are pleural plaques and why are they important in asbestos-related lung diseases?

A

Pleural collagen, often calcified.

Marker of exposure.

Not pre-malignant.

Aetiology unclear.

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30
Q

What is diffuse pleural thickening and why is it important in asbestos-related lung disease?

A

Follows benign effusion.

Obliteration of costophrenic angle.

Can cause.

-restriction due to thickened pleura. -SOB, respiratory failure.

No effective treatment.

May progress slowly (without further treatment).

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31
Q

What is asbestosis and why is it important in asbestos-related lung disease?

A

Pulmonary fibrosis

  • Subpleural, basal, UIP pattern.

With/without plaques.

History of heavy exposure.

No effective treatment.

May progress (without further exposure).

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32
Q

What is mesothelioma and why is it important in asbestos-related lung disease?

A

Rapidly progressive and usually incurable pleural cancer

Lung encased by tumour

Often presents as an unexplained pleural effusion

Progressive breathlessness, chest pain, weight loss

Average survival 8-14 months.

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33
Q

How can you prevent OLDs?

A

Requirement under COSHH.

Focus on exposure prevention or minimisation.

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34
Q

What procedures can you do to help prevent OLDs?

A

–Elimination (eg asbestos)

–Substitution (eg latex to nitrile gloves)

–Engineering controls (eg exhaust ventilation)

–Worker education

–RPE (masks and respirators)

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35
Q

What can you do if there is an individual risk to a patient?

A

Yearly questionnaire/spirometry/CXR

Identify ill health early

Prevent further harm by reducing/preventing exposure

Review control measures to protect other workers

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36
Q

What are the two types of obstruction?

A

Acute and Chronic.

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37
Q

What are the features of acute obstruction?

A

Can survive localised effects…inspiratory stridor or very few effects

Major airway obstruction often life limiting.

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38
Q

What usually causes acute obstruction and what does it cause? What does it show in pulmonary function tests?

A

Obstruction by tumour or foreign body

Causes distal collapse (atelectasis) or over expansion (valve effect)

Later may be complicated by secretions +++ >> distal lipoid or infective pneumonia

Usually normal pulmonary function tests

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39
Q

What are the Asthma-clinical categories?

A

Extrinsic and Intrinsic.

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40
Q

What is involved in extrinsic asthma factors?

A

Atopic = IgE / Type 1 hypersensitivity

Occupational = Type 3 hypersensitivity

Allergic bronchopulmonary aspergillosis

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41
Q

What is involved in intrinsic asthma factors?

A

Aspirin, cold, infection, stress, exercise, SO2, pollutants etc - induced.

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42
Q

What causes extrinsic asthma?

A

Enviromental agents like dust, pollens, foods, animal dusts etc.

Family history often +

Other atopic disorders (hay fever, eczema)

Exposure >> effect.

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43
Q

What is the pathogenesis of asthma?

A

Bronchial obstruction with distal overinflation or atelectasis

Mucus plugging of bronchi

Bronchial inflammation (mixed)

Seromucinous gland hypertrophy

Bronchial wall smooth muscle hypertrophy

Thickening of bronchial basement membrane.

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44
Q

What factors are involved with the pathogenesis of asthma?

A

Leukotrienes C4, D4, E4

Prostaglandins D2, E2, F2α

PAF

Mast cell tryptase

Both early & late phase.

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45
Q

What is intrinsic asthma associated with?

A

Associated with reccurent chest infections

Chronic bronchitis

Not immune-mediated

Possibly unusually hyper-reactive airways.

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46
Q

How is aspirin-induced asthma caused?

A

Unknown mechanism

Possibly increased locally leukotrienes or decreased prostaglandins

Usually associated with recurrent rhinitis with nasal polyps

and/or skin urticaria.

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47
Q

What is Allergic bronchopulmonary aspergillosis and what does it do?

A

Aspergillus fumigatus.

Induces both immediate type I reaction

And delayed immune complex type III. hypersensitivity reaction.

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48
Q

What are the key features of chronic obstruction?

A

Reversible (variable %) and intermittent often

Centered on bronchi or bronchioles ‘Obstructive’ pulmonary function tests

Usually many airways involved = diffuse process. Can adapt possibly.

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49
Q

What are some chronic obstructive diseases?

A

Chronic bronchitis and/or emphysema

Asthma

Bronchiectasis

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50
Q

What are both bronchitis and emphysema grouped under?

A

COPD

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51
Q

Who does chronic bronchitis affect?

A

Affects middle aged heavy smokers

Some following pollution chronically

Recurrent low grade bronchial infections

>>> Haemophilus influenzae, Streptococcus pneumoniae, viruses (respiratory syncytial virus, adenovirus).

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52
Q

What is the pathological basis of chronic bronchitis?

A

Viruses

Mucus hypersecretion with bronchial mucous gland hypertrophy

Respiratory bronchiolitis

Tobacco smoking-induced mainly

Some asthma effects

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53
Q

What does chronic bronchitis produce? (Symptoms)

A

Productive cough (cough and sputum) for 3 months in 2 consecutive years

Cough

Production of mucus (sputum), which can be clear, white, yellowish-gray or green in color — rarely, it may be streaked with blood

Fatigue

Shortness of breath

Slight fever and chills

Chest discomfort

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54
Q

What are the differential diagnosis for chonic bronchitis?

A

Alpha1-Antitrypsin Deficiency

Asthma

Bronchiectasis

Chronic Obstructive Pulmonary Disease (COPD)

Chronic Sinusitis

Gastroesophageal Reflux Disease

Influenza

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55
Q

What are the investigations for chronic bronchitis?

A

Chest X-ray can help rule out other lung conditions, such as pneumonia.

Sputum (bacteria).

A pulmonary function test.

CT scan.

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56
Q

What are the management options for chronic bronchitis?

A

A bronchodilator.

Theophylline is an oral medication that relaxes the muscles in your airways.

Steroids

Pulmonary rehabilitation. It often consists of exercise, nutritional counseling, and breathing strategies.

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57
Q

What is the progression of chronic bronchitis?

A

Often starts mild….severe

Hypercapnia

Hypoxaemia

Cyanosis (blue bloaters)

Right heart failure and/or respiratory.

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58
Q

What are some bronchial abnormalities with chronic bronchitis?

A

Mucus hypersecretion

Chronic inflammation

Irritation and inflammation leading to squamous metaplasia.

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59
Q

What is emphysema?

A

Enlargement of alveolar airspaces with destruction of elastin in walls.

Permanent enlargement of airspaces distal to terminal bronchioles due to destruction of walls.

Centri-acinar, pan-acinar and distal acinar

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60
Q

What are the causes of emphysema?

A

Cigarette smoking. (MAINLY)

Alpha-1-antitrypsin deficiency

Coal dust exposure

Cadmium toxicity

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61
Q

What is the pathogenesis of emphysema?

A

Pathogenesis probably revolves around recruitment of neutrophils in response to free oxygen radicals with release of IL8, LTB4 and TNF.

Also released are destructive enzymes e.g. neutrophil elastase.

Ultimate result = tissue damage.

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62
Q

What does emphysema cause? What does this prevent?

A

Gas trapping effect from emphysema

Prevents full exhalation of air, particularly if large bullae.

No increased risk of cancer

But

Pulmonary hypertension

Poor oxygen delivery to tissues

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63
Q

What are the symptoms of emphysema?

A

1/3 of lung capacity is destroyed before symptoms

‘pure’ emphysema appears with reduced PaCO2 and normal PaO2 at rest due to overventillation (‘pink puffers’)

Weight loss due to metabolic demands ++

Right heart failure

Overinflated chest

Poor oxygen delivery to tissues.

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64
Q

What are the differential diagnosis of emphysema?

A

Bronchiectasis

Bronchitis

Lymphangioleiomyomatosis

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65
Q

What are the investigations for emphysema?

A

Blood tests- Concentration of red blood cells, increased, lack of oxygen in the body. This process is called secondary polycythaemia.

Chest x-ray– This helps to show hyperexpansion of the lungs. Enlarged and empty and may flatten out the diaphragm.
Bullae (dilated airspaces) from severe emphysema at the outside of the lungs. Chest x-ray may be normal.

ECG or Echocardiogram– right heart failure (a complication of emphysema and COPD).

Pulmonary/Lung Function tests– Spirometry is the best test to detect airflow limitation and obstruction.

Blood gases- Normal, later stages of disease, low oxygen and high carbon dioxide levels.

High resolution CT – best test for detecting emphysema and bullae (big dilated air spaces).

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66
Q

What is the treatment for emphysema?

A

Stop smoking

Medications (tiotropium (antimuscarinic)) corticosteroids (prednisone) beta 2 agonist.

Oxygen therapy

Respiratory therapy

Surgery

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67
Q

What is Bronchiectasis and what is it due to?

A

Is the permanent dilatation of bronchi and bronchioles

Due to

Obstruction

Severe inflammation

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68
Q

Which parts of the lung are affected by bronchiectasis and why?

A

Usually the lower lobes are affected

Pooling of secretions with further infection

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69
Q

What is the morphology of bronchiectasis?

A

Dilation of bronchi and bronchioles

Inflammation during acute exacerbations

Inflammation and fibrosis extend into adjacent lung tissue

Cylindrical, saccular or fusiform bronchioles

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70
Q

What are the symptoms of bronchiectasis?

A

Chronic cough with expectoration of large quantities of foul- smelling sputum

Flecked with blood sometimes.

Finger clubbing

Coarse inspiratory crepitations.

Wheeze (asthma, COPD, ABPA).

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71
Q

What are the differential diagnosis for bronchectasis?

A

Alpha1-Antitrypsin Deficiency

Aspiration Pneumonitis and Pneumonia

Asthma

Bacterial Pneumonia

Bronchitis

Chronic Obstructive Pulmonary Disease (COPD)

Cystic Fibrosis

Emphysema

Gastroesophageal Reflux Disease

Parapneumonic Pleural Effusions and Empyema Thoracis

Tuberculosis (TB)

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72
Q

What are the complications with bronchiectasis?

A

Pneumonia

Fungal colonisation

Emphysema

Septicaemia

Meningitis

Metastatic abscesses (e.g. brain, heart)

Amyloid formation.

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73
Q

What are the tests for bronchiectasis?

A

Sputum culture.

Chest X-Ray - Cystic shadows, thickened bronchial walls.

HRCT chest: To assess extent and distribution of disease.

Spirometry - Obstructive.

Bronchoscopy to locate site of haemoptysis, exclude obstruction and obtain samples for culture.

Other tests: serum immunoglobulins; CF sweat test; Aspergillus precipitins or skin-prick test.

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74
Q

What is the management for bronchiectasis?

A
  • Postural drainage should be performed twice daily. Chest physiotherapy may aid sputum expectoration and mucous drainage.
  • Antibiotics to bacterial sensitivities. Patients known to culture Pseudomonas will require either oral

Ciprofloxacin or IV antibiotics.

  • Bronchodilators (eg nebulized salbutamol) may be useful in patients with asthma, COPD, CF, ABPA.
  • Corticosteroids (eg prednisolone) for ABPA.
  • Surgery may be indicated in localized disease or to control severe haemoptysis.
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75
Q

What are interstitial lung diseases?

A

Increased amount of lung tissue

Increased stiffness and decreased compliance

Restrictive lung defect of the pulmonary function

\Reduced Tco, VC, FEV1

Relatively normal FEV1/FVC ratio and PEFR.

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76
Q

Where are interstital lung diseases found? What is the similar pathology?

A

Alveolar-capillary wall is the site of lesion

non-compliant lung with loss alveolar surface

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77
Q

What are acute interstitial lung diseases mostly due to?

A

Adult respiratory distress syndrome Due to……

Drug and toxin reactions

Gastric aspiration

Radiation pneumonitis

Diffuse intrapulmonary haemorrhage.

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78
Q

What are the causes of adult respiratory distress syndrome?

A

Shock

Trauma, direct pulmonary or multisystem trauma

Infections (often severe viral or bacterial)

Gas inhalation (NO2, SO2, smoke, Cl2)

Narcotic abuse

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79
Q

What is adult respiratory distress syndrome?

A

Diffuse alveolar damage with hyaline membranes

Fatal in many cases

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80
Q

What are the symptoms of acute respiratory distress syndrome?

A

Causes acute respiratory distress with tachypnoea, dyspnoea, pulmonary oedema and arterial hypoxaemia refractory to O2 therapy.

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81
Q

What do Cytotoxic drugs do?

A

Lead to low grade alveolitis with healing interstitial fibrosis.

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82
Q

What does Paraquat do?

A

Acts by release of hydrogen peroxide and the superoxide free radical.

It remains in high concentrations in the lungs after ingestion.

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83
Q

What are some Chronic interstitial diseases? (Differential diagnosis of eachother)

A

Fibrosing alveolitis (CFA, UIP)

Pneumoconioses

Sarcoidosis

Diffuse malignancies

Rheumatoid diseases

Etc LCH, LAM, NSIP, GIP.

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84
Q

What are the signs and symptoms of fibrosing alveolitis?

A

Dry cough;

exertional dyspnoea;

malaise;

weight decrease;

arthralgia.

Finger and toe clubbing

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85
Q

What does it fibrosing alveolitis result in? What is the aetiology?

A

Results in an end-stage fibrosis (honeycomb lung)

Unknown aetiology

Restrictive pattern of the pulmonary function tests

>>> cor pulmonale

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86
Q

What are the tests for fibrosing alveolitis?

A

Blood: ABG decrease in oxygen, increase in CO2

CRP increase;

immunoglobulins increase;

ANA (30% +ve), rheumatoid factor (10% +ve).

CXR: Lung volume decrease; bilateral lower zone reticulonodular shadows; honeycomb lung (advanced disease).

CT shows similar changes to the CXR but is more sensitive and is an essential tool for diagnosis.

Spirometry: Restrictive; decrease transfer factor.

BAL (bronchoalveolar lavage) may indicate activity of alveolitis: lymphocytes (good response/prognosis) or neutrophils and eosinophils (poor response/prognosis).

Lung biopsy may be needed for diagnosis.

The histological changes observed on biopsy are referred to as usual interstitial pneumonia (UIP).

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87
Q

What are the management options for idiopathic pulmonary fibrosis?

A

Best supportive care: oxygen, pulmonary rehabilitation, opiates, palliative care input.

High-dose steroids are NOT used except where the diagnosis of IPF is in doubt.

All patients should be considered for current clinical trials or lung transplantation

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88
Q

What does fibrosing alveolitis produce?

A

Abnormally large irregular spaces separated by thick fibrous septa (honeycomb lung),

UIP (usual interstial pneumonia) histology

The subpleural regions are predominantly affected.

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89
Q

What is pneumoconiosis? What type of material can cause it?

A

Lung disease caused by inhaled dust Organic or inorganic dust (mineral)

Reaction varies:

Inert

Fibrous.

Allergic.

Neoplastic.

Co-existing disease may aggravate the lung debility.

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90
Q

What are the different ways a lung responds to inhaled dust?

A

Inert: coal worker’s pneumoconiosis

Fibrous: progressive massive fibrosis, asbestosis and silicosis

Allergic: extrinsic allergic alveolitis

Neoplastic: mesothelioma, lung cancer.

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91
Q

What happens in coal workers’ pneumoconiosis?

A

Coal is ingested by alveolar macrophages (dust cells)

They aggregate around bronchioles

The consequences vary from trivial to lethal.

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92
Q

What do each of these words mean? Anthracosis. Macular CWP. Nodular CWP.

A

Anthracosis: the presence of coal dust pigment in the lung

Macular CWP: aggregates of dust laden macrophages with no significant scarring

Nodular CWP : nodules >10mm in a background of extensive macular CWP, with no significant scarring.

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93
Q

What is Caplan’s syndrome?

A

The association between rheumatoid arthritis, pneumoconiosis, and pulmonary rheumatoid nodules.

94
Q

What is progressive massive fibrosis?

A

Due to progression of CWP, which causes progressive dyspnoea, fibrosis, and, eventually, cor pulmonale. CXR: upper-zone fi- brotic masses (1–10cm).

95
Q

How do you treat pneumoconiosis and progressive massive fibrosis?

A

Avoid exposure to coal dust; treat co-existing chronic bronchitis; claim compensation (in the UK, via the Industrial Injuries Act).

96
Q

What causes silicosis?

A

Silicates are inorganic minerals abundant in stone and sand

2µm fibres toxic to macrophages, leading to their death with release of proteolytic enzymes.

Tissue destruction and fibrosis

Nodules are formed after many years of exposure.

97
Q

What are the clinical features of silicosis?

A

Progressive dyspnoea,

increase incidence of TB,

CXR shows diffuse miliary or nodular pattern in upper and mid-zones and egg-shell calcification of hilar nodes.

Spirometry: restrictive ventilatory defect.

98
Q

How do you treat silicosis?

A

Avoid exposure and claim compensation.

99
Q

What are the causes of extrinsic allergic alveolitis?

A

Classic types =

Bird fancier’s lung.

Farmer’s lung.

Caused by fungus (poorly stored / mouldy hay)

Type 3 hypersensitivity >>> Bronchiolitis Later: chronic inflammation and granulomas Resolve or lead to fibrosis.

100
Q

What are the clinical features of extrinsic allergic alveolitis?

A

4–6h post-exposure:

Fever, rigors, myalgia, dry cough, dyspnoea, crackles (no wheeze).

Chronic: Increasing dyspnoea, weight decrease, exertional dyspnoea, type I respiratory failure, cor pulmonale.

101
Q

What are the tests for extrinsic allergic alveolitis?

A

Acute:

Blood: FBC (neutrophilia); ESR increase; ABGS; positive serum precipitins (indi- cate exposure only).

CXR: upper-zone mottling/consolidation; hilar lymphadenopathy (rare).

Lung function tests: reversible restrictive defect; reduced gas transfer during acute attacks.

Chronic:

Blood tests: positive serum precipitins.

CXR: upper-zone fibrosis; honeycomb lung.

Lung function tests: persistent changes (see above).

Bronchoalveolar lavage (BAL) fluid shows  lymphocytes and mast cells.

102
Q

What are the management options extrinsic alergic alveolitis?

A

Acute:

Remove allergen and give O2 (35–60%), then:

Oral prednisolone (40mg/24h PO), followed by reducing dose.

Chronic:

Avoid exposure to allergens, or wear a facemask or +ve pressure helmet.

Long-term steroids often achieve CXR and physiological improvement.

Compensation (UK Industrial Injuries Act) may be payable.

103
Q

What is sarcoidosis?

A

Granulomatous disease affecting mainly the lungs, but also lymph nodes in a greater frequency

104
Q

What is the Kveim test?

A

Subcutaneous injection of sterile homogenised sarcoid tissue induces granulomas in affected patients

105
Q

What are some cancers of the lung?

A

Lymphangitis (carcinomatosa)

Lepidic (bronchioloalveolar) carcinoma

106
Q

What do each of these represent? Mab. sone. terol. lone. nib.

A

mab = monoclonal antibody (e.g Reslizumab)

sone = corticosteroid (e.g Dexamethasone)

terol = brochodilators (e.g Salmeterol)

lone = corticosteroid (e.g prednisolone)

nib = kinase inhibitor (e.g Nintedanib)

107
Q

What two regions do the lungs consist of?

A

Conducting and respiratory regions.

108
Q

What does the respiratory region consist of?

A

respiratory bronchioles, alveolar ducts, and alveolar sacs.

109
Q

What do inhalers and nebulisers deliver?

A

Inhalers deliver a dry powder formula whilst nebulisers deliver medication in the form of an aerosol.

110
Q

What is the difference between the respiratory region and conducting region of the lungs?

A

Conducting airways: smaller surface area and lower regional blood flow. High filtering capacity (mucus, cilia) removes up to 90% of delivered drug particles Respiratory region: accounts for more than 95% of the lung’s surface area and is directly connected to the systemic circulation via the pulmonary circulation.

111
Q

What are the different delivery methods for inhaled drugs?

A

PRESSURIZED METERED-DOSE INHALERS (PMDIS) THE DEVICE IS ACTIVATED BY THE USER PRESSING DOWN ON THE TOP OF THE CONTAINER, RESULTING IN THE RELEASE OF A FINE SPRAY CONTAINING PROPELLANT AND DRUG. SPACER DEVICES SLOW DOWN THE PARTICLES OF THE DRUG AND ALLOW MORE TIME FOR EVAPORATION OF THE PROPELLANT SO THAT MORE OF THE DRUG CAN BE INHALED. DRY POWDER INHALERS (DPIS) DPIS DO NOT HAVE A PROPELLANT — INSTEAD, ON ACTIVATION, THE DEVICE RELEASES A SMALL AMOUNT OF DRUG IN POWDER FORM, WHICH IS THEN INHALED (THIS REQUIRES THE PERSON TO HAVE SUFFICIENT INSPIRATORY EFFORT TO BREATHE IN THE POWDER). NEBULIZERS NEBULIZERS WORK BY DISPERSING A LIQUID INTO A FINE MIST WHICH CAN BE INHALED THROUGH A MASK OR MOUTHPIECE. THEIR MAIN ADVANTAGE IS THAT NO COORDINATION IS REQUIRED BY THE USER, AND HIGH DOSES OF DRUG CAN BE DELIVERED TO THE AIRWAYS.

112
Q

What are some factors to consider of inhaled therapeutics?

A

SOLUBILITY. PRESENTLY, SOME OF THE LEAST-SOLUBLE DRUGS ADMINISTERED BY INHALATION ARE INHALED CORTICOSTEROIDS (ICS) FOR ASTHMA, SUCH AS BECLOMETHASONE DIPROPIONATE (BDP) AND FLUTICASONE PROPIONATE (FP) CHARGE AND TISSUE RETENTION. (LUNG TISSUE BINDING) THIS CAN PREVENT ABSORPTION AND INCREASE HALF LIFE. ENCAPSULATION. ALLOWS CONTROLLED RELEASE BY USE OF EXCIPIENTS (MOLECULES THAT MODIFY PROPERTIES OF MEDICINES E.G. IMPROVES SOLUBILITY AND DISPERSION, MASK TASTE ETC.

113
Q

What are the advantages of inhaled drugs?

A

LUNGS ARE ROBUST AND ABLE TO SAFELY HANDLE REPEATED EXPOSURE TO THERAPEUTICS. INHALED MEDICINES CAN ACT DIRECTLY ON THE LUNG OR ENTER THE SYSTEMIC CIRCULATION. FASTEST SYSTEMIC UPTAKE OTHER THAN IV ADMINISTRATION VERY RAPID ABSORPTION LUNGS ARE NATURALLY PERMEABLE TO PEPTIDES (VIA EPITHELIAL CELLS) LARGE SURFACE AREA (ALVEOLAR SURFACE ~75m2) FEWER DRUG METABOLISING ENZYMES IN THE LUNG COMPARED WITH BLOOD/LIVER NON-INVASIVE PORT OF ENTRY INTO THE SYSTEMIC CIRCULATION POTENTIALLY FEWER SYSTEMIC SIDE EFFECTS.

114
Q

What diseases cause bronchoconstriction?

A

Asthma and COPD.

115
Q

What happens in bronchoconstriction?

A

Constriction of the airways due to tightening of airway smooth muscle (ASM) lumenal occlusion by mucus and plasma airway wall thickening Leads to airflow obstruction.

116
Q

What are the two main categories of bronchodilators?

A

ADRENERGIC (SYMPATHETIC) BRONCHODILATION ANTI-CHOLINERGIC (PARASYMPATHETIC) BLOCK BRONCHOCONSTRICTION.

117
Q

What are bronchodilators: B2 adrenoreceptor agonists? and what are some examples?

A

b2-adrenoceptor agonists act on b2-adrenoceptors to cause smooth muscle relaxation and bronchodilation. Also inhibit histamine release from lung mast cells SABA: Short acting b2-adrenoceptor agonists e.g. Salbutamol LABA: Long acting b2-adrenoceptor agonists e.g. Formoterol and Salmeterol). ultra-LABAs (e.g Indacaterol, Olodaterol) allow once-daily dosing. Inhaled medicines, either aerosolised or as dry powder. LABAs are often combined with inhaled corticosteroids for the treatment of asthma and with an inhaled long-acting antimuscarinic agent (LAMA) for treating COPD patients.

118
Q

How does the ASM become contracted?

A

ACETYLCHOLINE (Ach) CONTRACTS ASM BY ACTIVATING MUSCARINIC RECEPTORS ON SMOOTH MUSCLE CELLS.

119
Q

What do antagonists do to stop ASM contracting?

A

ANTAGONISTS (anticholinergics) BLOCK ACh BINDING TO MUSCARINIC RECEPTORS.

120
Q

What are some examples of some muscarinic receptor antagonists?

A

ATROPINE IS A NATURALLY OCCURRING ANTICHOLINERGIC FOUND IN DEADLY NIGHTSHADE. ATROPINE REVERSES BRONCHOCONSTRICTION CAUSED BY PARASYMPATHETIC NERVE STIMULATION IPRATROPIUM BROMIDE & TIOTROPIUM BROMIDE ARE NEWER SYNTHETIC DERIVATIVES OF ATROPINE WITH FEWER SIDE EFFECTS.

121
Q

What diseases does inflammation occur?

A

Pneumonia. Asthma COPD. IPF.

122
Q

What cells are involved in inflammation of the lung?

A

INFLAMMATORY CELLS SUCH AS NEUTROPHILS AND EOSINOPHILS INAPPROPRIATELY PERSIST IN THE AIRWAY AND LEAD TO DIRECT TISSUE DAMAGE PERPETUATION OF INFLAMMATION

123
Q

What is the main treatment for inflammation? What do they do for the patient?

A

GLUCOCORTICOIDS (AKA CORTICOSTEROIDS) SUPPRESS INFLAMMATION VIA SEVERAL MECHANISMS MOST EFFECTIVE ANTI-INFLAMMATORY FOR ASTHMA INHALED CORTICOSTEROIDS (ICS): IMPROVE THE QUALITY OF LIFE OF PATIENTS WITH ASTHMA IMPROVE LUNG FUNCTION REDUCE FREQUENCY OF EXACERBATIONS CAN PREVENT IRREVERSIBLE AIRWAY CHANGES RELATIVELY INEFFECTIVE IN COPD, CF, IPF PARADOX BECAUSE BOTH ASTHMA AND COPD INVOLVE INFLAMMATION SEVERE ASTHMATICS CAN BECOME RESISTANT

124
Q

How do inhaled corticosteroids reduce inflammation?

A

AT A CELLULAR LEVEL GLUCOCORTICOIDS REDUCE THE NUMBERS OF INFLAMMATORY CELLS IN THE AIRWAYS SUPPRESS THE PRODUCTION OF CHEMOTACTIC MEDIATORS REDUCE ADHESION MOLECULE EXPRESSION INHIBIT INFLAMMATORY CELL SURVIVAL IN THE AIRWAY ICS SUPPRESS INFLAMMATORY GENE EXPRESSION IN AIRWAY EPITHELIAL CELLS

125
Q

What are the side effects of inhaled corticosteroids?

A

TITRATING TO LOWEST EFFECTIVE DOSE REDUCES SIDE EFFECTS HIGH-DOSE ICS ARE OFTEN USED IN COPD. THIS OVERUSE OF GLUCOCORTICOIDS IS LIKELY TO PRODUCE SEVERAL LONG-TERM SIDE EFFECTS, SUCH AS LOSS OF BONE DENSITY ADRENAL SUPPRESSION CATARACTS, GLAUCOMA.

126
Q

Why are some people resistant to corticosteroids?

A

POSSIBLE GENETIC CAUSES – COULD THIS ALLOW US TO PREDICT WHICH PATIENTS WILL BE RESISTANT? POOR GR BINDING AND NUCLEAR TRANSLOCATION REDUCED DOWNSTREAM CELLULAR SIGNALLING FOLLOWING CORTICOSTEROID:GR BINDING.

127
Q

How do B2 AGONISTS AND ICS: HELPING EACH OTHER ALONG?

A

GLUCOCORTICOIDS INCREASE THE TRANSCRIPTION OF THE B2-RECEPTOR GENE, RESULTING IN INCREASED EXPRESSION OF CELL SURFACE RECEPTORS. LONG-ACTING B2-AGONISTS INCREASE THE TRANSLOCATION OF GR FROM CYTOPLASM TO THE NUCLEUS AFTER ACTIVATION BY GLUCOCORTICOIDS +++GR to nucleus THIS ALL LEADS TO AN OVERALL GREATER EFFICACY AND NEED FOR LOWER DOSES

128
Q

What diseases and involved in BRONCHIECTASIS?

A

Cystic fibrosis. Asthms COPD.

129
Q

What is BRONCHIECTASIS?

A

OBSTRUCTIVE LUNG DISEASE ABNORMAL DILATION OF THE BRONCHI, EXCESSIVE SPUTUM PRODUCTION, CHEST PAIN PERMITS INFECTION Destruction of wall. Destruction of cilia. increased mucus.

130
Q

How do you treat bronchiectasis?

A

ANTIBIOTICS TREAT INFECTIVE ELEMENTS OF BRONCHIECTASIS, PHYSICAL THERAPY CLEARS AIRWAYS. SURGERY AND TRANSPLANTATION FOR SEVERE DISEASE STRATEGIES AIM TO REDUCE SYMPTOMS RATHER THAN UNDERLYING CAUSE OF DISEASE MUCOLYTICS TREAT HYERSECRETION B2 AGONISTS MOST USEFUL IN COPD/ASTHMA/BRONCHIECTASIS OVERLAP SYNDROMES ANTICHOLINERGICS HAVE LIMITED EFFECT ICS HAVE LIMITED EFFECT.

131
Q

What is fibrosis?

A

EXCESSIVE FIBROUS CONNECTIVE TISSUE LEADS TO PERMANENT SCARRING, AIRWAY WALL THICKENING AND BREATHING DIFFICULTIES. A COMMON END-STAGE OF A NUMBER OF HETEROGENOUS CONDITIONS HALLMARK OF THE INTERSTITIAL LUNG DISEASES

132
Q

What is the interstitium of the lung?

A

The interstitium of the lung is a lace-like network of tissue that extends throughout the lungs and provides support to the air sacs (alveoli). Tiny blood vessels traverse the interstitium and facilitate gas exchange between the blood and air.

133
Q

What is IDIOPATHIC PULMONARY FIBROSIS?

A

PROGRESSIVE AND IRREVERSIBLE FOR MANY YEARS, IPF WAS CONSIDERED A PRINCIPALLY INFLAMMATORY DISEASE, DUE TO INCREASES IN INFLAMMATORY CELLS IN THE LUNGS. HOWEVER, A GROWING BODY OF EVIDENCE INDICATES THAT IPF IS AN EPITHELIAL- DRIVEN DISEASE WHEREBY AN ABERRANTLY ACTIVATED LUNG EPITHELIUM PRODUCES MEDIATORS OF FIBROBLAST MIGRATION, PROLIFERATION AND DIFFERENTIATION INTO ACTIVE MYOFIBROBLASTS. THESE MYOFIBROBLASTS SECRETE EXAGGERATED AMOUNTS OF EXTRACELLULAR MATRIX (ECM) THAT SUBSEQUENTLY REMODEL THE LUNG ARCHITECTURE.

134
Q

What is the treatment of IPF?

A

TREATMENT OPTIONS ARE LIMITED (PARTICULARLY FOR IDIOPATHIC PULMONARY FIBROSIS) AND TRANSPLANTATION IS BEST OPTION FOR SEVERE CASES. SOME FORMS OF FIBROSIS RESPOND TO CORTICOSTEROIDS UNTIL RECENTLY THE TREATMENT STRATEGY WAS AMELIORATION OF SYMPTOMS/PRESERVING LUNG FUNCTION. PIRFENIDONE AND NINTEDANIB ARE NEW DRUGS THAT SIGNIFICANTLY SLOW THE RATE OF DISEASE PROGRESSION IN IPF.

135
Q

What are the two types of lung tumour?

A

Bronchial Pleural.

136
Q

What are the majority of lung tumours?

A

Malignant.

137
Q

What are the cell types of lung cancer?

A

15% small cell lung cancer 85% non small cell lung cancer squamous adenocarcinoma (adenocarcinoma-in situe).

138
Q

What are the SITES OF METASTATIC DISEASE FROM LUNG CANCER?

A

lymph glands bone brain liver adrenal glands

139
Q

What are the symptoms of metastatic disease?

A

bone pain headache seizures neurological deficit hepatic pain abdominal pain

140
Q

Which cancers can spread to the lung?

A

breast colorectal prostate kidney melanoma thyroid lymphoma.

141
Q

What are the causes of lung cancer?

A

Cigarettes Occupational – asbestos, radon, nickel, chromate, arsenic, uranium…. Lung fibrosis.

142
Q

What are the symptoms of lung cancer?

A

Cough Recurrent chest infections Haemoptysis Increasing shortness of breath Extra-pulmonary changes (directly/indirectly due to the cancer) General malaise Weight loss

143
Q

What does paraneoplastic mean?

A

Paraneoplastic syndromes are rare disorders that are triggered by an altered immune system response to a neoplasm. They are defined as clinical syndromes involving nonmetastatic systemic effects that accompany malignant disease.

144
Q

What are some paraneoiplastic symptoms of lung cancers?

A

Secretion of PTH SIADH Secretion of ACTH and other hormones Hypertrophic pulmonary osteo-arthropathy (HPOA) Myasthenic syndrome (Eaton Lambert) Finger Clubbing Migratory thrombophlebitis Non-infective endocarditis (Libman Sacks) Disseminated intravascular coagulation (DIC)

145
Q

What are the majority of lung neoplasms?

A

Majority are carcinoma (90%) Metastatic carcinoma is more common than primary lung carcinoma.

146
Q

What are the features of a small cell lung carcinoma?

A

A high grade epithelial neoplasm with strong cigarette smoking association. Has usually spread by presentation Chemotherapy is primary/ standard treatment.

147
Q

What are the features of a non small cell lung carcinoma?

A

A variable grade epithelial neoplasm with cigarette smoking association. May have metastasised by presentation/diagnosis Chemotherapy may be offered, but surgery and radiotherapy mainstay of treatment.

148
Q

What are the two types of pleural neoplasms?

A

Pleural fibroma Malignant mesothelioma

149
Q

What are the features of pleural fibroma?

A

Mostly benign small number are malignant….local spread and metastatic potential

150
Q

What does asbestos cause?

A

plaques persistent pleural effusion pleural fibrosis lung cancer asbestosis (diffuse interstitial fibrosis) MESOTHELIOMA

151
Q

What is the definition of COPD?

A

COPD, a common preventable and treatable disease, is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in individual patients..

152
Q

Is COPD restrictive or obstructive lung disease?

A

Obstructive.

153
Q

What are the reasons why airflow is limited in COPD?

A

Small Airways Disease Airway inflammation Airway fibrosis, luminal plugs Increased airway resistance Parenchymal Destruction Loss of alveolar attachments Decrease of elastic recoil

154
Q

What is COPD a cross between and why?

A

Emphysema due to loss of attachments. Chronic obstructive bronchitis because of fibrosis inflammation.

155
Q

What are the vascular changes with COPD?

A

Poor V/Q match – low Tlco and Kco Low PaO2 Poor ventilation may give high pCO2 Obliteration and vasoconstriction gives pulmonary hypertension.

156
Q

What are the symptoms and signs of COPD?

A

Old patients, smokers, male predominance Shortage of breath Cough, phlegm Wheeze Raised respiratory weight Hyperexpansion/barel shaped chest Cyanosis Weight loss ‘cor pulmonale’ = ‘heart failure’ raised JVP, SOA but CO maintained

157
Q

What are the two phenotypes of COPD?

A

Pink puffer – weight loss, breathless, emphysematous, maintained pO2 Blue bloater – cough, phlegm, cor pulmonale, respiratory failure

158
Q

What are the risk factors for COPD?

A

Preventable - Cigarette smoke. Occupational dust and chemicals. Environmental tobacco smoke. Indoor and outdoor air pollution. Not preventable - Genes. Infections Socio-economic status. Aging population.

159
Q

What is involved in a MRC dyspnoea test?

A

1 SOB marked exertion 2 SOB on hills 3 Slow or stop on flat 4 Exercise tolerance 100-200 yards on flat 5 Housebound/SOB on minor tasks.

160
Q

What are the CAT questions?

A

Cough Phlegm Chest tightness Breathlessness going up hills/stairs Activity limitation at home Confidence leaving the home Sleep and energy.

161
Q

What is the differential diagnosis of COPD?

A

Other causes of SOB Heart failure Pulmonary embolus Pneumonia Lung cancer Asthma Broncheictasis.

162
Q

What are the key differences between COPD and asthma?

A

Spirometry. Always abnormal May be normal Serial PEF. Minimal variation Day-to-day and diurnal variation Reversibility Usually <15% Usually >15%

163
Q

What is different in the pathology between COPD and asthma?

A

Same inflammation. COPD has more fibrosis and alveolar destruction. COPD has less basement membrane.

164
Q

What has the best effect at reduces COPD?

A

Smoking cessation. Exercise plan.

165
Q

What are some therapeutic options for treating COPD?

A

Beta2-agonists Short-acting beta2-agonists Long-acting beta2-agonists Anticholinergics Short-acting anticholinergics Long-acting anticholinergics Combination short-acting beta2-agonists + anticholinergic in one inhaler Combination long-acting beta2-agonist + anticholinergic in one inhaler Methylxanthines Inhaled corticosteroids Combination long-acting beta2-agonists + corticosteroids in one inhaler Systemic corticosteroids Phosphodiesterase-4 inhibitors

166
Q

What is a key prescribed bronchodilator?

A

The principal bronchodilator treatments are beta2- agonists, anticholinergics, theophylline or combination therapy for COPD.

167
Q

What do corticosteroids do? What does it put patients at risk of?

A

Regular treatment with inhaled corticosteroids improves symptoms, lung function and quality of life and reduces frequency of exacerbations for COPD patients with an FEV1 < 60% predicted. pneumonia.

168
Q

What is an exacerbation of COPD?

A

an acute event characterized by a worsening of the patient’s respiratory symptoms that is beyond normal day-to-day variations and leads to a change in medication.”

169
Q

What is the most common cause of COPD exacerbations?

A

The most common causes of COPD exacerbations are viral upper respiratory tract infections and infection of the tracheobronchial tree.

170
Q

What are the normal ranges of these properties? pH PaO2 PaCO2 HCO3

A

7.35 - 7.45. 10 - 14. 4.5 - 6.0. 22 - 26.

171
Q

What are the neural controls of breathing?

A

Cerebral cortex Conscious control of breathing. Medulla oblongata Breathing centre.

172
Q

What are the chemicals controls of breathing?

A

Medulla oblongata. Chemoreceptors respond to rising blood level of carbon dioxide and lowered blood level of oxygen. Carotid bodies. chemoreceptors respond to rising blood level of carbon dioxide and lowered blood level of oxygen. Aortic bodies. Chemoreceptors respond to rising blood level of carbon dioxide and lowered blood level of oxygen.

173
Q

What are the different classes of respiratory failure? What features does each have? What causes each one?

A

Type 1: Low PaCO2, normal (or low) paCO2, normal or high A-a gradient. Limited of ventilation, perfusion or diffusion. Type 2: low paO2, high CO2, usually normal A-a gradient (acute or chronic). Alveolar hypoventilation. CO2 enters alveoli, but not removed.

174
Q

What is hypercapnea?

A

High partial pressure of carbon dioxide (PaCO2).

175
Q

What are the signs of hypercapnea?

A

Bounding pulse. Flapping tremor. Confusion. Drowsiness. Reduced consciousness.

176
Q

What are the different causes of respiratory failure?

A

Failure to maintain patent airway. (obstruction) Type 1 (if severe type 2) Failure to ventilate alveoli. Type 1 or 2. Failure to diffuse oxygen into blood. Type 1. Perfusion. Type 1.

177
Q

What sort of diseases cause airway obstruction?

A

Asthma. Sleep apnoea

178
Q

What sort of diseases cause alveolar hypoventiulatiuon?

A

Obesity hypoventilatiuon. Chest wall deformity. Neuromuscular weekness. Myaesthenia gravis. Motor neurone disease. Guillan-Barre syndrome.

179
Q

What diseases cause a diffusion limitation?

A

Emphysema. Interstitial lung disease. IPF. Sarcoidosis. Pneumoconiosis. Drug-induced lung disease (bleomycin, methotrexate).

180
Q

What is perfusion without ventilation?

A

A shunt. Lots of blood, no air.

181
Q

What is ventilation without perfusion?

A

Dead space. Lots of air, no blood.

182
Q

How do you treat respiratory failure?

A

Treat underlying cause.

183
Q

What is a continuous positive airways pressure?

A

Devices which pushes air into lungs.

184
Q

What diseases cause obstruction of airways?

A

Asthma. COPD. OSA. Pneumonia.

185
Q

What diseases cause hypo-ventilation of the airways?

A

COPD. Neuromuscular weakness. Obesity. Chest wall deformity. Reduced drive.

186
Q

What disease cause diffusion limitation?

A

IPF. Other ILDs. Emphysema.

187
Q

What disease cause perfusion mismatch?

A

Pulmonary embolism. Cardiac failure. Shunt. Pulmonary hypertension.

188
Q

Who are the people at risk of pneumonia?

A

Infants and the elderly. COPD and certain other chronic lung diseases. Immunocompromised. Nursing home residents. Impaired swallow. Diabetes. Congestive heart disease. Alcoholics and intravenous drug users.

189
Q

What is the pathogenesis of pneumonia?

A

Pneumococci temporary colonise pharynx – They are microaspirated and usually cleared by AM But in some infections the macrophages ability to kill becomes overwhelmed, So they produce a proinflammatory response which attracts neutrophils, recruited to kill the bacateria This will result in dead bacteria + dead neutrophils + tissue fluid + inflammatory proteins = inflammatory exudate or ‘pus’ in the airspaces. Often the cost of this process is collateral damage to the lung which takes some time to heal.

190
Q

What are the symptoms of pneumonia?

A

Fever, sweats, rigors. Cough. Sputum. Classically’ rusty sputum suggests S. pneumoniae But may be none, particularly with organisms such as Mycoplama, Chlamydophila and Legionella ‘atypical pathogen’s Short of breath Pleuritic chest pain (pain worse on deep breathing) particularly S. pneumoniae Systemic features including weakness, malaise Extra-pulmonary features neurological or gastrointestinal with Legionella sp. rash with mycoplasma.

191
Q

What are the signs of pneumonia?

A

Abnormal vital signs; raised heart rate, raised respiratory rate, low blood pressure Fever dehydration Signs of lung consolidation on percussion and auscultation Dull to percussion Decreased air entry Bronchial breath sounds Crackles ± wheeze Increased vocal resonance ± Hypoxia and signs of respiratory failure especially if chronic lung disease or severe pneumonia.

192
Q

How can you investigate if somebody has suspected pneumonia?

A

Chest X-ray Full blood count for White blood cell count (WBC) aids diagnosis and a marker of severity Biochemistry for urea and electrolytes and Liver function tests (renal function required to asses severity, other tests for complications) C-reactive protein helps with diagnosis, assessment of severity and recovery Pulse oximetry assess severity and if required arterial blood gas define respiratory failure Microbiological tests.

193
Q

What do you look for in a chest X-ray?

A

Look for ‘air bronchogram’ in consolidated area Multi-lobar suggestive of S. pneumoniae, S. aureus, Legionella sp. Multiple abscesses or pneumatoceles of S. aureus Air fluid level in abscess Upper lobe cavity K. pneumoniae (but must exclude TB!) Interstitial or diffuse shadowing more suggestive of viral or Pneumocystis pneumonia (PCP) in HIV or immunocompromised Pleural collections require aspiration and management to avoid empyema Features suggestive of alternative diagnosis; TB , lung cancer.

194
Q

How do you manage pneumonia?

A

Supportive therapies & antibiotics ABCD approach e.g. CPAP (T1RF and pneumonia), IV fluids, vasopressors (NAdr) – vasoconstriction and adequate glucose control Antibiotics – empirical initially then guided on MC&S Anaerobic cover if aspiration pneumonia e.g. metronidazole Uncomplicated CAP (mild): Amoxicillin (0.5g-1g TDS) or macrolide +/- flucloxacillin (s.aureus = virulent!) Complicated CAP Moderate severity – amoxicillin + macrolide PO/IV Severe – co-amoxiclav IV (1.2g TDS) +/- rifampicin or a macrolide. Thromboprophylaxis w/ LMWH if admitted for >12hours ANALGESIA!! Note: patients may take up to 6 months to fully recovers from CAP – residual symptoms.

195
Q

What are the assessments of CAP severity?

A

‘CURB65’ One point for each of Confusion Urea ≥7mmol/L Respiratory rate≥ 30/min Blood pressure; low systolic < 90mm/Hg or diastolic ≤60mm/Hg Age ≥ 65 Predicts mortality 0=0.7%, 1 =2.1%, 3= 9.2% 4-5=15-40% Implications; 0-1 = mild, only admit if social circumstances or single worrying feature 2= moderate, admit to hospital 3-5 = severe, admit and monitor closely, 4-5 consider admission to critical care unit In community, no urea available so use: ‘CRB65’ 0=mild, 1-2 moderate and 3-4 severe.

196
Q

What are the different pathogens causing pneumonia?

A

Streptococcus pneumoniae (40%) Mycoplasma pneumoniae (~10% peaks in epidemic seasons) Chlamydophila pneumoniae (~10%) Legionella pneumophila and other spp.(<5%) Haemophilus influenzae (<5%) Klebsiella pneumoniae (rare; homeless and in hospital) Staphylococcus aureus (low % in community but increased after influenza and in hospital especially) Viruses (≥10%).

197
Q

What percentage of asthmatics are atopic?

A

25%.

198
Q

What are the two main types of asthma?

A

Eosinophilic. Associated with allergy. Also non-allergic variant. Non-eosinophilic.

199
Q

What is asthma if not eosinophilic?

A

Overlaps with smoking and obesity.

200
Q

What are the reasons for atopic asthma?

A

Fungal allergy. Common aeroallergens. Occupation, pets, exposures.

201
Q

What happens in eosinophilic asthma?

A

Allergen comes in interacts with mast cell which releases prostaglandin D2 which activates eosinophils with migration and survival. Allergen comes in interacts with APC which complexes with a T cell this then: Activates eosinophils. Interacts with B cell which interacts with mast cell. Interacts with smooth muscle cell. Also affects epithelial layer.

202
Q

What happens in non-eosinophilic asthma?

A

Cigarette smoke pollutants and airway microbiome PAMPs from viruses or bacteria affect air way lumen. Monocytes and macrophages on epithelial lining activates neutrophils. They also activates T cells which in turn cause changes in smooth muscle cells. T cells also affect mast cells.

203
Q

What are the differences between asthma and COPD?

A

COPD a later disease dominantly of smokers. More of a relentless progressive SOB with wheeze as part of the symptom complex. Less diurnal variation, less day-to-day variation. Winter symptoms, sputum production. Overlap occurs.

204
Q

What tests can you do for asthma?

A

Blood count: eosinophils. Tests for atopy and allergy: SPTs and RAST. Chest XR often useful. (Oxygen saturations).

205
Q

What would lung function testing show?

A

Airways obstruction may be present (reduced FEV1, reduced FEV1/FVC ratio) PEFR reductions from percent predicted, variability (>20% predicated 3/7 days) Increased responsiveness to challenge agents (mannitol, methacholine)

206
Q

What would reversibility testing in asthma show us and how?

A

Increase in lung capacity with bronchodilators or anti-inflammatory treatment Increase of 12% in FEV1 together with increase of 200 ml in volume is positive, ≥400 ml increase makes asthma highly likely (20% variability in PEFR also suggests asthma).

207
Q

What are the specific tests or airway inflammation?

A

Becoming more common Exhaled nitric oxide (FeNO), a marker of eosinophilic inflammation. But not specific, suppressed in smokers, elevated with viral infections and rhinitis. Direct measurement of cells in the airways can reliably guide treatment.

208
Q

What are the major characteristics of asthma?

A

Major characteristics Treatment with continuous or near continuous oral steroids. Requirement for high dose inhaled steroids.

209
Q

What are the minor characteristics of asthma?

A

Additional daily reliever medication (beta agonists, theophylline, LTRA) Symptoms needing reliever medication on daily or near daily basis Persistent airway obstruction (FEV1<80%, diurnal variation PEFR >20%) ≥1 emergency visits p.a. ≥3 steroid courses p.a. Prompt deterioration with ≤25% reduction in oral or inhaled steroid dose Near-fatal event in past.

210
Q

What are the classes of drug available for asthma?

A

Bronchodilators: beta agonists, leukotriene receptor antagonists, theophyllines, long acting beta agonists, anticholinergics Anti-inflammatory drugs: steroids New biologics: omalizumab, mepolizumab.

211
Q

Why do you need steroids in asthma?

A

Steroids to reduce airway inflammation and decrease mortality risks.

212
Q

Why can’t many people have oral steroids?

A

Systemic: diabetes, cataracts, osteoporosis, hypertension, skin thinning, easy bruising, growth retardation, osteonecrosis of the femoral head Topical: hoarse voice, oral candida, skin thinning, easy bruising, cataracts (in high dose) Adrenal suppression.

213
Q

What options can you give for severe eosinophilic asthma?

A

Anti-IgE (omalizumab) for atopic allergic disease anti-IL-5 (mepolizumab) Oral steroids, additional immunosuppressants (guided by overall atopic disease burden).

214
Q

What are the risk factors for TB?

A

Born in high prevalence area. IVDU Homeless. Alcoholic. Prisons. HIV+.

215
Q

How is TB spread?

A

Spread in aerosol from infected individual’s lung to another lung, or via spitting or sneezing on plates or hands.

216
Q

How can you catch TB?

A

Enternally, M.bovis cause abdominal TB, contracted by butchers / abattoir workers.

217
Q

What are the chances of showing symptoms if a patient becomes infected with TB?

A

5%. 95% mount an effective immune response that encapsulates and contains the organism forever.

218
Q

What happens in pulmonary infection only?

A

Bacilli settle in lung Apex. Macrophages and lymphocytes seal in and contain and kill majority of infecting bacilli.

219
Q

What happens in pulmonary TB?

A

2-5 % develop clinically evident primary pulmonary disease, Bacilli + macrophages coalesce to form a granuloma, this is called the Primary (Ghon) focus mediastinal lymph nodes which enlarge. Primary focus + mediastinal LN = Ghon Complex As granuloma grows it develops into a cavity. More likely in apex of lung as there is more air and less blood supply / immune cells The cavity is full of TB bacilli, which are expelled when patient coughs.

220
Q

What are the systemic features of TB?

A

Weight loss* Low grade fever Anorexia Night sweats* Malaise.

221
Q

What are the pulmonary features of TB?

A

cough > 3/52 (most other causes resolve by then) Chest pain Breathlessness Haemoptysis May be associated with Consolidation, collapse, pleural effusion, pericardial effusion depending on the site of granuloma / lymph node and subsequent rupture.

222
Q

What are some extra pulmonary TB features?

A

Lymph node TB swelling +/- discharge Miliary TB Bone Pain or swelling of joint, Potts disease with spinal cord lesion Abdominal TB Ascites, abdominal lymph nodes, ileal malabsorption Genito-urinary TB epididymitis, frequency, dysuria and haematuria. CNS TB Meningitis + CN palsy Tuberculoma.

223
Q

How can you diagnose TB?

A

Sputum Urine CSF Pleural fluid Biopsy specimen Any Lymph nodes: Cervical, axillary, inguinal, mediastinal, abdominal Peritoneum, omentum Bone Brain. Normochromic normocytic anaemia Thrombocytosis Raised ESR / CRP Hypoalbuminemia Hypergammaglobulinemia Hypercalcemia Sterile pyuria (whites cells in renal tract TB).

224
Q

How can you diagnose latent TB?

A

Tuberculin skin test ‘Mantoux’ protein derived from organism injected intradermally (technically difficult) stimulates type 4 delayed hypersensitivity reaction not sensitive: immunosuppressed or miliary TB wont react (false negatives) only moderately specific (false positives) won’t easily distinguish infection from disease.

225
Q

What is the treatment for active TB?

A

TB is curable Treat with at least 4 drugs for at least 6 months Standard treatment in UK: rifampicin. 6 months isoniazid. 6 months pyrazinamide 2 months ethambutol. 2 months

226
Q

What does rifampicin do?

A

Bacteriocidal, blocks protein synthesis, effective throughout treatment course SE: red urine, hepatitis, drug interactions.

227
Q

What does isoniazid do?

A

Bacteriocidal for rapidly growing bacilli (blocks cell wall synthesis), most effective in initial stages SE: hepatitis, neuropathy .

228
Q

What does pyranziamide do?

A

Bacteriocidal initially, less effective later SE: hepatitis, arthralgia / gout, rash.

229
Q

What does ethambutol do?

A

Bacteriostatic, blocks cell wall synthesis SE: optic neuritis.

230
Q

Why does the treatment for TB take so long?

A

Early killing of bacteria taken down to a very low number, some bacteria lay dormant and when they reactivate it is a good chance for them to be killed.

Bateman - Phase 2a COPY (15 decks)

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