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Year 2 > Resp: Asthma treatment, Hypersensitivity pneumonitis, Bronchiectasis, Cystic fibrosis > Flashcards

Resp: Asthma treatment, Hypersensitivity pneumonitis, Bronchiectasis, Cystic fibrosis Flashcards

1
Q

How is asthma treated

A
  1. Bronchodilators
    SABA: Salbutamol (partial agonist)
    Terbutaline
LABA (12 hours): Salmeterol 
Formoterol 
2. Muscarinic antagonists 
3. Methylxanthines
4. Anti-infllamtory steroids
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2
Q

Why are LABAs more longer acting

A

They are more lipophilic so remain in tissue for longer

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3
Q

What receptor does salbutamol bind to

A

B2

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4
Q

Where is B1 found

A

Heart

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5
Q

Where is B3 found

A

Adipose tissue

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6
Q

Pharmacology of B2 agonists

A
  1. Bind to B2 receptor coupled with Gs proteins
  2. Adenyl cyclase converts ATP to cyclic AMP
  3. Increases cyclic AMP to bronchodilation

ALSO inhibit mast cell activity

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7
Q

Why should B2 agonists not be given in high concentration

A
  1. They may develop B2-recpetor desensitisation
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8
Q

Name a short-acting muscuranic antagonist

A

Ipratropium

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9
Q

Name a long-acting muscuranic antagonist

A
  1. Tiotropium
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10
Q

What receptor do anti-muscurinic receptors bind to

A

M3

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11
Q

Pharmacology of M3 receptor binding

A
  1. ACh binds to M3 receptor bound to Gq protein resulting in phospholipase C converting phosphate to DAG
  2. Protein Kinase C production results in smooth muscle contraction
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12
Q

Why are methylxanthines given

A
  1. Phosphodiesterase inhibitor prevents conversion of cyclic AMP to 5’-AMP resulting in a build up of cyclic-AMP and thus increased smooth muscle relaxation
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13
Q

Name some methylxanthines

A
  1. LONG-ACTING: Theophylline (non selective so effects many systems) and aminophylline
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14
Q

What anti-inflammatory steroids are given to the patient

A
  1. Inhaled corticosteroids
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15
Q

When are inhaled corticosteroids given

A
  1. Patients who has a regular persistent symptoms
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16
Q

Name two types of corticosteroids

A
  1. Mineralocorticoids (aldosterone - Na retention)

2. Glucocorticoids (hydrocortisone - ensures glucose levels are correct and has anti-inflammatory properties)

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17
Q

Examples of inhaled corticosteroids

A
  1. Prednisolone
  2. Beclomatasone
  3. Budesonide
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18
Q

How do glucocorticoids suppress asthmatic attacks

A
  1. Gene transcription
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19
Q

Where is glucocorticoids receptor found

A

Promotor region of DNA has zinc fingers that anchor receptors to DNA and recognise discrete sequences on Glucocorticoid reposes element (either increases or decreases transcription)

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20
Q

Result of a negative GRE

A

SUPPRESSION OF CYTOKINES (TNF. IL-5, IL-3)

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21
Q

Result of a positive GRE

A

Results in increased lipocortin which inhibits PLA2:

DECREASED arachidonic acid

Causes a DECREASE in prostaglandins and leukotrienes

Reduced inflammation nd symptoms

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22
Q

Side-effects of corticosteroids

A
  1. Susceptibility to infection due to cytokine suppression

2. OSTEOPOROSIS and muscle wasting

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23
Q

Alternatives to corticosteroids

A
  1. Leukotriene receptor antagonist (montelukast)

2. Steroid-sparing agents

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24
Q

Name some steroid-sparing agents

A
  1. METHOTREXATE
  2. CICLOSPORIN
  3. IV immunoglobulin
  4. Anti-IgE monoclonal antibody (omalizumab)
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25
Q

Describe the structure of medication regime in a asthmatics

A
  1. SABA
  2. SABA + ICS (or leukotriene receptor antagonist)
  3. SABA + LABA + ICS
  4. SABA + LABA + ICS + 4th Drug (anti-IgE monoclonal)
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26
Q

What is hypersensitivity pneumonitis

A
  1. A type of interstitial lung disease

Where extracellular matrix deposition of complexes in lungs distal to bronchioles

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27
Q

What is the lung interstitum

A

The tissue and space around the air sacs of the lungs

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28
Q

What causes hypersensitivity pneumonitis

A
  1. Allergic reaction affecting small airways and alveoli in response to inhaled antigen or following ingestion of a causative drug
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29
Q

Pathophysiology of hypersensitivity pneumonitis

A
  1. Allergic response causes deposition of immune complexes (TYPE 3 hypersensitivity)
  2. Inflammation as complements are activated
  3. Inflammation attracts and activates alveolar and interstitial macrophages so that continued antigenic exposure results in the progressive development of pulmonary fibrosis
  4. Acutely, alveoli is infiltrated with inflammatory cells
  5. Chronically, granuloma forms and obliterative bronchiolitis occurs
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30
Q

What characteristic is seen in hypersensitivity

A

FARMERS LUNG

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31
Q

causes farmers lung

A
  1. Fungus in mouldy hay inhaled
  2. Type II hypersensitivity occurs
  3. Acute dyspnoea and coughs
  4. Early feature of bronchiolitis
  5. Later, chronic inflammatory cells are seen in the intersttium together with non-caveating granulomas
  6. Eventually results in pulmonary fibrosis
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32
Q

Risk factors of hypersensitivity pneumonitis

A
  1. Famers
  2. Bird/pigeon keepers
  3. Cheese-workers
  4. Malt-workers
  5. Humidifier fever
  6. Pre-existing lung disease
  7. Regular use of hot tubs
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33
Q

What fungus causes farmers lung

A
  1. Micropolyspora fauna

2. Aspergillus umbrosuus

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34
Q

What causes hypersensitivity pneumonitis

A
  1. Avian proteins in droppings
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35
Q

What causes hypersensitivity pneumonitis in cheese-workers

A

Penicillium casei

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36
Q

What causes hypersensitivity pneumonitis in malt-workers

A

Aspergillus clavatus

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37
Q

Clinical presentation of hypersensitivity pneumonitis

A

ACUTE:

  1. Fever
  2. RIgors
  3. Myalgia
  4. Dry Cough
  5. Dyspneoa
  6. Crackles
  7. Chest-wheeze

Resolves after removal of antigen

Subacute: Occurs at lower-level exposure
1. Less sever symptoms of acute and is repeated

Recurrent pneumonia

Improvement seen in weeks

Chronic: Cyanosis and clubbing
Weight loss
Increasing dyspnoea
Type I respiratory failure

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38
Q

Differential diagnosis of hypersensitivity pneumonitis

A
  1. Infection
  2. Connective tissue disorders (causes interstitial lung disease)
  3. Pulmonary fibrosis
  4. Asthma
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39
Q

How is hypersensitivity pneumonitis diagnosed

A
  1. CXR
  2. FBC
  3. Lung function test
  4. Bronchoalveolar lavage
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40
Q

What is seen in a chest X-ray for hypersensitivity pneumonitis

A
  1. Fibrotic shadow in upper zone of the lung

2. Diffuse small nodules and increased reticular shadowing may be present but not specific

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41
Q

What is seen in the FBC for hypersensitivity pneumonitis

A
  1. Raised white cell count

2. Increased ESR

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42
Q

What is seen on live function test for hypersensitivity pneumonitis

A
  1. Reversible restrictive defect

2. Reduced gas transfer during acute attacks

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43
Q

What is seen in bronchoalveolar lavage for hypersensitivity pneumonitis

A
  1. Analysis of lymphocyte count and CD4/CD8 ratio
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44
Q

How is hypersensitivity pneumonitis treated

A

ACUTE:

  1. Remove allergen
  2. Give O2 (35-60%)
  3. Oral prednisolone

CHRONIC:

  1. Avoid exposure to allergen
  2. Long term steroids can often achieve CXR and physiological improvement
  3. Corticosteroids (Prednisolone)
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45
Q

What can cause bronchial carcinomas

A
  1. ASBESTOS
  2. Polycyclic hydrocarbons
  3. Radon in mines
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46
Q

Define pneumoconiosis

A
  1. Accumulation of dust in the lungs and reaction of the tissue in its presence
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47
Q

Pathophysiology of pneumoconiosis

A
  1. Particles are ingested by alveolar macrophages in small airways causing them to die and releasing enzymes = fibrosis
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48
Q

What is simple pneumoconiosis

A

Production of fine micro nodular shadowing in CXR

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49
Q

How do we grade simple pneumoconiosis

A
  1. On CXR
50
Q

What can simple pneumoconiosis progress to

A

Progressive massive fibrosis

51
Q

What is progressive massive fibrosis

A
  1. Patients develop round fibrotic massive in the upper lobes with necrotic central cavities
52
Q

What is seen on CXR for progressive massive fibrosis

A
  1. Upper zone fibrotic masses
53
Q

What is found in the FBC of people with PMF, asbestosis and silicosis

A
  1. RHEUMATOID FACTOR

2. ANA

54
Q

Pathophysiology of PMF

A
  1. Apical destruction
    Disruption of lung

Emphysema and airway damage

55
Q

What is seen in lung function tests for PMF

A
  1. Mixed restrictive and obstructive ventilatory defect with loss of volume, irreversible airflow limitation and reduced gas transfer
56
Q

Clinical presentation of PMF

A
  1. Dyspneoa
  2. BLACK sputum
  3. Resp failure
57
Q

How is PMF managed

A
  1. Avoid dust exposure

2. Claim compensation

58
Q

What is silicosis

A

It is the accumulation of crystalline silica dust in the lung causing inflammation in the interstitium of the upper lobes of the lungs

59
Q

Clinical presentation of silicosis

A
  1. Dyspnoea
  2. Persistent cough
  3. Fatigue
  4. Chest pain
  5. Fever
  6. Cyanosis
  7. Cor pulmonale
60
Q

What condition are patients with silicosis susceptible to

A

TB (pulmonary macrophages can’t kill the mycobacterium as silica damages them)

Causes fibrogenesis

61
Q

What does CXR show in silicosis

A

Small nodules in the UPPER lobes of the lung and think streaks of egg-shell calcification of the hilar nodes

62
Q

How else do we diagnose silicosis

A
  1. Spirometry (shows restrictive ventilator defect)
63
Q

How is silicosis managed

A

Stop exposure to silica
Oxygen administration
Bronchodilators

64
Q

What are the most hazardous asbestos fiber types that cause asbestosis

A
  1. Crocidolite (blue asbestos) - most likely to get trapped in th lung
  2. Amosite (brown asbestos)

MOST COMMONLY CAUSED BY CHRYSOLITE (white asbestos)

65
Q

What is asbestosis

A

Long-term inflammation and scarring of the lungs due to the presence of asbestos fibres

66
Q

Pathophysiology of asbestosis

A
  1. When fibres reach alveoli, fibres activate lung immune system = inflammatory reaction by lung macrophages.
  2. This is chronic!
  3. Macrophages phagocytese fibres and stimulate fibroblasts to deposit connective tissue
  4. Asbestos is reistrant to digestion so macrophages are killed
  5. Dying macrophages release cytokines to attract more macrophages and fibroblasts to the area
  6. Fibrogenesis takes place
  7. Some asbestos fibres become layered by iron-containing material.
  8. Inhaled fibres are transported to the interstitium of the lungs where inflammation takes place
67
Q

Why is crocidolite easily inhaled

A

Because it is thin and long, resistant to macrophages

68
Q

Clinical presentation of asbestosis

A
  1. Progressive dyspnoea
  2. Resporatory failure
  3. Finger clubbing and bilateral basal end-inspiratory crackles
69
Q

How is asbestosis common

A

Corticosteroids

70
Q

Where does byssinosis take place

A

Cotton mill farmers

71
Q

What is byssinosis

A
  1. Interstitial lung disease caused by exposure to cotton dust
72
Q

Clinical presentation of byssinosis

A
  1. Occur on the first day back at work with improvement as week progress
  2. Chest tightness
  3. Cough
  4. Breathlessness

All occur in the first hour in dusty areas of the cotton mill

73
Q

What is seen on the CXR for byssinosis

A

No changes seen

74
Q

What is berylliosis

A
  1. Beryllium inhalation causing interstitial lung disease
75
Q

When is beryllium used

A
  1. Aerospace industry
  2. Atomic reactors
  3. Electrical devices
76
Q

Clinical presentation of berylliosis

A
  1. Progressive dyspnoea with pulmonary fibrosis

2. Systemic illness

77
Q

Define bronchiectasis

A
  1. Chronic infection of the bronchi and bronchioles leading to permanent dilatation of these airways
  2. Bronchial walls become inflamed, thickened and irreversibly damaged
78
Q

What causes bronchiectasis

A
  1. Pulmonary inflammation and scarring due to infection, bronchial obstruction or lung fibrosis
79
Q

Why are people susceptible to bronchiectasis

A
  1. Mucociliary transport mechanism is impaired due to thickening of the bronchi and bronchioles
80
Q

In what gender is bronchiectasis common in

A

Women

81
Q

Risk factors for bronchiectasis

A
  1. Female
  2. AGE
  3. Post-Infection (most common)
  4. Congenital
  5. Mechanical bronchial wall obstruction
82
Q

What infections can cause bronchiectasis

A
  1. Previous pneumonia
  2. Mycobacterium tuberculosis
  3. Measles, whooping cough
  4. Pertussis
  5. Bronchiolitis
  6. HIV
  7. Ulcerative colitis
  8. Hypogammaglobulinaemia
  9. RA
83
Q

What congenital problems can lead to bronchiectasis

A
  1. CF

2. Primary ciliary dyskinesia

84
Q

Pathophysiology of bronchiectasis

A
  1. Failure of mucociliary clearance and impaired immune function contribute to insult to bronchial wall through recruitment of inflammatory cells and uncontrolled neutrophilic inflammation (bronchitis -> bronchiectasis -> fibrosis)
  2. Fibritic tissues contracts causing airways to dilate
85
Q

Clinical presentation of bronchiectasis

A
  1. Yellow sputum
  2. Haemoptysis (coughing blood)
  3. Bad breath (infection)
  4. Crepitations (crackles) and expiratory rhonchi may be head on auscultation
  5. Finger clubbing (CF particularly)
  6. Wheeze
86
Q

What is Rhonchi

A

Rattling reparatory sounds caused by secretions in bronchial airways

87
Q

Differential diagnosis of bronchiectasis

A
  1. COPD
  2. Asthma
  3. TN
  4. Chronic sinusitis
  5. Cough due to acid reflux
  6. Pneumonia
  7. Pulmonary fibrosis
  8. Cancer
  9. Inhalation of foreign
88
Q

Diagnosis of bronchiectasis

A
  1. CXR
  2. Sputum culture
  3. High resolution CT
  4. Spirometry
  5. Sinus X-rays
  6. Sweat test for patients under 40 (should see high Cl conc/ for CF)
  7. Bronchoscopy (locate site of haemoptysis, exclude obstruction and obtain culture samples)
  8. Immunology (total IgE to exclude bronchopulmonary aspergillosis)
89
Q

What is seen on CXR in bronchiectasis

A
  1. Dilated bronchi with thickened walls

2. Multiple cysts containing fluid (cystic shadows)

90
Q

What is seen on sputum culture in bronchiectasis

A
  1. See bacterial colonisation status
91
Q

What bacteria cause bronchiectasis

A
  1. Haemophilus influenza
  2. Strep. pneumoniae
  3. Staph. Aureus
  4. Pseudomonas aerguinosa
92
Q

Why is sputum culture done for bronchiectasis

A
  1. Exlude non-tuberculous mycobacterial disease
93
Q

Role of high res CT in bronchiectasis

A
  1. Thickened, dilate bronchi with cysts at ends of th bronchioles seen
  2. Airways larger than associated blood vessels
94
Q

What would spirometry show in bronchiectasis

A

Obstructive pattern

95
Q

How is bronchiectasis treated

A
  1. Improved mucus clearance
  2. Antibiotics
  3. Bronchodilators (nebuliser salbutamol)
  4. Anti-inflammatory agents (azithromycin)
  5. Surgery
96
Q

How do we improve mcuus clearance

A
  1. Postural drainage (patient is tipped so affected lobes can drain mucus - 3 times a day for 10-20 mins)
  2. Chest physio
  3. Mucolytics
97
Q

What antibiotics are given for bronchiectasis

A
  1. Oral ciprofloxacin for pseudomonas aerguinosa
  2. Oral amoxicillin for haemophilia influenzae or cephalosporin
  3. Staphylococcus aureus - flucloxacillin
98
Q

Define cystic fibrosis

A
  1. Autosomal recessive condition in CAUCASIANS
99
Q

What genetic mutation occurs in CF

A
  1. CFTR gene mutation (F508 deletion)
100
Q

Where is the CFTR gene located

A

Long arm of chromosome 7

101
Q

Role of CFTR

A

Transport Protein on membrane of epithelial cells that act as chloride channels (exports CL and Na passively allows down an osmotic gradient)

Causes movement of water out of the cell and into the mucus

102
Q

What happens to CFTR in cystic fibrosis

A
  1. Defective Cl- airway secretion and increased Na absorption causes increased H20 absorption from mucus epithelium into the cells leading to thickened secretions in multiple organs
103
Q

What organs are effected in CF

A
  1. LUNG AND GI involvement
104
Q

What happens in CF at the lung s

A
  1. Dehydration of airway surface liquid, mucus stasis, airway inflammation and infections

Leads to progressive airway obstruction and bronchiectasis

105
Q

Clinical presentation of CF in neonates

A
  1. Lungs in neonates is structurally normal at birth BUT:
    Failure to thrive
    Meconium ileus
    Rectal prolapse
106
Q

What is meconium ileum

A

Bowel obstruction due to thick meconium (early stools)

107
Q

Clinical presentation of CF in the lungs

A
  1. Cough
  2. Thick mucus
  3. Wheeze
  4. Recurrent infections
  5. Bronchiectasis + airflow limitation
    6, Sinusitis
  6. Nasal polyps
  7. Spontaneous pneumothorax
  8. Haemoptysis + breathlessness
108
Q

Clinical presentation of CF in the GI tract

A
  1. Thick secretions
  2. Reduced pancreatic enzymes (due to mucus blocking pancreatic duct)
  3. Pancreatic insufficiency (diabetes mellitus + steatorrhoea)
  4. Distal intestinal obstruction syndrome (meconium ileus in adults) causing reduced GI motility
  5. Reduced bicarbonate production
  6. aldigestion and malabsorption thus poor nutrition (pulmonary sepsis)
  7. Cholesterol gallstones and cirrhosis
  8. Peptic ulcers
109
Q

Other clinical presentation of CF

A
  1. Male infertility due to ATROPHY of vas deferent and epididymis
  2. Females develop secondary amenorrhea
  3. Salty sweat
  4. Clubbing
  5. Osteoporosis
110
Q

Diagnosis of CF

A
  1. Clinical history
  2. Genetic testing
  3. Faecal elastase test
  4. Microbiology culture
  5. Sweat test
  6. Absent vas deferent and epididymis
  7. GI disorders
111
Q

What is a motive sweat test

A

High Na and Cl conc. (greater than 60mmol/L)

112
Q

Why do we do a faecal elastase test

A

Exclude exocrine pancreatic disease - in CF patient there will be no levels due to mcuus blocking pancreas

113
Q

What microbes can cause infections in CF

A
  1. Pseudomonas aerguinosa
  2. Mycobacterium abscesses
  3. Enterobacter spp
  4. Klebsiella
114
Q

How is CF treated

A
  1. FEV1 and BMI should be recorded
  2. Education to improve QOL
  3. Stop smoking
  4. Prophylaxis antibiotics
  5. Pseudomonal and flu vaccination
  6. Salbutamol and beclometasone
  7. Mucolytics
  8. Pancreatic enzyme replacement
  9. ADEK vitamin replacement
  10. Screen for osteoporosis
  11. Amiloride
  12. Bilateral ung trnasplant
115
Q

What prophylactic antibiotic is given to people with CF

A
  1. FLUCLOXACILLIN

2. AMOXYCILLIN

116
Q

How to treat MRSA

A
  1. RIFAMPICIN

2. FUCIDIN

117
Q

How is p aerguinosa treated

A
  1. Ciprofloxacillin

2. Nebulised colomycin

118
Q

What mucolytics are given

A

Dornase Alba nebulised

Clears airways of mucus

119
Q

Why is AMiloride given

A

Inhibits Na transport so less thick mucus

120
Q

When is bilateral lung transplant

A

Patient needs to be on maximal therapy
HLA compatibility
Reasonable bone health

121
Q

When is bilateral lung transplant contraindicated

A
  1. Mycobacterium abscess since it can cause rapid decline of health

Year 2 (155 decks)

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