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

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

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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
Describe the structure of medication regime in a asthmatics
1. SABA 2. SABA + ICS (or leukotriene receptor antagonist) 3. SABA + LABA + ICS 4. SABA + LABA + ICS + 4th Drug (anti-IgE monoclonal)
26
What is hypersensitivity pneumonitis
1. A type of interstitial lung disease Where extracellular matrix deposition of complexes in lungs distal to bronchioles
27
What is the lung interstitum
The tissue and space around the air sacs of the lungs
28
What causes hypersensitivity pneumonitis
1. Allergic reaction affecting small airways and alveoli in response to inhaled antigen or following ingestion of a causative drug
29
Pathophysiology of hypersensitivity pneumonitis
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 4. Chronically, granuloma forms and obliterative bronchiolitis occurs
30
What characteristic is seen in hypersensitivity
FARMERS LUNG
31
causes farmers lung
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
32
Risk factors of hypersensitivity pneumonitis
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
33
What fungus causes farmers lung
1. Micropolyspora fauna | 2. Aspergillus umbrosuus
34
What causes hypersensitivity pneumonitis
1. Avian proteins in droppings
35
What causes hypersensitivity pneumonitis in cheese-workers
Penicillium casei
36
What causes hypersensitivity pneumonitis in malt-workers
Aspergillus clavatus
37
Clinical presentation of hypersensitivity pneumonitis
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
38
Differential diagnosis of hypersensitivity pneumonitis
1. Infection 2. Connective tissue disorders (causes interstitial lung disease) 3. Pulmonary fibrosis 4. Asthma
39
How is hypersensitivity pneumonitis diagnosed
1. CXR 2. FBC 3. Lung function test 4. Bronchoalveolar lavage
40
What is seen in a chest X-ray for hypersensitivity pneumonitis
1. Fibrotic shadow in upper zone of the lung | 2. Diffuse small nodules and increased reticular shadowing may be present but not specific
41
What is seen in the FBC for hypersensitivity pneumonitis
1. Raised white cell count | 2. Increased ESR
42
What is seen on live function test for hypersensitivity pneumonitis
1. Reversible restrictive defect | 2. Reduced gas transfer during acute attacks
43
What is seen in bronchoalveolar lavage for hypersensitivity pneumonitis
1. Analysis of lymphocyte count and CD4/CD8 ratio
44
How is hypersensitivity pneumonitis treated
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)
45
What can cause bronchial carcinomas
1. ASBESTOS 2. Polycyclic hydrocarbons 2. Radon in mines
46
Define pneumoconiosis
1. Accumulation of dust in the lungs and reaction of the tissue in its presence
47
Pathophysiology of pneumoconiosis
1. Particles are ingested by alveolar macrophages in small airways causing them to die and releasing enzymes = fibrosis
48
What is simple pneumoconiosis
Production of fine micro nodular shadowing in CXR
49
How do we grade simple pneumoconiosis
1. On CXR
50
What can simple pneumoconiosis progress to
Progressive massive fibrosis
51
What is progressive massive fibrosis
1. Patients develop round fibrotic massive in the upper lobes with necrotic central cavities
52
What is seen on CXR for progressive massive fibrosis
1. Upper zone fibrotic masses
53
What is found in the FBC of people with PMF, asbestosis and silicosis
1. RHEUMATOID FACTOR | 2. ANA
54
Pathophysiology of PMF
1. Apical destruction Disruption of lung Emphysema and airway damage
55
What is seen in lung function tests for PMF
1. Mixed restrictive and obstructive ventilatory defect with loss of volume, irreversible airflow limitation and reduced gas transfer
56
Clinical presentation of PMF
1. Dyspneoa 2. BLACK sputum 3. Resp failure
57
How is PMF managed
1. Avoid dust exposure | 2. Claim compensation
58
What is silicosis
It is the accumulation of crystalline silica dust in the lung causing inflammation in the interstitium of the upper lobes of the lungs
59
Clinical presentation of silicosis
1. Dyspnoea 2. Persistent cough 3. Fatigue 4. Chest pain 5. Fever 6. Cyanosis 7. Cor pulmonale
60
What condition are patients with silicosis susceptible to
TB (pulmonary macrophages can't kill the mycobacterium as silica damages them) Causes fibrogenesis
61
What does CXR show in silicosis
Small nodules in the UPPER lobes of the lung and think streaks of egg-shell calcification of the hilar nodes
62
How else do we diagnose silicosis
1. Spirometry (shows restrictive ventilator defect)
63
How is silicosis managed
Stop exposure to silica Oxygen administration Bronchodilators
64
What are the most hazardous asbestos fiber types that cause asbestosis
1. Crocidolite (blue asbestos) - most likely to get trapped in th lung 2. Amosite (brown asbestos) MOST COMMONLY CAUSED BY CHRYSOLITE (white asbestos)
65
What is asbestosis
Long-term inflammation and scarring of the lungs due to the presence of asbestos fibres
66
Pathophysiology of asbestosis
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
Why is crocidolite easily inhaled
Because it is thin and long, resistant to macrophages
68
Clinical presentation of asbestosis
1. Progressive dyspnoea 2. Resporatory failure 3. Finger clubbing and bilateral basal end-inspiratory crackles
69
How is asbestosis common
Corticosteroids
70
Where does byssinosis take place
Cotton mill farmers
71
What is byssinosis
1. Interstitial lung disease caused by exposure to cotton dust
72
Clinical presentation of byssinosis
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
What is seen on the CXR for byssinosis
No changes seen
74
What is berylliosis
1. Beryllium inhalation causing interstitial lung disease
75
When is beryllium used
1. Aerospace industry 2. Atomic reactors 3. Electrical devices
76
Clinical presentation of berylliosis
1. Progressive dyspnoea with pulmonary fibrosis | 2. Systemic illness
77
Define bronchiectasis
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
What causes bronchiectasis
1. Pulmonary inflammation and scarring due to infection, bronchial obstruction or lung fibrosis
79
Why are people susceptible to bronchiectasis
1. Mucociliary transport mechanism is impaired due to thickening of the bronchi and bronchioles
80
In what gender is bronchiectasis common in
Women
81
Risk factors for bronchiectasis
1. Female 2. AGE 3. Post-Infection (most common) 4. Congenital 5. Mechanical bronchial wall obstruction
82
What infections can cause bronchiectasis
1. Previous pneumonia 2. Mycobacterium tuberculosis 3. Measles, whooping cough 4. Pertussis 5. Bronchiolitis 6. HIV 7. Ulcerative colitis 8. Hypogammaglobulinaemia 9. RA
83
What congenital problems can lead to bronchiectasis
1. CF | 2. Primary ciliary dyskinesia
84
Pathophysiology of bronchiectasis
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
Clinical presentation of bronchiectasis
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
What is Rhonchi
Rattling reparatory sounds caused by secretions in bronchial airways
87
Differential diagnosis of bronchiectasis
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
Diagnosis of bronchiectasis
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
What is seen on CXR in bronchiectasis
1. Dilated bronchi with thickened walls | 2. Multiple cysts containing fluid (cystic shadows)
90
What is seen on sputum culture in bronchiectasis
1. See bacterial colonisation status
91
What bacteria cause bronchiectasis
1. Haemophilus influenza 2. Strep. pneumoniae 3. Staph. Aureus 4. Pseudomonas aerguinosa
92
Why is sputum culture done for bronchiectasis
1. Exlude non-tuberculous mycobacterial disease
93
Role of high res CT in bronchiectasis
1. Thickened, dilate bronchi with cysts at ends of th bronchioles seen 2. Airways larger than associated blood vessels
94
What would spirometry show in bronchiectasis
Obstructive pattern
95
How is bronchiectasis treated
1. Improved mucus clearance 2. Antibiotics 3. Bronchodilators (nebuliser salbutamol) 4. Anti-inflammatory agents (azithromycin) 5. Surgery
96
How do we improve mcuus clearance
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
What antibiotics are given for bronchiectasis
1. Oral ciprofloxacin for pseudomonas aerguinosa 2. Oral amoxicillin for haemophilia influenzae or cephalosporin 3. Staphylococcus aureus - flucloxacillin
98
Define cystic fibrosis
1. Autosomal recessive condition in CAUCASIANS
99
What genetic mutation occurs in CF
1. CFTR gene mutation (F508 deletion)
100
Where is the CFTR gene located
Long arm of chromosome 7
101
Role of CFTR
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
What happens to CFTR in cystic fibrosis
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
What organs are effected in CF
1. LUNG AND GI involvement
104
What happens in CF at the lung s
1. Dehydration of airway surface liquid, mucus stasis, airway inflammation and infections Leads to progressive airway obstruction and bronchiectasis
105
Clinical presentation of CF in neonates
1. Lungs in neonates is structurally normal at birth BUT: Failure to thrive Meconium ileus Rectal prolapse
106
What is meconium ileum
Bowel obstruction due to thick meconium (early stools)
107
Clinical presentation of CF in the lungs
1. Cough 2. Thick mucus 3. Wheeze 4. Recurrent infections 5. Bronchiectasis + airflow limitation 6, Sinusitis 7. Nasal polyps 8. Spontaneous pneumothorax 9. Haemoptysis + breathlessness
108
Clinical presentation of CF in the GI tract
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
Other clinical presentation of CF
1. Male infertility due to ATROPHY of vas deferent and epididymis 2. Females develop secondary amenorrhea 3. Salty sweat 4. Clubbing 5. Osteoporosis
110
Diagnosis of CF
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
What is a motive sweat test
High Na and Cl conc. (greater than 60mmol/L)
112
Why do we do a faecal elastase test
Exclude exocrine pancreatic disease - in CF patient there will be no levels due to mcuus blocking pancreas
113
What microbes can cause infections in CF
1. Pseudomonas aerguinosa 2. Mycobacterium abscesses 3. Enterobacter spp 4. Klebsiella
114
How is CF treated
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
What prophylactic antibiotic is given to people with CF
1. FLUCLOXACILLIN | 2. AMOXYCILLIN
116
How to treat MRSA
1. RIFAMPICIN | 2. FUCIDIN
117
How is p aerguinosa treated
1. Ciprofloxacillin | 2. Nebulised colomycin
118
What mucolytics are given
Dornase Alba nebulised Clears airways of mucus
119
Why is AMiloride given
Inhibits Na transport so less thick mucus
120
When is bilateral lung transplant
Patient needs to be on maximal therapy HLA compatibility Reasonable bone health
121
When is bilateral lung transplant contraindicated
1. Mycobacterium abscess since it can cause rapid decline of health

Year 2 (155 decks)

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