Phase 2a diseases > Respiratory > Flashcards

Respiratory Flashcards

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1
Q

What is COPD?

A
  • Chronic Obstructive Pulmonary Disease
  • Irreversible airflow limitation, usually progressive. Caused by persistent inflammatory response.
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2
Q

What are the two diseases that comprise COPD?

A
  • Emphysema.
  • Chronic bronchitis.
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3
Q

What is the clinical presentation of COPD?

A

Respiratory presentation:

  • Chronic productive cough.
  • Wheezing
  • SOB
  • Worsens with exercise.
  • Barrel chest.

Other symptoms:

  • Fatigue (often due to sleep disruption).
  • Ankle oedema.
  • Decreased exercise tolerance.
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4
Q

What are the differentials for COPD?

A
  • Asthma. Earlier onset, often with FH of type 1 hypersensitivity. Daily variability of symptoms too.
  • Congestive heart failure. Will have raised BNP.
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5
Q

What is the pathophysiology of COPD?

A
  • Chronic inflammation affecting central and peripheral airways, lung parenchyma, alveoli and the pulmonary vasculature.
  • The repeated damage and repair leads to structural and physiological changes in the lungs:
  • Airway narrowing/remodelling.
  • Increased numbers of goblet cells.
  • Increased size of mucous-secreting glands in the airways.
  • Alveolar loss.
  • Vascular changes causing pulmonary hypertension.
  • The emphysema is caused by elastin breakdown, which results in loss of alveolar integrity.
  • Innate immunity (macrophages, neutrophils) play an important role in COPD.
  • Increasing evidence there is eosinophilic involvement too.
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6
Q

What are the 2 most common causes of COPD?

A
  • Smoking
  • Occupational irritants (such as car fumes).
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7
Q

What are the risk factors for COPD?

A
  • Smoking.
  • Old age.
  • FH.
  • Occupational exposure to chemicals.
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8
Q

What are the diagnostic tests for COPD?

A
  • Spirometry. Will show FEV1/FVC < 0.7, suggesting obstructive disease.
  • Physical examination: Tachypnoea, use of accessory muscles, expiratory wheeze, coarse crackles.
  • Sometimes CXR to exclude other pathologies.
  • Alpha-1 antitrypsin (AAT) should always be measured at least once to check for AAT deficiency COPD.
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9
Q

What is the treatment for COPD?

A

1st line:

  • STOP SMOKING.
  • SABA. Short-acting B agonist. (salbutamol) as a rescue inhaler for all patients.
  • LAMA. Long acting muscarinic antagonist (tiotropium) OR LABA. Long-acting B agonist (salmeterol).
  • Consider adding an ICS (ciclesonide) for patients with severe COPD.

If extremely severe, consider oxygen therapy.
If sleep apnoea develops, consider ventilation overnight.

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10
Q

What are the potential complications of COPD?

A
  • Cor pulmonale. Right sided heart failure. Occurs due to pulmonary hypertension.
  • Recurrent pneumonia. Usually Strep. Pneumoniae of haemophillus Influenza. (amoxicillin).
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11
Q

What is asthma?

A
  • Asthma is a chronic respiratory condition associated with airway inflammation and type 1 hypersensitivity (IgE mediated).
  • Usually causes intermittent symptoms.
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12
Q

What are the two different types of asthma?

A
  • Extrinsic. This is triggered by external, allergic factors. (Type 1 hypersensitivity).
  • Intrinsic. Triggered by non-allergic factors (e.g. stress, cold).
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13
Q

What is the clinical presentation of asthma?

A
  • Expiratory wheeze
  • Dyspnoea
  • Chest tightness
  • Dry cough (exacerbated by exercise/cold conditions).
  • Night-symptoms indicate more severe asthma.
  • Patients often have family members with asthma.
  • Patients often have other allergy-related conditions.
  • KEY FEATURE OF ASTHMA: Will have regular but distinctive exacerbations/attacks of disease.
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14
Q

What is the pathophysiology of asthma?

A

Mainly caused by inflammation. A variety of triggers will begin the inflammatory cascade within the bronchial tree:

  • Leukocyte numbers increased in the bronchial wall, bronchial membranes and the secretions.
  • Lymphocytes will produce ILs to start the inflammatory cascade, and IgE will be produced (IgE is strongly associated with allergic disease).
  • Smooth muscle in bronchial walls will contract, causing airway obstruction. It will also hypertrophy over time, narrowing the airway further.
  • Airways will remodel to contain more smooth muscle and an increased number of goblet cells.
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15
Q

What is the aetiology of asthma?

A
  • Largely unknown
  • An element of atopy (IgE antibodies produced as a result of exposure to common particles.)
  • Increased responsiveness to inhaled stimuli (higher levels of histamine/methacholine produced).
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16
Q

What is the epidemiology of asthma?

A
  • 15-20% of population affected by 20, so very common.
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17
Q

What are the diagnostic tests for asthma?

A
  • History
  • Evidence of obstruction (Can be gained using PEF (peak expiratory flow) or spirometry during episodes/attacks).
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18
Q

What are the treatment options for asthma?

A

1) ICS-Formoterol (LABA + corticosteroid) as needed, OR salbutamol (SABA) + ICS (2 seperate inhalers).
2) Can introduce a daily low-dose ICS for preventative measure if 1st line doesn’t work.

Potentially use a montelukast (LTRA) if ICS isn’t appropriate.

3) Use ICS-formoterol OR salmeterol (LABA) + ICS preventatively, with salbutamol (SABA) as a reliever.

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19
Q

What are the potential complications of asthma?

A
  • Pneumonia (infection of lung/s)
  • Pneumothorax (collapsed lung)
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20
Q

What are the two types of rhinitis?

A
  • Allergic
  • Non-allergic.
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21
Q

What is the most common form of rhinitis?

A
  • Hey fever. This is a type of seasonal allergic rhinitis that occurs due to pollen exposure in spring/summer.
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22
Q

What is the pathophysiology of allergic rhinitis?

A
  • Exposure to allergen.
  • Dendritic cells present the allergen’s antigens to the immune system, triggering IgE production.
  • IgE binds to mast cells, sensitising them.
  • When re-exposure to the allergen occurs, mast cells degranulate to begin the inflammatory cascade:
  • Histamine release.
  • IL secretion.
  • Migration of inflammatory cells.
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23
Q

What are the two phases of effects seen following mast cell degranulation?

A

Early phase:

  • Due to histamine.
  • Within minutes of allergen exposure.
  • Symptoms include pruritus, sneezing, rhinorrhea,

Late phase:

  • Due to inflammatory cell infiltration.
  • A few hours after initial exposure.
  • Symptoms include nasal congestion/ mucus production.
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24
Q

What are the risk factors for rhinitis?

A
  • FH of atopic disease (allergic asthma, eczema etc.)
  • Allergen exposure.
  • <20 years old.
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25
What are the diagnostic tests used for rhinitis?
- Trials of antihistamines or intranasal corticosteroids. - If needed, an allergy skin prick test.
26
What treatment is given for rhinitis?
1st line: - Avoidance of allergens (if possible). - Anti-histamines. 2nd line or if rhinitis more severe: - Intranasal corticosteroid (beclometasone or budesonide)
27
What is the clinical presentation of rhinitis?
- Pruritus. - Rhinorrhea (thin discharge from nose). - Red/swollen/watery eyes. - Nasal congestion. - Sneezing.
28
What is bronchiectasis?
- Permanent dilatation of the bronchi due to destruction of the elastic and muscular components of the bronchial wall. - Usually occurs as a result of recurrent/severe infection of the respiratory tract.
29
What is the clinical presentation of bronciectasis?
- Intermittent episodes of expectoration (coughing or spitting material up from the lungs) and infection, but as disease progresses can become more frequent (e.g. daily). - Persistent, productive cough. - Dyspnoea - Wheezing/ crackling lungs.
30
What is the pathophysiology of bronchiectasis?
- Recurrent colonisation of the airways with microorgansisms, causing chronic inflammation. This results in: - Permanently dilated and thickened bronchi. - Increased mucous production. - Impaired mucocilliary clearance. - Infiltration by inflammatory cells, which then release cytokines and cause further bronchial damage.
31
What are the risk factors for developing bronchiectasis?
- Cystic fibrosis. Most commonly identified primary cause of bronchiectasis. - Immnosuppresive conditions such as HIV. - alpha-1 antitrypsin deficiency. - Recent severe pulmonary infection.
32
What is the criteria used to classify the severity of bronchiectasis called?
BSI: Bronchiectasis severity index.
33
What diagnostic tests are available for bronchiectasis?
- HRCT (high-resolution computed tomography). Can be used to see bronchial wall dilation and thickening. GOLD STANDARD. - CFTR to check for CF. - Spirometry. Shows an obstructive pattern of disease (FEV1/FVC \< 0.7).
34
What are the treatment options for bronchiectasis?
- Physiotherapy/exercises to aid mucocilliary clearance. - Nebulised saline + salbutamol (pharmacological induction of mucociliary clearance). - Amoxicillin is the first line of antibiotics if acute infection occurs. NOTE: If patient also has COPD or asthma, choice of bronchodilator should be dependant on guidance for that condition.
35
What is cystic fibrosis?
- Severely life-limiting disease caused by autosomal recessive mutation, leading to abnormal CFTR chloride channels.
36
What is the clinical presentation of CF?
Symptoms associated with respiratory disease: - Clubbing - Wheeze - Recurrent respiratory complaints. - Nasal polyps. Symptoms associated with pancreatic/intestinal disease: - Failure to thrive - Low BMI - Increased appetite
37
What is the pathophysiology of cystic fibrosis?
- Mutation in the gene responsible for producing the CFTR chloride channels. - Results in Cl transport channels on epithelial surfaces being dysfunctional, leading to mucous secretions being more thick and sticky. This causes: - Pancreas. Blockage of the pancreatic ducts, and activation of the pancreatic enzymes trapped inside the pancreas. This leads to auto-destruction of the pancreas and a lack of digestive enzymes. - Intestine. Formation of bulky stools, with the potential to cause intestinal obstruction. - Respiratory. Reduced mucociliary clearance due to thicker secretions. This increases likelihood of chronic infection/inflammation, which leads to destruction of lung tissue. NOTE: It is usually the respiratory aspect of CF that kills the patient.
38
What are the risk factors for CF?
- FH of CF. - Both parents are carriers. (1 in 4 chance as the disease is autosomal recessive). - White ethnicity.
39
How is CF monitored?
- CF patients should be seen approximately every 3 months by a CF specialist. - Assessment of their lung function, diet and drugs will be carried out.
40
What are the diagnostic tests for cystic fibrosis?
- Sweat test. High levels of Cl- in sweat indicative of CF (98% sensitive). - Heel-prick test (newborns). If positive, this only raises suspicion and a subsequent sweat test needs to be done for a conclusive result. - Genetic testing. See if a mutation of a CFTR-coding gene is present.
41
What are the potential treatments for cystic fibrosis?
FOR ONGOING RESPIRATORYDISEASE: 1st line: - Salbutamol (SABA) + inhaled saline + dornase alfa (all for mucociliary clearance). - Inhaled tobramycin (antibiotic) if the patient has been colonised by pseudomonas aeruginosa. - CFTR modulators (ivacaftor - all of these drugs end in "-ftor"). FOR ONGOING GI DISEASE WITH PANCREATIC INSUFFICIENCY: - Pancreatic enzyme replacement (pancreatin) - H2 antagonist (famotidine) or PPI (omeprazole) to keep the pH of the GI tract up, increasing the effectiveness of the pancreatin enzymes.
42
What are the main classes of lung cancer?
Mesothelioma (cancer of the pleura). Strongly associated with asbestos exposure. Small cell carcinoma (highly malignant and aggressive). Non small cell carcinoma. Most common. 3 subtypes: - Adenocarcinoma. Most common lung cancer overall, and the most common lung cancer in non-smokers. - Squamous cell carcinoma. Most common lung cancer in smokers. - Large cell carcinoma.
43
What are the symptoms of lung cancer?
- Persistent cough. - Haemoptysis. - Weight loss. - Fatigue. - Clubbing. - Chest/shoulder pain. - Potential for lymphadenopathy. - Horner's syndrome (sympathetic chain disturbance) or loss of sensation/atrophy in hand (brachial plexus disturbance). - Recurrent laryngeal compression can cause hoarse voice.
44
Which lung cancer is most commonly found peripherally? Which lung cancer is most commonly found centrally?
Peripherally - adenocarcinoma. Centrally - large cell carcinoma.
45
What are the risk factors associated with lung cancer?
- Smoking - FH (especially 1st degree relative). - Radon exposure (mining). - COPD - Older age (median age is 70). - Asbestos exposure (especially mesothelioma!)
46
What is the histological presentation of a small cell carcinoma?
- Small, densely packed cells. - Anuclear.
47
What are the investigations used for lung cancer?
- CXR. Low sensitivity, so only used if the risk is low as it is cheap and quick. - Contrast CT. Used straight away for higher risk patients (e.g. 70 year old smoker with chronic haemoptysis) or if CXR is worrying. - Biopsy. Usually obtained by transbronchial needle aspiration. Allows for the typing/sub-typing of the cancer and planning of treatment.
48
What are the treatment options for pleural mesothelioma?
- Surgical (lobectomy/pneumonectomy) is GS. Unlikely to be curative for small cell carcinoma or mesothelioma. - Radiotherapy. - Chemotherapy. Cisplatin often the drug of choice.
49
Where does lung carcinoma commonly metastasise to?
- Bone (most common) - Liver - Brain - Adrenal glands - Lymph nodes.
50
What is the pathophysiology of Horner's syndrome
Disruption of the sympathetic nervous supply to one side of the face. Causes: - Drooping eyelid. - Pupil constriction. - Absence of sweating on one side of the face.
51
What is the most common lung cancer in non-smokers?
- Adenocarcinoma
52
What is the most common lung cancer overall in the population?
- Adenocarcinoma.
53
What is the most common lung cancer in smokers?
- Squamous cell carcinoma (over half of the lung cancers seen in smokers).
54
What are the two types of COPD?
- Emphysema (Alveolar damage). - Chronic bronchitis (long term inflammation of the bronchi).
55
What is alpha-1 antitrypsin deficiency?
- An autosomal codominant disorder. - Mutation of the SERPINA1 gene at the protease inhibitor (PI) locus. - Results in the production of mutant AAT, causing inflammatory lung damage and liver damage.
56
What is the clinical presentation of alpha-1 antitrypsin deficiency?
- Panacinar emphysema. - Obstructive lung disease. - Bronchiectasis. - Liver disease - Typical COPD presentation.
57
What is the main risk factor for alpha-1 antitrypsin deficiency?
- FH of AAT deficiency (could be one or two parents as the SERPINA1 mutation is co-dominant).
58
What are the investigations used for alpha-1 antitrypsin deficiency?
- AAT measurement. Low AAT raises suspicion. - Spirometry. FEV1/FVC \< 0.7 indicates obstructive disease such as AAT deficiency.
59
What is the pathophysiology of alpha-1 antitrypsin deficiency?
- Mutation of the SERPINA1 gene at the protease inhibitor locus (PI). - Results in the production of mutant alpha-1 antitrypsin. - This mutant AAT results in less clearance of neutrophilic elastase, leading to inflammatory lung damage. - Mutant AAT may polymerise and build up in the liver, causing liver disease.
60
What is the treatment for alpha-1 antitrypsin deficiency?
- Standard COPD treatment (Salbutamol for rescue, tiotropium LAMA for maintenance). - Treat liver disease as appropriate: diuretics, transplant etc. - Stop smoking - Hep A/B vaccine
61
What are the common differentials for alpha-1 antitrypsin deficiency?
- Asthma. More response to ICS. - COPD. More likely to be associated with smoking, and occurs at an older age. - All differentials can be evaluated using an AAT test. If AAT is low, alpha-1 antitrypsin deficiency likely cause.
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