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Phase 2a diseases > Respiratory > Flashcards

Respiratory Flashcards

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
Q

What are the diagnostic tests used for rhinitis?

A
  • Trials of antihistamines or intranasal corticosteroids.
  • If needed, an allergy skin prick test.
26
Q

What treatment is given for rhinitis?

A

1st line:

  • Avoidance of allergens (if possible).
  • Anti-histamines.

2nd line or if rhinitis more severe:
- Intranasal corticosteroid (beclometasone or budesonide)

27
Q

What is the clinical presentation of rhinitis?

A
  • Pruritus.
  • Rhinorrhea (thin discharge from nose).
  • Red/swollen/watery eyes.
  • Nasal congestion.
  • Sneezing.
28
Q

What is bronchiectasis?

A
  • 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
Q

What is the clinical presentation of bronciectasis?

A
  • 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
Q

What is the pathophysiology of bronchiectasis?

A
  • 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
Q

What are the risk factors for developing bronchiectasis?

A
  • Cystic fibrosis. Most commonly identified primary cause of bronchiectasis.
  • Immnosuppresive conditions such as HIV.
  • alpha-1 antitrypsin deficiency.
  • Recent severe pulmonary infection.
32
Q

What is the criteria used to classify the severity of bronchiectasis called?

A

BSI: Bronchiectasis severity index.

33
Q

What diagnostic tests are available for bronchiectasis?

A
  • 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
Q

What are the treatment options for bronchiectasis?

A
  • 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
Q

What is cystic fibrosis?

A
  • Severely life-limiting disease caused by autosomal recessive mutation, leading to abnormal CFTR chloride channels.
36
Q

What is the clinical presentation of CF?

A

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
Q

What is the pathophysiology of cystic fibrosis?

A
  • 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
Q

What are the risk factors for CF?

A
  • FH of CF.
  • Both parents are carriers. (1 in 4 chance as the disease is autosomal recessive).
  • White ethnicity.
39
Q

How is CF monitored?

A
  • 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
Q

What are the diagnostic tests for cystic fibrosis?

A
  • 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
Q

What are the potential treatments for cystic fibrosis?

A

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
Q

What are the main classes of lung cancer?

A

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
Q

What are the symptoms of lung cancer?

A
  • 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
Q

Which lung cancer is most commonly found peripherally?

Which lung cancer is most commonly found centrally?

A

Peripherally - adenocarcinoma.

Centrally - large cell carcinoma.

45
Q

What are the risk factors associated with lung cancer?

A
  • Smoking
  • FH (especially 1st degree relative).
  • Radon exposure (mining).
  • COPD
  • Older age (median age is 70).
  • Asbestos exposure (especially mesothelioma!)
46
Q

What is the histological presentation of a small cell carcinoma?

A
  • Small, densely packed cells.
  • Anuclear.
47
Q

What are the investigations used for lung cancer?

A
  • 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
Q

What are the treatment options for pleural mesothelioma?

A
  • Surgical (lobectomy/pneumonectomy) is GS. Unlikely to be curative for small cell carcinoma or mesothelioma.
  • Radiotherapy.
  • Chemotherapy. Cisplatin often the drug of choice.
49
Q

Where does lung carcinoma commonly metastasise to?

A
  • Bone (most common)
  • Liver
  • Brain
  • Adrenal glands
  • Lymph nodes.
50
Q

What is the pathophysiology of Horner’s syndrome

A

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
Q

What is the most common lung cancer in non-smokers?

A
  • Adenocarcinoma
52
Q

What is the most common lung cancer overall in the population?

A
  • Adenocarcinoma.
53
Q

What is the most common lung cancer in smokers?

A
  • Squamous cell carcinoma (over half of the lung cancers seen in smokers).
54
Q

What are the two types of COPD?

A
  • Emphysema (Alveolar damage).
  • Chronic bronchitis (long term inflammation of the bronchi).
55
Q

What is alpha-1 antitrypsin deficiency?

A
  • 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
Q

What is the clinical presentation of alpha-1 antitrypsin deficiency?

A
  • Panacinar emphysema.
  • Obstructive lung disease.
  • Bronchiectasis.
  • Liver disease
  • Typical COPD presentation.
57
Q

What is the main risk factor for alpha-1 antitrypsin deficiency?

A
  • FH of AAT deficiency (could be one or two parents as the SERPINA1 mutation is co-dominant).
58
Q

What are the investigations used for alpha-1 antitrypsin deficiency?

A
  • AAT measurement. Low AAT raises suspicion.
  • Spirometry. FEV1/FVC < 0.7 indicates obstructive disease such as AAT deficiency.
59
Q

What is the pathophysiology of alpha-1 antitrypsin deficiency?

A
  • 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
Q

What is the treatment for alpha-1 antitrypsin deficiency?

A
  • 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
Q

What are the common differentials for alpha-1 antitrypsin deficiency?

A
  • 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.

Phase 2a diseases (18 decks)

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