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Resipiratory > Session 8 - Asthma, COPD, Bronchiectasis and Cystic fibrosis > Flashcards

Session 8 - Asthma, COPD, Bronchiectasis and Cystic fibrosis Flashcards

1
Q

What are some main symptoms of asthma?

A

Wheezing, shortness of breath, chest tightness and cough (vary over time, frequency and intensity).

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2
Q

Why does asthma cause difficulty breathing air out of lungs?

A
  • Bronchoconstriction
  • Airway wall thickening
  • Increased mucus
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3
Q

What may trigger or worsen asthma symptoms?

A

Viral infections, Allergens, Tobacco smoke, Exercise, and Stress.

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4
Q

What is the definition of asthma?

A

Asthma is a heterogeneous disease, usually characterised by chronic airway inflammation.

It is defined by history of respiratory symptoms (wheeze, shortness of breath, chest tightness, coughing) that vary over time with intensity, together with variable expiratory airflow.

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5
Q

What are the causes of asthma?

A
  • Genetic susceptibility

- Environmental risk (e.g. allergens, smoke, pollutants, obesity, etc)

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6
Q

Which factors increase the probability that a patient’s symptoms are due to asthma?

A
  • More than one type of the symptoms.
  • Worse at night/ early morning
  • Symptoms vary over time and intensity
  • Are triggered by viral infections, exercise, allergens, change in weather, laughter, irritants (car exhaust), fumes, smoke or strong smells.
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7
Q

Which factors decrease probabiltiy that symptoms are due to asthma?

A
  • Isolated cough, no other symptoms
  • Chronic sputum production
  • Shortness of breath associated with dizziness, light headed, or tingling.
  • Chest pain
  • Exercise induced dyspnoea. (noisy inspiration)
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8
Q

What is the pathophysiology of asthma?

A
  • Airway inflammation
  • Classically eosinophilic but may be non-eosinophilic.
  • Airway oedema
  • Mucus hypersecretion
  • Desquamation of epithelium
  • Smooth muscle hyperplasia
    All causes airflow obstruction and increase bronchial hyper-responsiveness.
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9
Q

What is airway remodelling?

A

The changes to the airways as a result of the inflammation and hyper-responsiveness in asthma.

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10
Q

On what basis is asthma diagnosed?

A
  • A History of characteristic symptom patterns.

- Evidence of variable outflow limitation, from bronchodilator reversibility testing etc.

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11
Q

How is variable airflow limitation confirmed?

A

Confirm there is an airflow limitation.

  • FEV1/FVC is reduced (at least once, when FEV1 is low).
  • Ratio normally >0.75 - 0.80 in healthy adult (>0.90 children)

Confirm lung function varies more than a healthy individual.

  • > variation, > probability of asthma.
  • Excessive bronchodilator reversibility (Adults: > FEV1 of >12%, and >200ml)
  • Significant increase in FEV1 or PEF after 4 weeks of controller treatment.
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12
Q

What is the nitric oxide test?

A

Test to see how much nitric oxide is breathed out. It is used to see the liklihood that your airways are inflamed and help inform treatment.

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13
Q

How else is airway inflammation detected with tests?

A

Peripheral blood eosinophil count.

Induced sputum

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14
Q

What can differentiate asthma from COPD?

A
  • Age (COPD tends to be >35)
  • Cough (COPD = persistent, productive
  • Smoking (typical in COPD)
  • Dyspnoea (variable in asthma, persistent in COPD)
  • Nocturnal symptoms (breathless in COPD, Coughing,
  • wheezing with asthma)
  • Family History - common in asthma
  • Atopy (common with asthma)
  • Diurnal symptoms (asthma)
  • Spirometry - reversible with asthma usually.
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15
Q

Define Atopy.

A

The genetic tendency to develop allergic diseases.

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16
Q

Define Diurnal.

A

Variation throughout the day.

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17
Q

What is the difference in immune cells present with Asthma and COPD?

A

COPD
Neutrophils
Macrophages
CD8 + cells

Asthma
Eosinophils
Mast Cells
CD4 + cells

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18
Q

If there is a high probability someone has suspected asthma what treatment is given?

A
  • 6 Weeks inhaled corticosteroids (or 2 week prednisolone).

- B2 agonist can relieve symptoms but doesn’t treat inflammation.

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19
Q

What are the treatment plans if there is intermediate or low probability the patient is suspected of asthma?

A

Intermediate

  • If asymptomatic watchful waiting.
  • If symptomatic initiate treatment and assess response.

Low
- Investigate or treat for other more likely diagnosis.
(and assess response)

20
Q

What are the aims for asthma control?

A
  • No daytime symptoms
  • No awakening due to it
  • No need for the rescue medication
  • No asthma attacks
  • No limitations on activity (exercise)
  • Normal lung function.
    (minimal side effects)
21
Q

What does ‘SIMPLE’ mean, for effective asthma management?

A 
S moking cessation
I nhaler technique
M onitoring
P harmacotherapy
L ifestyle
E ducation
22
Q

If the control of the asthma is poor on the initial/ current treatment, what addon therapies are used?

A
  • Increased inhaled corticosteroid dose.

- Increased dose of Long acting beta 2 adrenoceptor agonist. (LABA)

23
Q

How are acute severe asthma episodes treated?

A
  • High flow oxygen (sats 94-98%)
  • Nebulised salbutamol (w/ O2)
  • Oral Prednisolone (short term)

Severe/life threatening

  • Add nebulised ipratropium bromide
  • Can consider iV magnesium/ aminophylline if not improvement.
24
Q

What investigations are done in suspected COPD patients?

A
  • Measurement of airflow obstruction, with spirometry. (Forced Expiratory Manoeuvre).
  • Airflow Obstruction = FEV1 <80% predicted, or FEV1/FVC ratio <70%

Along with a good history (e.g. age, smoking status, and productive cough, can diagnose COPD!)

25
Q

How is stable COPD managed?

A
  • Smoking Cessation!
  • Pulmonary rehabilitation (community course)
  • Bronchodilators (
26
Q

What are the causes of bronchiectasis?

A
  • Post infective - whooping cough, TB
  • Immune deficiency - hypogammaglobulinaemia
  • Mucociliary clearance defects - CF, etc

Many others

27
Q

How does bronchiectasis clinically present?

A
  • Chronic cough
  • Daily Sputum production - can vary in quantity, colour and consistency.
  • Breathlessness on exertion
  • Intermittent haemoptysis
  • Nasal symptoms
  • Chest pain
  • Fatigue
28
Q

In what way is bronchiectasis managed?

A
  • Physio / airways clearance
  • Sputum sample/ culture
  • Exclude immunodeficiency
  • Flu vaccine
  • Pulmonary rehabilitation
    (management plan for infective exacerbation)
29
Q

What is the pathophysiology at work in cystic fibrosis?

A
  • Genetic defect in CFTR gene (cystic fibrosis transmembrane conductance regulator).
  • Ineffective cell surface chloride transport
  • Causes thick, dehydrated body fluids in organs which have CFTR.
30
Q

How does CF usually present?

A
  1. Meconium ileus
    - In 15-20% of newborn CF infants, bowel is blocked by the sticky secretions. Intestinal obstruction, bilious vomit, abdo distension, delay in passing meconium.
  2. Intestinal malabsorption
    - Over 90% CF individuals have intestinal malabsorption. (usually evident in infancy)
    - Main cause is severe deficiency of pancreatic enzymes.
  • Chest infections
  • Newborn screening
31
Q

What is the treatment for cystic fibrosis?

A 
Key is maintaining lung health (chest physio, infection management), and nutritional state - BMI, pancreatic status etc.
Targeted therapies (genotype specific).
Management of comorbidities.
32
Q

What is the mechanism of action for bronchodilators like salbutamol?

A
  • Ligand binds B2 adrenergic receptor.
  • Activates adenylyl cyclase
  • Increases cAMP - activates PKA.
  • PKA phosphorylates MLCK, leading to relaxation of smooth muscle in airway.
33
Q

What are the adverse effects of B2 agonists?

A
  • Tachycardia (atrial B2 receptors)
  • Tremor (skeletal B2 receptors)
  • Anxiety
  • Palpitations
  • Hypokalaemia (skeletal muscle uptake K+)
34
Q

What are the adverse effects of B2 agonists?

A
  • Tachycardia (atrial B2 receptors)
  • Tremor (skeletal B2 receptors)
  • Anxiety
  • Palpitations
  • Hypokalaemia (skeletal muscle uptake K+)
35
Q

What is pulmonary rehabilitation?

A
  • Education about exercise with control of breathlessness, to help strengthen respiratory muscles and prevent deconditioning due to doing no exercise (as often happens in COPD).
  • Nutritional advice, etc.
36
Q

What final measure may be used in COPD if all treatments are ineffective?

A

Long term oxygen therapy.

  • Used at least 16 hrs a day.
  • Offered if pO2 consistently below 7.3 kPa.
  • (must be non smoker, not retain high levels of CO2)
37
Q

What surgical interventions can be carried out for COPD patients?

A

Lung volume reduction: - to reduce the hyperinflation.

Lung transplant may be option in younger patients.

38
Q

What is non-invasive ventilation?

A

Ventilatory support through patients upper airway using a mask.
(Useful for acute exacerbations of COPD with type 2 respiratory failure and mild acidosis)
Must be conscious!

39
Q

What is non-invasive ventilation?

A

Ventilatory support through patients upper airway using a mask.
(Useful for acute exacerbations of COPD with type 2 respiratory failure and mild acidosis)
Must be conscious!

40
Q

What is bronchiectasis?

A

Chronic dilation of one or more bronchi. The bronchi exhibit poor mucus clearance and there is predisposition to recurrent or chronic bacterial infection.

41
Q

Which diagnostic tool can confirm bronchiectasis?

A

High Resolution CT

42
Q

Which common organisms could cause bronchiectasis?

A

Haemophilus influenzae
Streptococcus pneumoniae
Fungus - aspergillus, candida
Pseudomonas aeruginosa.

43
Q

How is an exacerbation of bronchiectasis defined?

A

Deterioration in 3 or more key symptoms for at least 48 hours.

  • Cough
  • Sputum (volume/ consistency/ purulence)
  • Breathlessness (exercise intolerance)
  • Fatigue
  • Haemoptysis.
44
Q

How is an exacerbation of bronchiectasis defined?

A

Deterioration in 3 or more key symptoms for at least 48 hours.

  • Cough
  • Sputum (volume/ consistency/ purulence)
  • Breathlessness (exercise intolerance)
  • Fatigue
  • Haemoptysis.
45
Q

How is CF diagnosed?

A
  • One or more characteristic phenotypic features.
  • History of CF in sibling
  • Positive newborn screening result
    and
  • Increased sweat chloride concentration
  • Identification of two CF mutations (genotyping)
46
Q

What are some main cystic fibrosis complications?

A
  • Bronchiectasis
  • Haemoptysis
  • Chronic sinusitis
  • Nasal polyposis
  • Diabetes mellitus (cystic fibrosis related diabetes)
  • Pancreatic insufficiency
  • Distal intestinal obstruction syndrome
  • Chronic liver disease
  • Gall stones
  • Arthritis
  • Male infertility
  • Congenital bilateral absence of the vas deferens. (CBAVD)

Many more!

Resipiratory (9 decks)

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