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Respiratory Sytem > Asthma and COPD > Flashcards

Asthma and COPD Flashcards

1
Q

What is Asthma?

A

Chronic inflammation of the airways where obstruction is often reversible, either spontaneously or with treatment

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2
Q

What are 5 defining characteristics of Asthma?

A
  • Chronic Inflammatory Process
  • Susceptibility
  • Variable/intermittent airflow obstruction
  • Airway hyper responsiveness
  • Reversibility
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3
Q

Describe the pathophysiology of Asthma

A
  • Macrophages process and present antigens to T cells, activating Th2 (T Helper) cells
  • Cytokines released, which attract and activate inflammatory cells (mast cells, eosinophils). Th2 cells also activate B cells, which produce IgE
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4
Q

In Atopic Asthma, what does Atopy mean?

A

Means that patient has a triad of Asthma, Hayfever and Eczema

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5
Q

Typically, exposure to antigens result in a 2 phase response.

What are 2 phases?
What time periods do they occur over?
What type of hypersensitivity are they examples of?

A

Immediate response;

  • Within 20 mins
  • Example of Type I hypersensitivity

Late Phase response;

  • Within 3 to 12 hours
  • Example of Type IV hypersensitivity
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6
Q

Describe the Immediate Response to Antigens being presented to T cells in Asthma

A
  • Caused by interaction of Allergens and specific IgE antibodies
  • Leads to Mast Cell Degranulation, Mucus Production and Bronchoconstriction (Bronchial smooth muscle contraction)
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7
Q

Describe the Late Phase Response to Antigens being presented to T cells in Asthma

A
  • Inflammatory cells (Mast cells, Eosinophils, Neutrophils etc) release mediators and cytokines
  • These cause Airway Inflammation and Shedding of Epithelial cells
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8
Q

List 5 ways Airway inflammation reduces airway diameter

A
  • Mucosal swelling/ Oedema
  • Thickening of bronchial walls
  • Excess production of Abnormal Mucus (Thick, slow moving)
  • Smooth muscle contraction
  • Epithelium shed and incorporated into thick mucus
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9
Q

Describe the usual cough of asthma patients

A

Due to abnormal mucus cough is usually dry/ only productive of scanty, white sputum

(In severe cases, many airways are occluded by mucus plugs)

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10
Q

Why can non-allergic stimuli like cold air and fumes trigger asthma attacks?

A

Inflammation causes hyper-responsiveness of airways

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11
Q

Chronic poorly controlled asthma can lead to airway remodelling, which may not be reversible.

What are 3 changes?

A
  • Hypertrophy + Hyperplasia of Smooth Muscle
  • Hypertrophy of mucus glands
  • Basement membrane thickening
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12
Q

What are 3 effects of airway narrowing in Asthma patients?

A
  • Wheezing + other clinical features of asthma
  • Results in an obstructive pattern on Spirometry (Reduced FEV and FVC ratio)
  • Air trapping with increased Residual Volume
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13
Q

Describe the effects on Gas Exchange due to ;

  • Mild to Moderate Asthma
  • Severe attacks of Asthma
A

Mild/ Moderate;

  • Reduced pCO2, reduced pO2
  • Type 1 respiratory failure

Severe (Less CO2 can be exchanged due to exhaustion and more extensive involvement of airways);

  • Increased pCO2, reduced pO2
  • Type 2 respiratory failure
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14
Q

List 8 triggers of Asthma

A
  • Allergens
  • Cold air
  • Exercise
  • Fumes
  • Cigarette smoke
  • Perfumes
  • Emotional distress
  • Drugs (NSAIDS and Beta Blockers)
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15
Q

How do you treat Asthma?

A
  • Patient education (Remove triggers)
  • Vaccinations (Influenza and pneumococcal)
  • Drug treatment, Bronchodilators and Steroids
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16
Q

What are 4 ways Acute Severe Asthma presents?

A
  • Can’t complete full sentences
  • O2 sats< 92%
  • Tachypnoea (25) and Tachycardia (110)
  • Peak Flow Rate at 33-50% of max value
17
Q

What are 6 ways Life Threatening Asthma presents?

A

Any 1 of;

  • Cyanosis
  • Drowsiness, poor respiratory effort
  • ‘Silent chest’
  • O2 sats< 90%
  • Peak Flow rate< 33%
  • Arrhythmia, Hypotension
18
Q

Describe the ABG analysis of Acute Severe Asthma

A

Hyperventilation leads to;

  • Reduced pCO2
  • Unchanged pO2

Therefore, Respiratory Alkalosis and pH increases

19
Q

Describe the Aetiology of COPD

A
  • Tobacco smoking is responsible for 90% of COPD cases
  • Air pollution and occupational exposure are other causes

Alpha1 Antitrypsin deficiency is a less common cause;

  • Imbalance in proteinases and antiproteinases
  • Leads to Destruction of Alveolar Walls-> Emphysema
  • Usually presents at an early age
20
Q

List 6 pathological changes of COPD

A
  • Enlargement of mucus secreting glands
  • Increased no. of goblet cells (replace ciliated epithelium)
  • Ciliary dysfunction
  • Elastin breakdown-> Alveolar Wall destruction-> Loss of Elastic Recoil
  • Formation of larger air spaces-> Reduced SA for gas exchange
  • Vascular bed changes-> Pulmonary hypertension
21
Q

What is the final outcome of Chronic Bronchitis, a component of COPD?

A
  • Excessive mucus secretion

- Impaired removal of secretions (due to ciliary dysfunction)

22
Q

What are 3 ways the changes due to Emphysema and Chronic Bronchitis lead to increased airway resistance

A
  • Airways obstructed by secretions
  • Narrowing of small bronchioles (usually kept open by radial traction)
  • Reduced elastic recoil-> Reduced expiratory force-> Air trapping
23
Q

What does Progressive Hypoxia in COPD lead to?

A
  • Pulmonary vasoconstriction + Vascular smooth muscle thickening-> Pulmonary Hypertension
  • RH Failure (Cor pulmonale)
24
Q

Describe the clinical features of COPD before examination

A

Cough;

  • Chronic for 3 consecutive months
  • Productive but sputum quality may change

Shortness of Breath;
- Initially on exertion, may progress to at rest

25
Q

Describe 6 clinical features of COPD on examination

A
  • Tachypnoea
  • Use of accessory muscles of respiration
  • Barrel chest
  • Hyper resonance on percussion (due to hyper-inflation and air trapping)
  • Reduced intensity breath sounds
26
Q

List 3 late features of COPD

A
  • Central Cyanosis
  • Flapping tremors due to Hypercapnia
  • Signs of RH Failure, secondary to pulmonary hypertension
27
Q

List 6 investigations that can be done for COPD

A
  • Lung Function Tests
  • Spirometry
  • DLCO (Diffusing Capacity for CO, reduced)
  • Alpha-1 Antitrypsin level
  • Pulse oximetry/ ABG Analysis
  • CXR
28
Q

Compare Asthma and COPD in Spirometry results

A

Asthma;

  • Obstructive pattern with FEV/ FVC< 30%
  • Results improve after Bronchodilator treatment

COPD;

  • Obstructive pattern with FEV/ FVC< 30%
  • Results don’t improve after Bronchodilator treatment
29
Q

Describe the use of CXR in investigating COPD

A

Hyper-inflated lungs may result in;

  • Flattened diaphragm
  • Hyper lucent lungs
  • Increased antero-posterior diameter of chest
  • May also show COPD complications such as Pneumonia and Pneumothorax
  • Useful to rule out other pathologies
30
Q

List 7 treatments for COPD

A
  • Smoking cessation
  • Patient education
  • Vaccinations (Influenza and Pneumococcal)
  • Bronchodilators, Antimuuscarinics, Steroids
  • Pulmonary rehabilitation (exercise programme, nutrition advice)
  • Long term O2 treatment
  • Surgical interventions (Last step, volume reduction/ transplant/ removal of large bullae
31
Q

Define Acute Exacerbation of COPD (Most common cause is infection)

A
  • Change in patient’s baseline Dyspnoea, Cough, and/ or Sputum
  • Beyond normal day to day variations and acute in onset
32
Q

How do Acute Infectious Exacerbations of COPD present?

A
  • Fever
  • Chest pain
  • Acute, severe hypercapnia
33
Q

What are 5 management methods of Acute Exacerbations of COPD

A
  • Antibiotics
  • Bronchodilators
  • Oral steroids
  • O2 therapy, while monitoring pCO2
  • Non invasive/ Invasive ventilation
34
Q

What are 5 complications of COPD?

A
  • Pneumonia
  • Pneumothorax
  • Respiratory failure
  • Cor pulmonale (RH Failure)
  • Polycythaemia (More RBCs made to carry more O2)
35
Q

What is a classic sign of someone having an asthma attack?

A
  • Upright, posture

- Slightly leaning forward

Respiratory Sytem (21 decks)

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