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Respiratory > Lecture 10- Obstructive airway diseases > Flashcards

Lecture 10- Obstructive airway diseases Flashcards

1
Q

example of obstructive lung diseases

A

asthma

COPD

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2
Q

COPD

A

emphyseme and chronic bronchitis

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3
Q

asthma overview

A
  • Chronic inflammatory airway disease
  • Affects small airways
  • Intermittent and variable airway obstruction and hyper reactivity in the airways
  • Usually reversible
    • Can be spontaneous
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4
Q

pathophysiology of asthma can be

A

atopic (more prevalent ) or non-atopic asthma

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5
Q
  • Atopic means
A

Susceptible individual

  • Triad of
    • Asthma
    • Eczema
    • Hay fever
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6
Q

atopic asthma lined to

A

allergens- Type 1 hypersensitity reaction

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7
Q
  • Type 1 hypersensitivity
    • *
A
  1. Allergen (1st exposure)
  2. Comes into contact with APC e.g. macrophage
  3. Process information about allergen to T helper 2 cell
  4. Causes a cascade of events which involves antibody production–> IgE
  5. IgE attach themselves to the surface of mast cells which release histamine and leukotrienes when antibodies sense re- exposure to antigen–>cause mast cell degranulation cause inflammation :
    1. Mucus production
    2. Bronchoconstriction – parasympathetic nervous system (oedema- sweeling in the airway)
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8
Q

Non-allergic asthma, or non-atopic asthma, is a type of asthma that

A
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9
Q
  • Symptoms of asthma
A
  • Breathlessness
  • Chest tightness
  • Wheeze –> poor airflow
    • May be a symptom or sign
  • Dry cough - nocturnal
    • Worse at night because parasympathetic NS more prevalent at night
  • Atopy
  • Intermittent symptoms
  • Triggers (allergen)/ hyper-responsive
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10
Q

signs of asthma

A
  • Increase RR, HR and decreased O2 sats
  • Wheeze
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11
Q

investigations for asthma

A

Peak flow (PEFR)

Spirometry

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12
Q

peak flow takes into account

A
  • Sex
  • Age
  • Height
  • not usually race
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13
Q

spirometry results for asthma

A
  • Decreased FEV: FVC ratio <70%
  • If you give bronchodilator you will see reversibility in form of bronchodilation which will increase FEV/ FVC ratio
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14
Q

management if low probability of being asthma

A
  • no typical features, other diagnosis more likely
    • Want to investigate other causes to rule out
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15
Q

management if intermediate probability of being asthma

A
  • Intermediate prob -borderline- some not all symptoms. Treatment for other cause isn’t working
    • Investigate for definitive diagnosis- spirometry
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16
Q

management if high prob of being asthma

A
  • High prob- typical presentation
    • Start treatment straight away
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17
Q

Long term treatments for asthma

A
  • Patient education- removed triggers
  • Pharmacology (inhalers)​
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18
Q
  • Asthma Patient education- remove triggers
A
  • Say bye to the cat
  • Remove dust
  • Remove smoke
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19
Q

first line drugs for asthma

A
  • B2 agonists- Salbutamol (blue enhaler)
    • Short acting- - relieves symptoms in short term
  • Inhaled corticosteroid- preventor (brown inhaler)
    • ​Dampen down inflammation which causes narrowing of airways
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20
Q

B2 agonists- Salbutamol (blue enhaler) works by

A
  • Promote bronchodilation via the sympathetic NS (B2 receptor in the lungs)
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21
Q
  • Asthma long term treatment : If they have to use the reliver 3+ times a week or if they are being woken up at night
    • Need to check inhaler technique
    • Move to Step 2
      • Add-on therapies:
A
  • Inhaled long acting beta agonist (salmeterol)
    • Inhaled Cortical Steroid
      • Purple inhaler (with both in)
  • With blue reliver
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22
Q

Long term asthma treatment: step 3

A
  • Increase dose of ICS to medium dose
  • Add leukotriene receptor antagonist

If still not responding… have you made the right diagnosis

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23
Q
  • Management will change depending on
A
  • age
    • May introduce a spacer–> don’t need to have coordinated breathing technique
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24
Q

emergency managemnt asthma - 2 scenarios

A

acute severe asthma

life threatening asthma

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25
Q
A
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26
Q
A
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27
Q
  • Acute serve asthma
    • Assessment when they are brought in
A
  • A–> E assessment
    • A- may not be able to complete sentences
    • B
      • O2 sats may be low but O2>92%
      • Wheeze
      • RR >25
      • PEFR – 33-50% of their known best peak expiratory value
        • E.g. precited peak flow 400, but only getting 180 –> would qualify in the 33-50% bracket.
    • C
      • HR >110
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28
Q
  • Life threatening asthma
A
29
Q

ABGs in….

Acute serve asthma

A
  • Decreased CO2 (blowing of CO2)
  • Increased pH
    • Respiratory alkalosis
  • Low O2
    • Type 1 respiratory failure
30
Q

ABGs in… life threatening asthma

A

Life threatening

  • Can look normal
  • LOOK AT THE PATIENT
    • Treatment is working
    • Patient deteriorating (rising CO2 due to decreased respiratory rate- may need ventilation if cant support own breathing)
31
Q

emergency management of asthma

A
  • Oxygen
  • Salbutamol nebuliser – short acting
  • Steroid (oral or through vein)
  • Admit +/- ITU
  • CXR
32
Q

COPD = umbrella term for:

A
  • Emphysema
  • Chronic bronchitis
33
Q

COPD is the

A
  • 4th leading cause of death
  • Signif morbidity
34
Q

Emphysema

A
  • Damage to walls of alveoli
  • Rather than lots of small alveoli, they breakdown forming larger alveoli –> unable to support bronchioles
    • Bronchioles collapse and trap air inside the lungs
  • Changes in emphysema are irreversible
35
Q

causes of emphyseme

A
  • Smoking (must stop smoking to stop it getting worse)
  • Alpha 1- antitrypsin deficiency
36
Q
  • Alpha 1- antitrypsin deficiency
A
  • Not truly a deficiency- malformed alpha 1-antitrypisn–> cant leave the liver, therefore builds up in the liver and can cause liver disease directly
    • In the lung main function
    • Balance action of protease and elastase enzymes which are produced in the presence of inflammation, infection, or smoking
    • If no alpha 1-antitrypsin, then elastase can break down the structure of the lung
37
Q

Chronic bronchitis

A
  • Chronic inflammation of the bronchioles
  • Inflammatory changes like asthma
  • Instead of responding to allergen, it responds to irritants like cigarette smoke
    • Not T1 hypersensitivity
  • Non-reversible
  • Increased mucus and inflammation that causes narrowing of the airway –>not bronchoconstriction
38
Q

difference between asthma and chronic bronchitis

A
  • Increased mucus and inflammation that causes narrowing of the airway –>not bronchoconstriction
39
Q

Symptoms of chronic bronchitis

A

Chronic productive cough

40
Q
  • Risk factors for COPD
A
  • Smoking
  • More common in male (cultural)
  • Increased age
  • Childhood respiratory disease
  • Genetic e.g. A1AT deficiency
  • Exposure
41
Q
  • Symptoms of COPD
A
  • Breathlessness and wheeze (airway narrowing)
  • Chronic bronchitis
    • Productive cough
42
Q

diagnosis of COPD based on

A

spirometry and CXR

43
Q

COPD Spirometry

A
  • Will show obstructive airway pattern- reduced FEV: FVC ratio
  • <70%
  • Poor bronchodilator reversibility (not caused by bronchoconstriction)
44
Q
  • COPD CXR
A
  • Can see bigger alveoli–>air trapping–> shows up as hyperdense
  • Hyperinflated chest – how many ribs can you seen
45
Q

symptomatic test for COPD

A

MRC dyspnoea scale

46
Q

severity of COPD based on

A
  • decreased FEV1
47
Q

prevention of COPD

A

quit smoking

48
Q

pharmcological management of COPD

A
  • SABA (short acting beta agonists) /LABA (long acting beta agonists)
  • Antimuscarinics (ipratropium bromide or tiotropium- long acting)
  • Steroids (ICS)
49
Q
  • Non-pharmacological management of COPD
A
  • Vaccines
  • Chest physiotherapy
50
Q

Acute exacerbation of COPD

  • In response to
A
  • Infection- viral/bacterial
  • Irritants
51
Q

Acute exacerbation of COPD symptoms

A
  • Increased dyspnoea
  • Cough
  • Productive/ green sputum
  • Wheeze
52
Q

Acute exacerbation of COPD signs

A
  • Breathless
  • Using accessory muscles-tripoding
  • Pursed lip breathing
  • Look cyanosed
53
Q

investigations for acute exacerbations of COPD

A
  • CXR
  • ABG
  • FBC, CRP
  • U&Es
  • Cultures
    • Sputum
    • Blood culture (if fever- sepsis
54
Q
  • Management of Acute exacerbation of COPD
A
  • SABA and SAMA nebuliser
  • Steroid orally/ IV
  • Antibiotics if bacterial
  • +/- O2- 88-92% target
55
Q

what do we need to consider carefully when managing pts with COPD

A

giving oxygen

  • different response to normal people due to different hypoxic drive
56
Q

Hypoxic drive in normal people

A
  • Increase pCO2- CO2 retention
  • Resets central chemoreceptors in the brain
    • Chemoreceptors are sensitive to absolute pH
      • Increased pCO2= decreased pH
    • Sends a message to respiratory centre to hyperventilate (acute setting)
57
Q
  • Hypoxic drive in COPD pts
A
  • Hyperventilation cannot fix the increased pCO2
  • In pts with chronic lung disease, their levels of pCO2 are continually high
    • Worse gas exchange (reduced SA)
  • Even hyper ventilation will not blow off the CO2
  • Need to involve the kidneys
    • Retain HCO3- to buffer increased CO2
    • Improved low pH in the brain and therefore hyperventilation stops (not sensing levels of cO2, sensing pH)
      • H+ still high as well as HCO3- high- brain think this looks normal
  • The brain is very sensitive to increased CO2 to drive respiration (main force of resp drive)
    • If you have chronically high Co2 levels, brain will not detect changes due to compensation by the kidney
  • Back up option
    • Peripheral chemoreceptors which detect changes in Oxygen
      • Much less sensitive than central chemoreceptors
      • O2 has to drop very low for the hypoxia to be the determining driver for respiration
58
Q

COPD patients and oxygen

A

This is why pts with COPD are given very controlled amounts of oxygen- we aim for a lower range of saturation as is normal for them

59
Q
  • If we over correct the oxygen in a COPD patient…
A
  • we will completely remove the hypoxic drive detected by the peripheral chemoreceptors
    • Oxygen levels may come back up to normal but the CO2 will still be high
    • Respiratory rate will plummet
60
Q

how do we tightly control pO2 in COPD pts

A
  • venturi marks
    • Very heavily controlled oxygen to make sure we don’t damage hypoxic drive
  • Aiming for 88%-92% oxygen

However in emergency situation and you don’t know if they have COPD- give oxygen normally and correct later.

61
Q

longterm complications of COPD

A

chronic hypoxia

chronic resp failure

polycythaemia

62
Q

Chronic hypoxia

1.

A
  • State of chronic hypoxia due to under perfused lungs can lead to pulmonary hypertension
  1. If under perfused area of lung- vasoconstriction to divert blood flow
  2. If much of the lung is chronically hypoxic- more widespread vasoconstriction
  3. Pressure in blood vessels goes up- pulmonary hypertension
  4. Harder for right side of the heart to pump blood into pulmonary circulation
    1. Right sided heart failure (Cor pulmonale- caused by pathology in the lungs)
63
Q

Cor pulmonale

A

Right sided heart failure

  • caused by pathology in the lungs- pulmonary hypertension due to vasconconstriction of pulmonary blood vessels
64
Q

Chronic respiratory failure

A

Co2 retention can lead to type 2 resp failure due to chronic poor ventilation of the lungs

65
Q

Polycythaemia

A

due to chronic hypoxia–> body is doing all it can to increase oxygen carrying capacity –> increases number of RBC–>Polycythaemia

66
Q

Respiratory failure is divided into type I and type II.

A

Type I respiratory failure involves low oxygen, and normal or low carbon dioxide levels.

Type II respiratory failure involves low oxygen, with high carbon dioxide.

67
Q

summary of difference between asthma and COPD

A
68
Q

Explanation by Dr Christides:Changes in ventilation in people with chronic CO2 retention with oxygen therapy

A
  • High CO2 because of lung disease
    • Initially CO2 diffuses across the BB reacting with H2O increasing carbonic acid- that rapidly dissociates to H+ and HCO3- brain extracellular fluid pH drops because H+ increase
    • Choroid plexus increases re-absorption of HCO3—restores HCO3-: CO3 reaction – brain ECF pH restored
  • But at a higher PaCO2 levels (Those with COPD)
    • Therefore ventilation now adjusted by hypoxaemia triggering peripheral chemoreceptor
    • If O2 given and PaO2 increase and Hb increases
      • CO2 levels may increase for 2 main reasons
        • V/Q mismatch and Haldane (this is the main problem)
          • Haldane- oxygenated Hb carries less CO2
          • Exacerbation of V/Q mismatch
            • If alveoli not well ventilated - O2 levels fall- constriction of pulmonary arteries- decreased perfusion to maintain V/Q as close to 1:1
              • Perfusion needs to go to healthy alveoli
            • If we give oxygen
              • Still poor ventilation to alveoli, but have increased o2
              • Therefore we lose the pulmonary vasoconstriction- worsening V/Q mismatch <1
              • Still cant get rid of CO2 due to poor ventilation
                • Lose diffusion gradient for CO2
        • Loss Hypoxia/ hypoxaemia drive minor role (minor role)
          • Carrying more CO2

Respiratory (27 decks)

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