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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
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* **Acute serve asthma** * **Assessment when they are brought in**
* **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
28
* **Life** threatening asthma
29
**ABGs in….** Acute serve asthma
* Decreased CO2 (blowing of CO2) * Increased pH * Respiratory alkalosis * Low O2 * Type 1 respiratory failure
30
ABGs in... life threatening asthma
**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
**emergency management of asthma**
* Oxygen * Salbutamol nebuliser – short acting * Steroid (oral or through vein) * Admit +/- ITU * CXR
32
**COPD = umbrella term for:**
* Emphysema * Chronic bronchitis
33
**COPD is the**
* **4th leading cause of death** * **Signif morbidity**
34
**Emphysema**
* 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
causes of emphyseme
* Smoking (must stop smoking to stop it getting worse) * **Alpha 1- antitrypsin deficiency**
36
* **Alpha 1- antitrypsin deficiency**
* 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
**Chronic bronchitis**
* 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
difference between asthma and chronic bronchitis
* Increased mucus and inflammation that causes narrowing of the airway --\>not bronchoconstriction
39
**Symptoms of chronic bronchitis**
Chronic productive cough
40
* **Risk factors for COPD**
* Smoking * More common in male (cultural) * Increased age * Childhood respiratory disease * Genetic e.g. A1AT deficiency * Exposure
41
* **Symptoms of COPD**
* Breathlessness and wheeze (airway narrowing) * Chronic bronchitis * Productive cough
42
diagnosis of COPD based on
spirometry and CXR
43
COPD **Spirometry**
* Will show obstructive airway pattern- reduced FEV: FVC ratio * \<70% * Poor bronchodilator reversibility (not caused by bronchoconstriction)
44
* **COPD CXR**
* Can see bigger alveoli--\>air trapping--\> shows up as hyperdense * Hyperinflated chest – how many ribs can you seen
45
symptomatic test for COPD
MRC dyspnoea scale
46
severity of COPD based on
* decreased FEV1
47
prevention of COPD
quit smoking
48
pharmcological management of COPD
* SABA (short acting beta agonists) /LABA (long acting beta agonists) * Antimuscarinics (ipratropium bromide or tiotropium- long acting) * Steroids (ICS)
49
* Non-pharmacological management of COPD
* Vaccines * Chest physiotherapy
50
**Acute exacerbation of COPD** * **In response to**
* Infection- viral/bacterial * Irritants
51
**Acute exacerbation of COPD symptoms**
* Increased dyspnoea * Cough * Productive/ green sputum * Wheeze
52
Acute exacerbation of COPD signs
* Breathless * Using accessory muscles-tripoding * Pursed lip breathing * Look cyanosed
53
investigations for acute exacerbations of COPD
* CXR * ABG * FBC, CRP * U&Es * Cultures * Sputum * Blood culture (if fever- sepsis
54
* **Management of Acute exacerbation of COPD**
* SABA and SAMA nebuliser * Steroid orally/ IV * Antibiotics if bacterial * +/- O2- 88-92% target
55
what do we need to consider carefully when managing pts with COPD
giving oxygen - different response to normal people due to different hypoxic drive
56
**Hypoxic drive in normal people**
* 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
* Hypoxic drive in COPD pts
* 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
**COPD patients and oxygen**
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
* If we over correct the oxygen in a COPD patient...
* 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
how do we tightly control pO2 in COPD pts
* 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
longterm complications of COPD
chronic hypoxia chronic resp failure polycythaemia
62
**Chronic hypoxia** 1.
* 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
Cor pulmonale
Right sided heart failure - caused by pathology in the lungs- pulmonary hypertension due to vasconconstriction of pulmonary blood vessels
64
**Chronic respiratory failure**
Co2 retention can lead to type 2 resp failure due to chronic poor ventilation of the lungs
65
**Polycythaemia**
due to chronic hypoxia--\> body is doing all it can to increase oxygen carrying capacity --\> increases number of RBC--\>Polycythaemia
66
Respiratory failure is divided into type I and type II.
**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
summary of difference between asthma and COPD
68
**Explanation by Dr Christides:Changes in ventilation in people with chronic CO2 retention with oxygen therapy**
* 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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