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PH2113 Disease & Drugs 1 > U2 COPD, inhalers and ICS > Flashcards

U2 COPD, inhalers and ICS Flashcards

1
Q

In what ways are asthma and COPD similar?

A
  1. Similar symptoms
  2. Both obstructive pulmonary diseases

Impaired pulmonary airflow
Increasing flow resistance
Feeling of breathlessness

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2
Q

What is the presenting symptom of COPD?

A

Persistent chesty cough

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3
Q

What causes mucous buildup in COPD patients?

A
  • excess caused by pulmonary inflammation
  • loss of cilia on epithelial cells (minimal mucous clearance)
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4
Q

What is a major impact of mucous buildup for COPD patients?

A

Increased frequency of chest infections

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5
Q

What is the most common cause of death in those with COPD?

A

Pneumonia

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6
Q

How does wheezing in patients with COPD differ from those with asthma?

A

Wheezing in COPD is persistent

Wheezing with asthma - episodic

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7
Q

What causes persistent wheezing?

A
  1. Airway narrowing; long-term obstruction
  2. Oedema, swelling of bronchial wall
  3. Mucous buildup in lungs
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8
Q

What does an Alpha-1-antitrypsin deficiency cause?

A
  1. Genetic COPD
  2. Early onset COPD
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9
Q

What is the function of Alpha-1-antitrypsin?

How does it work?

A

Protein protecting the lungs from inflammation and disease

Protease inhibitor - inactivates neutrophil elastase; enzyme that breaks down lung tissue

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10
Q

In what sorts of patients is COPD most prevalent?

A
  • smokers
  • over 35
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11
Q

In what two ways are asthma and COPD the most similar?

A
  1. Airway hyper-responsiveness
  2. Periods of worsening symptoms - exacerbations
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12
Q

What are the main differences between COPD and asthma?

A

COPD - increasing breathlessness
Asthma - episodic breathlessness

COPD - symptoms will get worse
Asthma - symptoms get worse if untreated

COPD - no hereditary links
Asthma - some hereditary links

COPD - frequent chest infections
Asthma - less increased freq of chest infections

COPD - presents in older patients
Asthma - any age

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13
Q

What % of COPD patients are smokers?

What % of smokers develop COPD?

A

90%

15%

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14
Q

What is thought to be a contributory factor in causing non-smokers to develop COPD?

A

Exposure to small aerosol particles

E.g. concern about air pollution in city centres due to fine particle aerosols from diesel motors

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15
Q

How much as the incidence of COPD risen over the last 10 years?

A

30%

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16
Q

How do tissue changes in COPD patients differ from those in asthmatics?

A
  • irreversible structural changes
  • no pharmacological treatments to prevent progression
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17
Q

What is the predominant inflam cell found in the lungs of COPD patients?

A

Neutrophil

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18
Q

What feature common to asthma patients does not effect COPD patients?

A

Thickening of smooth muscle in the bronchiole wall

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19
Q

What should COPD be thought of as?

A

An exaggerated irritant response that leads to an inflammatory response

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20
Q

What are the characteristics of parasympathetic tone?

A
  • slow HR
  • lower bp
  • increased digestive activity
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21
Q

How does the body respond to irritation in the lung?

Why doesn’t this work?

A

Increasing parasympathetic tone to reduce exposure to atmospheric irritant

Source of irritation is within the lung not external to it and increase in ACh causes bronchoconstriction

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22
Q

What is one cause of hyper-responsiveness which is present in patients with both asthma and COPD?

A

Loss of integrity of protective epithelial cell lining
Reduces barrier between irritant receptors and atmosphere, increasing likelihood of irritant response

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23
Q

What causes long-term swelling (oedema) of bronchial wall?

A

Increased vascular permeability during inflam for ease of access for immune cells

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24
Q

In what patients is damage to the alveolar extracellular matrix in the lung prevalent?

A

COPD and severe asthma patients

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25
Q

What are the consequences of damage to alveolar extracellular matrix?

A
  1. Loss of lung elasticity
  2. Enlargement of respiratory air-spaces = emphysema
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26
Q

What could cause death in COPD patients?

A
  1. Infection
  2. Loss of lung capacity due to loss of elasticity
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27
Q

What is the main underlying cause of COPD?

A

Inappropriate pulmonary inflam - like asthma

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28
Q

What is the only known strategy that can intervene in COPD disease progression?

A

Smoking cessation

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29
Q

What is the only proven intervention for COPD that has been proven to slow its’ progression?

A

smoking cessation

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30
Q

In what two ways can COPD be non-pharmacologically managed?

A
  1. smoking cessation
  2. mental health care
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31
Q

What is involved in pharmacological COPD management?

A

palliative care

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32
Q

Why aren’t corticosteroids used in COPD treatment?

A

relatively ineffective at limiting inflammation in COPD

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33
Q

What sort of smoking cessation is best for COPD patients?

A

give up completely instead of gradually cutting down

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34
Q

What is an accepted method of risk reduction for smokers at risk of COPD?

A

vaping instead

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35
Q

Why is vaping concerning?

A
  1. unsure of long-term effects
  2. industry not heavily regulated, vapes not endotoxin-free
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36
Q

Why is it significant that vapes could contain endotoxins?

A

endotoxins - fragments from bacteria cell walls

shown to induce COPD-like syndrome in animal models

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37
Q

What kind of COPD patients are offered pulmonary rehabilitation?

A

those whose mobility is effected by the disease

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38
Q

What does pulmonary rehabilitation involve?

A
  1. disease education
  2. dietary advice
  3. fitness regimes
  4. psychological care
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39
Q

What does pulmonary rehabilitation improve for the patient?

What does it not effect?

A

quality of life

disease progression

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40
Q

To what COPD patients is oxygen therapy offered?

A

those who have severe impairment to airflow ie
FEV1 < 30% of normal
ie patients experiencing hypoxia

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41
Q

Why could oxygen supplementation in COPD patients cause respiratory depression?

A

usually increased CO2 levels cause urge to breathe but in COPD patients with chronically high CO2, their bodies may rely more on low O2 levels to trigger breathing

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42
Q

Why would pulse oximeters be used to calculate how much oxygen someone should be supplemented with?

A

O2 supplementation needs to be titrated to O2 saturation levels that require the use of pulse oximeters

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43
Q

What cautions need to be considered in patients receiving O2 supplementation?

A

O2 highly flammable so avoid
- static sparks e.g. moustaches
- SMOKING ie. open flames

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44
Q

What types of surgical procedures can be offered to COPD patients?

A
  1. bullectomy
  2. lung transplantation (one or both)
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45
Q

What is a bullectomy?

Why can this be helpful?

A

removal of obstructed, inflated bronchioles ie. alveolae that have collapsed into eachother forming large sacs (bullae)

inflated bronchioles can obstruct other unaffected airways due to their size

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46
Q

What is one difficulty in choosing lung transplantation for COPD patients?

A

patient has to
- have sufficiently advanced COPD to justify a transplant
- be fit enough for surgery

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47
Q

Why would pharmacotherapy be initiated for COPD patients?

A

To target potential factors that exacerbate the condition, prepare patient to know what to do in response and how to limit impact of such factors

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48
Q

What is the meaning of exacerbation?

What could a COPD exacerbation involve?

A
  • changes to phlegm e.g. thicker, change in colour
  • worsening breathlessness
  • worsening cough
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49
Q

What drugs would be recommended as first line to relieve breathlessness and exercise limitation in patients with only COPD?

A

SABA - short acting beta2 adrenoreceptor agonist and
SAMA - short acting muscarinic antagonist

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50
Q

For patients without asthma whose COPD symptoms are affecting their quality of life and are unresponsive to SABAs/SAMAs, what can be offered?

Why are they offered this?

A

LABA and LAMA combo

provides long-lasting pharmacological bronchodilation to help overcome the symptoms of breathlessness

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51
Q

For patients without asthma who have tried LABA and LAMA for day-to-day symptoms that affect quality of life but are still struggling, what is the next stage in the treatment plan?

Why is there a caution with this?

What is recommended if this is seen not to be effective?

A

initiation of 3 month trial with ICS

treatment with ICS in COPD can increase pneumonia risk

revert back to LABA/LAMA combo

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52
Q

Why would it be inappropriate to offer a LABA and ICS combo to a patient diagnosed with only COPD?

A

the ICS increases the risk of pneumonia against limited beneficial effects

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53
Q

How could exacerbations and persistent breathlessness be managed pharmacologically when the patient has both asthma and COPD?

How does this treatment help such patients?

A

LABA and ICS combo inhaler

LABA - offers long-term relief of bronchoconstriction by relaxation of airway smooth muscle
ICS - controls eosinophilic inflam (asthma) but does not influence neutrophilic inflam (COPD)

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54
Q

For patients who experience either one serious exacerbation or two moderate exacerbations, what is recommended?

Why?

A

LAMA + LABA + ICS in combi inhaler

evidence suggests ICS treatment can reduce freq of exacerbations in COPD patients; benefit of this outweighs increased pneumonia risk

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55
Q

When might antibiotics be offered to COPD patients?

A

when diagnosed with bacterial chest infection

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56
Q

Why might physiotherapy be offered to COPD patients?

A

to help mucus clearance

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57
Q

What are three hospital therapies for COPD treatment?

A
  1. IV theophylline (phosphodiesterase inhibitor)
  2. invasive ventilation
  3. non-invasive ventilation and doxapram
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58
Q

What might be the reasons for a COPD exacerbation?

A

bacterial or viral resp infection

exposure to allergen if patient also has asthma

stress increase

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59
Q

When can oral corticosteroids be beneficial for COPD patients?

A

those with viral infections e.g. COVID-19

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60
Q

What could resolve over diagnosis of childhood asthma?

A

more widespread use of spirometry to assess lung function

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61
Q

What percentage of chronic lung diseases are not diagnosed early?

A

85%

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62
Q

When does lung capacity decline?

A
  • with increasing age
  • when lungs become less compliant, stretchy (usually restrictive lung diseases but symptoms can present in end-stages of COPD)
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63
Q

What two parameters can be used to assess severity of lung disease?

A
  1. lung capacity
  2. air flow
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64
Q

What does a peak flow meter measure?

What are the units of measure?

A

maximum airflow that a patient can generate (max rate of exhalation) - flow rate generated in first 0.1 seconds of forced expiration

litres per minute; expiratory flow rate is extrapolated over 1 min on scale to provide reading

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65
Q

What are the advantages of a peak flow meter?

A
  • cheap
  • patients can monitor their own resp health
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66
Q

What can affect a peak flow reading?

What is the consequence of this?

A

reduced lung capacity - reduced expiratory flow rate
and airway obstruction - //

peak flow meter cannot distinguish between obstructive and restrictive diseases

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67
Q

Why do peak flow readings vary considerably across a healthy population?

A

lung capacity varies widely across the population
- is a function of thoracic volume therefore
- varies with height, gender, ethnicity

ie taller people have larger lung capacity than shorter people

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68
Q

Why is it recommended to stand when taking a peak flow reading?

A

the best readings are obtained when standing as this does not impair the ability of the diaphragm and abdominal muscles to affect the thoracic volume

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69
Q

How should a peak flow meter be used to obtain a peak flow reading?

A
  1. ensure marker set at zero
  2. exhale as fully as possible then deep breath in
  3. put meter in mouth and seal mouthpiece with lips
  4. exhale as hard and fast as possible

ensure fingers do not impede movement of marker down scale

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70
Q

Ideally, how many peak flow readings should be taken?

Which one is used/is an average reading taken?

A

3

best one is used ie. the highest volume

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71
Q

What are the advantages to a spirometer?

A

measures flow and capacity therefore can diagnose both obstructive and restrictive disease

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72
Q

What is the best way to measure lung function?

A

spirometry

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73
Q

What is FEV1? What is it affected by?

A

Forced Exhaled Volume in 1 second

airway diameter, lung capacity

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74
Q

What is FVC?

A

Forced Vital Capacity - total amount of air that can be exhaled (usable lung capacity)

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75
Q

How can lung capacity be calculated?

A

FVC + Residual Volume

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76
Q

What extra info is needed in order to work out what a normal range for FEV1 and FVC would be for an individual?

A

age, gender, height, ethnicity and smoking status

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77
Q

What is the main parameter used to determine whether there is evidence of obstructive disease?

what does this mean?

What ratio is indicative of an obstructive disease?

A

ratio of FEV1 : FVC

meaning the percentage of lung capacity that can be forcibly exhaled in 1 second

< 0.7

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78
Q

Why is it common to obtain an underestimated FVC?

A

patients will stop exhaling before they have completely emptied their lungs - encourage to keep going

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79
Q

What is the consequence of an underestimated FVC?

A

an overestimate of FEV1 to FVC ratio, might overlook potential of obstructive disease

80
Q

How would you expect values for FVC, FEV1 and FEV1 : FVC ratio to look for restrictive diseases e.g. scoliosis ?

A

FVC reduced < 80%
FEV1 reduced
FEV1 : FVC normal

81
Q

How would you expect FVC, FEV1 and FEV1 : FVC ratio to look for obstructive diseases?

A

FVC normal or reduced
FEV1 reduced < 80%
FEV1 : FVC reduced <70%

82
Q

For an inhaler to be effective in treating obstructive disease, where does the drug need to reach?

A

the small airways - those without cartilage to help keep them open - deep in the lungs

83
Q

What is arguably the most significant issue in regards to efficient aerosol delivery into the lungs?

A

inhaled aerosol must travel 90 degrees from the mouth into the airway

but aerosols have momentum - the higher the momentum, the more likely they are to travel straight and impact the throat instead of the lungs

84
Q

What influences aerosol momentum?

What sorts of particles are more likely to impact the throat?

Therefore what must be controlled for efficient drug delivery?

A

mass and speed

  • high speed particles
  • larger mass

particle speed
mass limitation

85
Q

Apart from impacting the throat, what is another consequence of too large a size of aerosol particulates as inhaler meds?

A

more likely to get stuck in an airway en route to the smaller airways in which the drug should be acting

86
Q

What is the possible consequence of having too small an aerosol particle size as an inhaler medication?

A

the particles may not deposit on the surface of the site of action, will be exhaled out of lung

87
Q

Why is breath holding after using an inhaler important?

A

to allow deposition of drug particles on airway walls

88
Q

What is the ideal size of aerosol particles for optimal tracheobronchial deposition?

A

between 2 and 5 microns

89
Q

What is the ideal size of aerosol particles for optimal alveolar deposition?

A

between 0.5 and 2 microns

90
Q

What does MDI mean?

How is an aerosol generated?

A

metered dose inhaler

via a pressurised cannister containing drug powder that sits on a valve;
depression of cannister generates a ‘spray’ of aerosolised drug particles through valve and into mouth

91
Q

What must be kept the same over the lifespan of an MDI? Why? How can this be achieved?

A
  1. dose on each actuation - particle aggregation prevention
  2. size of particles released to prevent early deposition - particle aggregation prevention
  3. force of ejection
92
Q

Why is it hard to maintain the force of ejection of the aerosol in a MDI over its lifespan?

A

the amount of compressed gas will reduce with each actuation

93
Q

What is the general technique for a MDI?

A

big exhalation
canister activation at beginning of breath
slow and deep breath

94
Q

Why is it important to take a slow and deep breath when using a MDI?

A

breathing too quickly will increase momentum of particles, result in larger proportion impacting on back of throat

95
Q

why is it important to complete a large exhalation before using a MDI, as well as activating the canister at the beginning of your breath?

A

to ensure that the particles are carried with airflow and reach deep into the lung

96
Q

What is a common problem with MDI technique among patients?

Why is this a problem?

A

spray hitting tongue or roof of mouth

  • reduce proportion of dose delivered to lung
  • reduced therapeutic efficacy
97
Q

What percent of the NHS carbon footprint can be accounted for by inhaler emissions?

What is the main reason for this?

A

3%

propellant use with MDIs

98
Q

How many doses of a Flutiform or Symbicort inhaler is equivalent to a 115 mile car journey in terms of carbon emissions? (ie. emits 35kg CO2)

A

120 doses

99
Q

What are propellants used for in MDIs?

What are they?

A

to generate the aerosol

greenhouse gases, large contributors to CO2 emissions

100
Q

What is meant by DPI?

A

dry powder inhaler

101
Q

Why are DPIs more environmentally friendly than MDIs?

A

they do not contain propellants therefore have much smaller carbon footprints

102
Q

How is the aerosol generated in a DPI?

How does a DPI work?

A

via force (and speed) of inspiration moving across delivery device, pulling drug out

  • holes punched in capsule to activate DPI
  • drug molecules attached to carrier molecules
    force of inspiratory flow moving over capsule must be sufficient to disaggregate the drug and pull into the aerosol
103
Q

What is the recommended technique for a DPI?

A

fast, strong inhale of breath

104
Q

What are the possible effects of insufficient inspiratory flow on a DPI?

A
  1. insufficient particles liberated into aerosol
  2. particles being too big
105
Q

What influences the size of the particles generated by a DPI?

How does this work?

What would be the consequence of insufficient inspiratory flow?

A

inspiratory effort and airflow

  1. vacuum generated in capsule with holes punched due to inspiratory flow
  2. generates turbulence causing drug molecules to dissociate from carrier

turbulence insufficient to disaggregate drug molecules so larger in size - more likely to impact on throat

106
Q

What sorts of molecules usually act as carrier molecules in DPIs?

A

lactose-based

107
Q

How efficient is an MDI with good inhaler technique? What does this mean?

Why is it not 100% efficient?

A

20% efficient - meaning 20% of delivered dose would be expected to reach small airways with good technique

80% lost by being impacted on throat

108
Q

What is the fate of drug deposited on the back of the throat?

A

is swallowed and absorbed from the gut

109
Q

How will good design of an MDI limit systemic penetration of the drug into circulation from the throat?

A

by limiting absorption or

ensuring a high degree of first-pass metabolism in the liver

110
Q

How does the drug deposited in the lungs reach systemic circulation?

A
  1. mucociliary clearance
  2. metabolism or absorption
111
Q

How efficient is an MDI with poor inhaler technique?

What does this mean? What are the consequences for the patient?

A

5% efficient ie 4x less dose reaches the airways with poor technique

  • dosing below therapeutic threshold and so therapeutic failure
  • more drug in GI, increased absorption into systemic circulation, increased likelihood of adverse effects
112
Q

What are the consequences of poor inhaler technique in regards to
i) relievers
ii) preventers

A

i) minimal effect felt so take another dose; poor technique can be offset by dose titration

ii) sub-therapeutic dosing because effect cannot be felt immediately anyway - no anti-inflam action

113
Q

Why are MDIs classed as monodispersed?

A

particles can be classed as being all of the same size as generated by the device itself

114
Q

What is an In-Check DIAL used for?

A

measures inspiratory flow

allows HC profs to train patients to use more/less force for optimal flow rate for MDI/DPI for better lung deposition by drugs

115
Q

How can an In-Check DIAL be reset before use?

A
  1. DIAL at top twists to change size of opening to stimulate resistance of different inhalers
  2. tap bottom of device to return red cursor to the bottom (start position)
  3. return magnetic weight to start position by turning device 180 degrees
116
Q

How should a patient use an In-Check DIAL after resetting?

A
  1. exhale away from mouthpiece
  2. form airtight seal around mouthpiece and inhale according to device selected
  3. position of red cursor should be written down
  4. process repeated twice more; highest reading taken
117
Q

What should be done with the results from the In-Check DIAL?

What can this ensure for both patients and HC profs?

A
  • values compared with target flows for specific device; should be in green area

ensures training for correct inspiratory flow,
able to ascertain if patient can generate enough inspiratory flow for certain DPIs

118
Q

What is an example of a DPI with a low resistance?

What should be recommended if a patient cannot generate sufficient inspiratory flow?

A

breezhaler

MDI

119
Q

What is a self-actuated MDI?

A

inhaler senses an inspiration and triggers the device to release a pressurised dose automatically

120
Q

What is a high efficiency MDI?

Why have they been designed?

What kind of drugs do they deliver?

A

designed to increase dose delivered to lung from 20% (classical MDI with good inhaler technique) to 40% by decreasing the whole dose released with each actuation

to reduce the potential for side effects due to systemic absorption

muscarinic receptor antagonists

121
Q

What is the easiest way to tell an MDI from a DPI?

A

MDI activation always results in a spray, DPI does not

122
Q

What is the most common error causing poor inhaler technique for both MDIs and DPIs?

A

incorrect speed of inhalation ie
MDIs - often too fast
DPIs - ofetn too slow

123
Q

What must the patient be counselled on regarding inhaler technique?

A
  1. appropriate speed of inhalation
  2. appropriate force of inhalation (might be high for DPIs with high resistance to flow)
  3. What the inhaler is for ie. preventer, reliever, both
  4. How it works
124
Q

What type of DPI has a relatively low resistance to flow and so is easier to use for many patients with obstructive diseases relative to other DPIs?

A

Accuhaler

125
Q

What were 3 key findings from the National Review of Asthma Deaths by the Royal College of Physicians in 2014?

A
  1. Personal asthma action plans (PAAPs), acknowledged to improve asthma care, were
    provided to only 23% of people who died from asthma
  2. There was evidence of excessive prescribing of reliever medication - 39% had been prescribed more than 12 short-acting reliever inhalers in the year before they
    died and they were likely to have had poorly controlled asthma
  3. There was evidence of under-prescribing of preventer medication. To comply with recommendations,
    most patients would usually need at least 12 preventer prescriptions per year. 80% issued with fewer than 12 preventer inhalers in the previous year
126
Q

What is the whole process of correct use of an MDI?

A
  1. remove cap and shake
  2. breathe out, put open end in mouth
  3. start breathing in normally
  4. depress trigger
  5. continue breathing in as much as possible
  6. hold breath for 10 secs
  7. breathe out
  8. wait 30 secs before repeating as needed, replace cap
127
Q

Why is good inhaler technique more important for preventer inhalers?

A

patient won’t titrate up dose like reliever because no immediate relief for them to sense

128
Q

What is a simple method of ensuring better inhaler technique, especially for preventers?

A

use of a spacer

129
Q

What are the advantages to using a spacer?

A
  1. it retains the drug aerosol therefore removing need to synchronise canister actuation with beginning of inhalation
  2. removes chances of spraying aerosol onto tongue or roof of mouth
  3. new spacers have a whistle that sounds if inspiration is too quick - EXPLAIN otherwise patients think they need to hear it to be inhaling correctly
130
Q

What are the two inspiratory techniques that can be used with a spacer?

A
  1. one slow, deep breath after actuation or
  2. five normal (tidal) breaths
131
Q

What is the whole process for the correct use of a DPI?

A
  1. remove cap and open trigger guard until click
  2. remove lever until click (makes dose available and moves dose counter on)
  3. breathe out
  4. hold device horizontal and put in mouth
  5. breathe in quick and hard
  6. hold breath for 10 secs
  7. breath out, wait 30 secs before repeating
132
Q

What is important to consider when counselling patients on their corticosteroids?

A
  • ensure patient understands what they are used for
  • advise on side effects and how to use safely

counsel in a way that gets message across but does not scare them

133
Q

What kinds of uses do corticosteroids have?

What are some examples of targets for corticosteroids?

A
  1. anti-inflammatory/immunosuppressive therapies e.g. asthma, IBD, rheumatoid arthritis
  2. adjunct treatment in cancer e.g. combined by cytotoxic drugs in leukaemia treatment
  3. replacement therapy e.g. Addison’s disease

topically - skin, lungs
systemically - nerves, blood, liver

134
Q

What are some common corticosteroids to be aware of?

A

hydrocortisone, beclametasone, fluticasone, prednisolone, deflazacort

135
Q

How can we recognise them as corticosteroids from the name?

A

many end with similar suffixes
- ‘sone’ e.g. fluticasone
- ‘olone’ e.g. prednisolone

look for root words that indicate steroid structure e.g.
- ‘cort’ as in cortisone e.g. hydrocortisone
- ‘flu’ e.g. fluticasone, fludrocortisone

NB there are many others these are just more common

136
Q

What is hypersecretion of glucocorticoids AKA adrenal hyperfunction?

In what type of patients is this more common?

A

body producing too many glucocorticoids

more common in women

137
Q

What is involved in adrenal hyperfunction?

What is the function of ACTH?

A

overproduction of ACTH from pituitary

drives production of cortisol (most common glucocorticoid) from the adrenal glands

138
Q

Diseases involving ACTH can be caused by what two mechanisms?

A
  1. overproduction by pituitary - accounts for 80% ACTH diseases
  2. ectopic ACTH-secreting tumour
  3. ACTH-independent adrenal cortical tumour
  4. ectopic CRH-secreting tumour (RARE)
139
Q

What is an ectopic ACTH-secreting tumour?

A

a neuroendocrine tumour, can develop in various parts of the body including the lungs

they secrete hormones that they shouldn’t and body cannot control it

140
Q

What is an ACTH-independent adrenal cortical tumour?

A

a tumour in the adrenal cortex where cortisol is made

141
Q

What is an ectopic CRH-secreting tumour?

What is the role of CRH?

A

tumour outside of hypothalamus that secrete corticotrophin releasing hormone

CRH is released from hypothalamus and drives production of ACTH in pituitary

142
Q

What are the possible consequences of adrenal hyperfunction?

A

Cushing’s disease (hypercortisolism) - excess pititary ACTH secretion

(iatrogenic) Cushing’s syndrome - due to anything that isn’t pituitary ACTH secretion ie. ectopic tumours or
prolonged glucocorticoid therapy which causes iatrogenic cushings syndrome

143
Q

Why are the clinical symptoms of Cushing’s so distinct?

A

ACTH involvement (or uninvolvement) has large influence

144
Q

What are the clinical symptoms of Cushing’s?

A
  1. high plasma and urine cortisol
  2. loss of diurnal variation in cortisol levels
  3. high plasma ACTH if pituitary problem or ACTH-secreting tumour or
  4. low or undetectable plasma ACTH if due to adrenal tumour or taking exogenous steroids
145
Q

Why is it unusual to have high levels of both cortisol and ACTH in blood?

A

normally when cortisol levels rise, ACTH no longer produced as it is the driver for cortisol production

146
Q

What are the diagnostic tests for hypersecretion?

What would you expect from the tests in people with Cushing’s disease/syndrome?

A
  1. measure cortisol in blood, urine, saliva - look for high levels especially at night when would normally be low
  2. ‘overnight dexamethasone suppression test’ - normally inhibits cortisol production for 24hrs
  3. Metyrapone (a competitive inhibitor of 11beta hydroxylase) should inhibit cortisol production normally

high levels of cortisol from all of these tests indicate possible cushing’s

147
Q

What are the side effects of taking high dose corticosteroids and/or Cushing’s disease/syndrome?

A
  • euphoria or depression
  • moonface
  • buffalo hump
  • hypertension
  • easy bruising
  • poor wound healing
  • thinning skin
  • fat redistribution from limbs to trunk

as well as obesity, osteoporosis, increased appetite, increased susceptibility to infection and negative nitrogen balance

148
Q

What are the non-pharmacological methods of treating Cushing’s?

A
  1. removal of pituitary, ectopic or adrenal tumour or adrenal cortex
    - plus corticosteroid replacement therapy for life when cortex removed
  2. gradual discontinuation of glucocorticoids
    - when glucocorticoid treatment is causing Cushing’s
149
Q

What drugs can be used to treat Cushing’s?
Under what circumstances?

Why are these drugs mostly seen in hospital pharmacy?

A
  1. Metyrapone
    - for patients with ling tumours that cannot be removed
    - for controlling symptoms prior to surgery
  2. Osilodrostat - 11beta hydroxylase (crucial for cortisol production) inhibitor
    - only for endogenous Cushing’s disease
    - caution with patients of Asian origin due to differences in bioavailability
  3. ketoconazole (antifungal - oral use for Cushing’s)
    - endogenous cushings disease only
    - increased risk of liver toxicity
  4. Pasireotide - somatostatin analogue
    - for use when surgery failed or inappropriate
    - lots of side effects

These drugs have many side effects; sometimes the risks will outweigh the benefits, also lots of monitoring is required

150
Q

What are the possible side effects of Metyrapone?

A
  • nausea and vomiting
  • dizziness
  • headaches
  • hypotension
  • sedation
151
Q

What are glucocorticoids?

A

They are a type of corticosteroid

  • Regulate glucose metabolism
  • Have potent anti-inflammatory and immunosuppressive effects
  • Mimic the action of cortisol, a natural hormone
152
Q

What does ‘endogenous’ mean in terms of disease?

A

refers to conditions or factors that originate from within the body or organism itself, rather than from external sources

153
Q

What are the possible serious side effects of corticosteroids?

A
  1. central serous chorioretinopathy
  2. elevation of plasma glucose
  3. osteoporosis
  4. growth suppression in children
  5. immunosuppression
  6. psychiatric reactions
  7. adrenal suppression
154
Q

What is central serous chrioretinopathy?

What should patients report and/or look out for when taking corticosteroids?

How common is this risk? For what sorts of administration routes does this apply?

What could be the appropriate course of action for patients with visual disturbances?

Is this a reversible side effect?

A

fluid accumulation and leakage from underneath the retina which can lead to the eventual detachment of the retina and consequent visual disturbances

patients should report
- blurred vision
- other visual disturbances

RARE risk but recently linked to local administration routes e.g. inhaled, topical dermal etc as well as systemic use corticosteroids ie. all administration routes

Patient may need opthalmology referral

Visual problems will remain even if corticosteroid use stopped

155
Q

How can corticosteroid use lead to increased plasma glucose levels?

What sorts of patients are most at risk?

For patients who are already diabetic how can the risk of further elevation of plasma glucose levels be managed?

Is this a reversible side effect?

A

Cortisol drives production of blood glucose and causes some insulin antagonism

Patients at risk should be observed:
- those with pre-diabetic blood levels
- those with reduced pancreatic function as can trigger type 2 diabetes

type 1 diabetics - monitor patients carefully
type 2 diabetics - consider dose adjustments

Reversible - glucose levels should return to normal upon stopping corticosteroid treatment

156
Q

When is the risk of osteoporosis from exogenous use of corticosteroids highest?

Why is calculating osteoporosis risk from corticosteroid use so complicated?

Is this a reversible side effect?

A

osteoporosis risk highest during first 6-12 months of corticosteroid use

osteoporosis risk dependent on dose, duration of corticosteroids and other risk factors

Osteoporosis will remain even if corticosteroid use stopped

157
Q

What is considered a high dose of glucocorticoid?

A

7.5mg + / day of prednisolone or equivalent

158
Q

What sorts of patients are most at risk of corticosteroid-related osteoporosis?
What would be the appropriate course of action for these patients?

For what sorts of patients would fracture probability be used instead of bone protective therapy?

What are the possible pharmacological management strategies for osteoporosis?

A

patients most at risk:
- post-menopausal women
- anyone over 70
- those on high dose glucocorticoids
- those with previous fragility fracture
these patients should be considered for bone protective therapy; this can apply even if for short-term use e.g. 2 months if on high dose or with previous fracture etc

fracture probability can be used for
- pre-menopausal women
- younger men

possible osteoporosis management
- bisphosphonates
- Calcium & Vit D
- HRT for women
- testosterone for men

159
Q

When is there a risk for growth retardation in children during corticosteroid use?

How can the presence of growth suppression be identified?

What are the possible consequences of growth suppression?

Why does it happen?

A

children most at risk of growth retardation:
- during systemic use
- with severe asthma - on very high doses
- over 6 weeks of corticosteroid use

Growth progression should be monitored against growth charts

possible consequences
- delayed puberty
- stunted height

steroids effect growth plates in bones

160
Q

What are the risks associated with immunosuppression?

What must be avoided with people taking sufficient steroids to cause immunosuppression?

How should infections be managed in immunosuppressed patients?

A

risks from immunosuppression
- opportunistic infections
- reduced response to infections

immunosuppressed patients must avoid
- live vaccines (will develop disease)
- chickenpox, shingles
- measles

infections should be treated aggressively

161
Q

What psychiatric reactions are possible with high dose systemic use of corticosteroids?

What patients are most at risk of such side effects?

What is the appropriate course of action if psychiatric reactions occur?

How should the patient be counselled about psychiatric reactions?

A

psychiatric reactions include euphoria, insomnia, mood swings, suicidal thoughts, paranoia, behavioural changes, depression

patients most at risk are those
- who already have neuropsychiatric disease
- who are at risk of developing psychiatric disease

if psychiatric reactions occur:
- reduce dose or
- discontinue steroid
generally cannot have the steroid again due to likelihood of similar rxns

counselling points:
- seek medical advice if depressed or having suicidal thoughts
- consider asking about family history or previous medical history to rule out predisposition

162
Q

Why can adrenal suppression occur from corticosteroid use?

How is glucocorticoid production in the body affected by 2 weeks of exogeneous steroid use?

How is glucocorticoid production in the bidy affected by 3 weeks (or more) of exogenous steroid use?

What are the risks associated with suddenly stopping steroid use having been taking them for three or more weeks?

A

use of exogenous steroids can switch off production of CRH and ACTH, decreasing production of glucocorticoids ie. cortisol

for 2 weeks use:
- downregulated ACTH and CRH
- will recover quickly after stopping steroid use

for 3 weeks use:
- adrenal cortex shrinks
- endogenous production of steroid stops completely, patient dependent on drug

patient taking steroids for 3 or more weeks who then suddenly stops is at risk of ADRENAL CRISIS - can be fatal

163
Q

What are the symptoms associated with adrenal crisis?

Why is it underdiagnosed?

How can it be treated?

A

adrenal crisis - acute illness, rare, can kill quickly

  • dehydration
  • loss of appetite
  • confusion, weakness
  • pyrexia

can lead to circulatory collapse, stroke, arrythmias and cardiac arrest - death or permanent disability

underdiagnosed because symptoms similar to other less serious illnesses

can be treated via immediate IV steroids e.g. hydrocortisone

164
Q

How can side effects associated with corticosteroid use be minimised?

A
  1. lowest effective dose for shortest time possible!
  2. alternate day regimens (not possible for asthma)
  3. morning dosing to match natural diurnal rhythms
  4. intermittent therapy with short courses where possible e.g. reduced risk of adrenal suppression
  5. use ‘steroid sparing’ agents e.g. azathioprine
  6. use local routes of administration before systemic where possible
165
Q

Why do steroid doses often need increasing when a patient is ill?

A

cortisol is stress hormone, often increased secretion in body when ill

those with adrenal suppression ie. on long-term steroids cannot increase their cortisol production themselves so need dose increase

166
Q

How can illness in steroid-taking patients be managed?

In what other patients does steroid dosing need to be considered when they are undergoing surgery?

A

infection:
- increased dose; recommended to double dose in times of ‘stress’

surgery:
- extra dose of hydrocortisone as pre-med
- extra doses of hydrocortisone in following 2-3 days
(replicating what the body would do normally)

vomiting:
- may need IV hydrocortisone

MUST also be considered in patients who have stopped taking steroids in the last 3 months if undergoing surgery

167
Q

What sorts of patients should be considered for gradual steroid withdrawal?

Why must these patients be withdrawn gradually?

A

Those whose disease is unlikely to relapse and have:
- 40mg+ prednisolone daily or equivalent or for more than 7 days
- had repeated evening doses
- > 3 weeks treatment
- recently received repeated courses
- history of previous long-term therapy
- other possible causes of adrenal suppression e.g. stress or alcohol

gradual withdrawal from steroids prevents:
- flare-up of disease steroids were treating
- withdrawal symptoms; allows body to start making own cortisol again

168
Q

What is the appropriate course of action should stress (e.g. infection, surgery, trauma) occur up to 1 week after gradually stopping a corticosteroid?

A

additional corticosteroid is needed to compensate for any potential adrenal suppression

169
Q

For patients taking oral corticosteroids for 2 weeks to a month, how should the dose be reduced?

A

by 50% per day

170
Q

For patients taking oral corticosteroids for over a month or high doses for shorter periods, how should the dose be reduced?

A

2.5-5mg reduction every 3-4 days

171
Q

What areas should be covered when counselling patients on their steroid use?

A
  1. side effects
  2. steroid treatment card where applicable
  3. compliance!!!
  4. accidental missed doses
  5. starting/stopping course
  6. infection and other illnesses
172
Q

What sorts of patients should be carrying a steroid treatment card?

A
  1. those on long-term courses (more than 3 wks)
  2. those on repeated short courses
  3. those taking inhaled high dose steroids
  4. those taking high dose steroids
173
Q

What is a steroid emergency card for?

What sorts of patients have this card?

A

supports early recognition and treatment of adrenal crisis in adults - for healthcare professionals

patients needing this card:
- those with adrenal insufficiency
- those with steroid dependence at risk of adrenal crisis

174
Q

Where can we access guidelines for adrenal insufficiency in children?

A

British Society for Paediatric Endocrinology and Diabetes (BSPED) guidelines

175
Q

How can we further study steroid use during the degree?

A
  • read PILs - see U2 L10
  • review conditions as we learn; why steroid as treatment? how do benefits outweigh risks?
176
Q

Why is inhalation the preferred formulation of administering corticosteroids for long term control of pulmonary inflammation?

A

corticosteroids extremely effective

when administered via airway, most of the adverse effects associated with the systemic administration are eliminated

177
Q

When does the BTS ladder recommend the use of ICS in therapy?

A

At step 2 of the therapeutic ladder

  • The threshold to progress from step 1 to step 2 is relatively low
  • incl exacerbation of asthma within last 2 years, experiencing symptoms more than 3 times a week or waking one night of the week due to asthma.
178
Q

Why are corticosteroids (ICS) the most effective preventer drugs for the prophylaxis of asthmatic patients?

A
  • extremely good anti-inflammatory agents due to their broad spectrum of activity
  • proven to reduce mortality in asthma patients
  • reduce progression of disease by reducing inflam driven airway remodelling
  • improve patient quality of life
179
Q

What is the general cause of patients who experience nocturnal asthma?

A
  • due to delayed phase of bronchoconstriction which is more severe and longer lasting than early phase
  • or due to bedbugs?? (but not proven)
180
Q

Which 2 factors is airway remodelling dependant on?

A
  • Inflammation and time

i.e changes in tissue structure take longer than timescale of bronchoconstriction as processes e.g gene expression + mitosis are involved

181
Q

List two time restraints that describe individual inflammatory responses.

A
  • episodic
  • self terminating
182
Q

Due to the fact that individual inflammatory is episodic and self terminating, how does that effect the frequency of airway remodelling in an asthmatic patient?

A
  • there is a level which you have a frequency of asthma attacks which wouldn’t result in airway remodelling = lower frequency
183
Q

In which situations does tissue remodelling linking to asthma occur?

A
  • in situations where inflammation is resident in the lung over long term.
  • this can happen if asthma attacks inc in frequency = limited resolution between attacks
184
Q

If an individual were to have more than three attacks a week (leading to a larger frequency of airway remodelling), what would be the treatment suggested?

A

corticosteroid treatment

185
Q

Why is corticosteroid treatment the suggested treatment for when someone is having three asthma attacks a week?

A
  • when there are more than three attacks in a week = not enough time for inflammation to resolve before the next inflammatory episode = tissue remodelling (TRP)
  • corticosteroids break cycle = allows lung to recover from inflam + cause it to fall below threshold required to drive TRP
186
Q

What is the effect of unchecked airway modelling on asthmatic patients?

A
  • inc frequency and severity of asthma in patients
187
Q

What is the effect of airway remodelling causing damage to epithelial cell layer within the lung?

A
  • loss of barrier = increase access to allergens/irritants to underlying sensory nerves = more likely triggered to cause bronchoconstriction.
188
Q

What are the main effects of corticosteroid treatment to the mechanisms of asthma?

A
  • every aspect of remodelling process
  • decrease n.o of inflam cells in lung = dec magnitude of inflam responses = limits release of mediators
  • accelerate termination of inflam response by inc levels of IL-10
189
Q

How do corticosteroids reduce oedema and mucous production caused by asthma?

A
  • reduce production of inflammatory mediators from epithelial cells
  • reduce the leakiness of pulmonary vasculature, limiting oedema, reduce mucus production, and limit goblet cell hyperplasia.
190
Q

How do corticosteroids increase the efficacy of other drugs such as salbutamol to treat asthma?

A

increase the number of beta-2 receptors on smooth muscle. This has the effect of making the airway smooth muscle more sensitive to beta-2 agonists

191
Q

What aspects of COPD has corticosteroids been clinically proven to treat?

A
  • reduces the frequency of acute exacerbation in moderate to severe COPD
192
Q

What is the clinical effect of corticosteroids on FEV1 value in patients?

A
  • study shown than when tested with a placebo, there was little difference between effect
  • it has been proven in studies to inc FEV1 20ml per year compared to placebo in asthma patients
  • therefore much less effective of decline on FEV1 value in COPD
193
Q

What is the percentage range of asthma patients that do not respond well to inhaled corticosteroid treatment?

A

1-10%

194
Q

What is the reason for some asthma patients not responding well to inhaled corticosteroid treatments?

A

may be due to:
- non-adherance
- poor inhaler technique
- asthma resistance to corticosteroids
- ability of neutrophil to cause activation + degranulation of eosinophil in corticoertoid insensitive manner = eosinophil function escape inhibitory effect of CS = inflam continues

195
Q

Why neutrophils are much less sensitive to inhaled corticosteroids compared to eosinophils?

A
  • pulmonary neutrophils express a much larger proportion of the GRβ splice variant
  • variant can bind to corticosteroids but does not subsequently affect DNA transcription
  • therefore, it can compete with GRα for corticosteroid binding and reduce the overall corticosteroid response.
196
Q

What is the difference in effects of activation between neutrophils and eosinophils?

A
  • neutrophils release a different spectrum of mediators compared to eosinophils.
  • ability of neutrophil elastase to activate eosinophils
  • if neutrophils less sensitive to corticosteroid = release of elastase cause activation + degranulation to eosinophils that in other methods of release would be effected by corticosteroid.
197
Q

Why is it important to shake a MDI?

A

To ensure drug is evenly distributed in canister - ensures even dosing

PH2113 Disease & Drugs 1 (5 decks)

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