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Block 5 Respiratory > Dental Management of Patients with Asthma & COPD > Flashcards

Dental Management of Patients with Asthma & COPD Flashcards

1
Q

List the composition of upper respiratory tract of a child:

A
  • Large occiput
  • Short neck
  • Large tongue (relative to head size)
  • Narrow nasal passages
  • Epiglottis positioned higher
  • Decreased airway characteristics
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2
Q

List composition of lower respiratory tract of a child

A
  • Short and narrow trachea
  • Sternum less rigid
  • Horizontally positioned ribs
  • Increased alveolar surface area, small total volume of gas exchange
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3
Q

Define Asthma according to Greenwood 2003

A

Chronic inflammatory disorder characterised by generalised airway obstruction and bronchospasm.

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4
Q

Define asthma according to Zhu and Hidalgo et al. 1996

A

Initially a reversible bronchoconstriction caused by airway hypersensitivity

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5
Q

Define asthma according to WHO

A

A disease characterised by recurrent attacks of breathlessness and wheezing, which vary in severity and frequency from person to person. In an individual, they may occur from hour to hour and day to day.

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6
Q

Prevalence of asthma?

A

Very common chronic obstructive disease of childhood + adulthood.

  • 2014/15: 10.8% of all Australians with asthma (2.5 million)
  • M = F for all ages, M > F for 0-14 yo
  • 2013/14: 37,700 hospital admissions for asthma, 389 deaths
  • ABTSI: 1.9x more likely to have asthma than non-ABTSI
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7
Q

Rank of asthma as non-fatal hospital burden in ages 5-14

A

No. 1

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8
Q

Rank of asthma as non-fatal hospital burden in ages 15-49

A

8th

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9
Q

rank of asthma as non-fatal hospital burden in ages 50-69

A

11th

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10
Q

Rank of asthma as non-fatal hospital burden in ages 70+

A

14th

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11
Q

Rank of asthma as non-fatal hospital burden in all ages

A

7th

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12
Q

Mild asthma?

A

Wheezing < 2 days/week, exercise tolerance

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13
Q

Moderate asthma

A

Wheezing 2-5 days/week, nocturnal symptoms, limited exercise tolerance

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14
Q

Severe asthma

A

Daily wheezing, exercise intolerance, frequent nocturnal symptoms

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15
Q

Global initiative for asthma (2016)

A
  • Severity + responsiveness to meds

- Controlled, partially controlled, uncontrolled

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16
Q

Triggers for asthma?

A

Exercise, seasonal, drug-induced

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17
Q

Mild-moderate episode of asthma

A
  • Cough (continuing), wheeze, chest tightness, shortness of breath
  • Tachycardia, tachypnoea, use of accessory muscles (typically lasts for minutes
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18
Q

Severe episode of asthma

A
  • Respiratory distress with tachypnea, nasal flaring

- Intercostal mm. retractions, cyanosis, pulsus paradoxus (typically lasts for hours to days)

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19
Q

Aetiology of asthma

A
  • Genetic predisposition

- Gene-by-environment interactions

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20
Q

Risk/triggering factors for asthma

A
  • Maternal smoking
  • Low socioeconomic status
  • Extended breastfeeding
  • Early viral respiratory infections
  • Exposure to allergens
  • Pollution
  • Antibodies, NSAIDs
  • Exercise
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21
Q

How to diagnose asthma

A
  • Clinical examination + various non-specific respiratory function tests
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22
Q

Defining features of asthma in >5 year old

A
  • Positive history of respiratory symptoms (wheeze, shortness of breath, chest tightness, cough)
  • Expiratory airflow limitation
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23
Q

It is difficult to diagnose asthma in <5 year olds as early S+S mimic several respiratory conditions.

A

True

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24
Q

Asthma is often diagnosed after successful treatment of an acute attack with?

A

Beta-2 agonists

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25
Q

Pathophysiology of acute airway inflammation

A

Release of chemical mediators from activated resident cells (mast cells) undergoing histamine degradation

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26
Q

Pathophysiology of subacute airway inflammation

A

Early cellular infiltrate (mainly eosinophils), releasing mediators with toxic effects on the respiratory epithelium

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27
Q

Pathophysiology of chronic inflammation

A
  • Irreversible airway obstruction due to eosinophils + lymphocytes (mainly CD4+ T lymphocytes) mediating a persistent, ongoing inflammation that results in a vicious cycle of extensive tissue damage and repair.
  • Subepithelial thickening, mucous gland hypertrophy, bronchial muscle wall hypertrophy
  • Decreased airway diameter -> airway resistance -> difficulty with expiration
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28
Q

Medical management and pharmacological management of asthma

A
  • Avoidance of precipitating factors
    Pharmacological management:
  • Bronchodilators (short + long acting beta2 agonists, anticholinergic agents, theophylline)
  • Anti-inflammatory agents (inhaled + systemic corticosteroids, nedocromil sodium)
  • Mast cell stabilisers (cromolyn sodium, nedocromil sodium)
  • Leukotriene antagonists (antileukotriene, e.g. Montelukast)
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29
Q

Preventative medication for asthma

A
  • Bronchodilators (long-acting, e.g. salmeterol)
  • Inhaled low-dose corticosteroids
  • cromolyn sodium / nedocromil sodium (usually an alternative to steroids)
  • Systemic corticosteroids (last resort for unresponsive cases)
  • Most children have an asthma plan prepared by their doctor
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30
Q

Acute management for asthma

A
  • Short-acting bronchodilators (e.g. salbutamol)

- Remove aggravating factors

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31
Q

Definition of COPD according to Qaseem et al. 2011

A

Broad category of irreversible respiratory diseases characterised by reduced expiratory flow

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32
Q

Definition of COPD according to Hupp 2006

A

COPD includes conditions such as emphysema and chronic bronchitis, both with different clinical presentations but that can coexist together causing irreversible structural changes to the airways.

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33
Q

Devlin’s definition of emphysema

A

Emphysema is characterised by permanent enlargement of airspaces distal to the terminal bronchioles. The elastic recoil of the alveoli is compromised affecting the tendency of the lungs to force air out. Gas exchange becomes insufficient due to the inability of lungs to expire air passively.

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34
Q

Devlin’s definition of bronchitis

A

Bronchitis is inflammation and thickening of the lining of the bronchial tubes affecting the airflow to the alveoli. This condition is characterised by excessive mucus secretion and productive cough at least for three consecutive months a year in 2 consecutive years.

35
Q

Most recent definition of COPD according to GOLD 2013

A

A clinical diagnosis of COPD should be considered in any patient who has dyspnoea, chronic cough or sputum production, and a history of exposure to risk factors for the disease. Spirometry is required to make the diagnosis in this clinical context; the presence of a post bronchodilator FEV1/FVC <0.70 confirms the presence of persistent airflow limitation and thus of COPD.

36
Q

Environmental factors for overlapping asthma-COPD

A
  • Smoking
  • Biomass exposure
  • Pollution
  • Infections
  • Microbiome
  • Diet
37
Q

Susceptibility factors for asthma-COPD

A
  • Genetics
38
Q

Specific molecular mechanisms for asthma-COPD

A
  • Aging
  • Diet
  • Obesity
  • Exposures
  • Infections
  • Treatment
  • Psychosocial factors
39
Q

Pathology of pure chronic bronchitis

A
  • Large airways (Trachea, bronchi): mucus hypersecretion, inflammation, chronic bronchitis
  • Small airways (bronchioles): peribronchiolar fibrosis, airway obstruction, chronic bronchiolitis
40
Q

Pathology of pure emphysema

A
  • Acinus (respiratory bronchiole, alveolar ducts, and alveoli): loss of elastic recoil, emphysema
41
Q

Describe type A emphysema

A
  • Predominant emphysema
  • Tended to be lean with no fluid retention
  • Maintained gas exchange through increased ventilatory effort
  • Often exhibiting mild hypoxemia only
42
Q

Describe Type B emphysema

A
  • Predominant bronchitis with cough and sputum production
  • Allowed their gas exchange to deteriorate
  • Poorer prognosis with the onset of fluid retention and cor pulmonale.
  • Worse hypoxaemia and hypercapnia as the disease progressed.
43
Q

Onset of chronic bronchitis

A

50 years

44
Q

Onset of emphysema

A

60 years

45
Q

Cough of chronic bronchitis

A

Chronic obstructive cough

46
Q

Cough of emphysema

A

Seldom coughing

47
Q

Dyspnoea of chronic bronchitis

A

Mild

48
Q

Dypsnoea of emphysema

A

severe

49
Q

Respiratory infections in chronic bronchitis

A

Frequent

50
Q

Respiratory infections in emphysema

A

Mild

51
Q

Partial pressure of carbon dioxide in chronic bronchitis

A

Elevated

52
Q

Partial pressure of carbon dioxide in emphysema

A

Normal

53
Q

Partial pressure of oxygen in chronic bronchitis

A

Decreased

54
Q

Partial pressure of oxygen in emphysema

A

Decreased

55
Q

Chest radiographs of chronic bronchitis show?

A

Prominent blood vessels, large heart

56
Q

Chest radiographs of emphysema show?

A

Hyperinflation, small heart

57
Q

Signs, symptoms and pathophysiology of emphysema

A
  • Shortness of breath
  • Alveolar destruction
  • Airway narrowing
  • Air trapping and hyperinflation
  • Loss of elasticity
58
Q

Signs, symptoms and pathophysiology of chronic bronchitis

A
  • Shortness of breath
  • Chronic cough
  • Excessive mucus production
  • Frequent infections
  • Airway narrowing
  • Air trapping and hyperinflation
  • Inflammation and swelling of airways
59
Q

Signs, symptoms and pathophysiology of chronic asthma

A
  • Shortness of breath
  • Airway narrowing
  • Air trapping and hyperinflation
  • Inflammation and swelling of airways
60
Q

List other findings in patients with COPD

A
  • Peripheral muscle weakness/wasting (weight loss)
  • Cardiovascular deconditioning
  • Hypoxaemia
  • Anaemia
  • Pulmonary hypertension
  • Osteoporosis
  • Diabetes
  • GORD
  • Anxiety/depression
61
Q

COPD is the ____ leading cause of death.

A

3rd

62
Q

Pathophysiology of COPD

A

Airway inflammation in COPD is characterised by a neutrophilic inflammation with increased numbers of macrophages and CD8+ T-lymphocytes. These cells release chemokines, cytokines and proteases that are instrumental in producing a chronic inflammatory state

63
Q

Pathophysiology of emphysema

A
  • In the alveoli, neutrophils and macrophages phagocytose toxic particles (e.g. smoke). This also results in a release of proteases.
  • These proteases destroy alveoli walls that then extend to larger air spaces (lung parenchyma). This then results in the formation of bullae that reduce the efficiency of gas exchange in the lungs.
  • There is also loss of elasticity due to the destruction of elastin by the same proteases. This causes airway collapse due to air trapping and hyperinflation of the lungs (barrel chest)
  • Poor gas exchange + airway narrowing = hypoventilation
64
Q

Pathophysiology of chronic bronchitis

A
  • Mucus hypersecretion due to increased degranulation by neutrophil-mediated elastase
  • Difficulty in clearing secretions results from: poor ciliary function (usually due to smoking); distal airway occlusion; ineffective cough secondary to respiratory muscle weakness; reduced peak expiratory flow
65
Q

Non-pharmacological management of COPD

A
  • Reduction in risk factors (smoking)
  • Exercise with pulmonary rehabilitation: reduced dyspnoea and improved QoL, improved mood/ reduced anxiety and depression; reduced hospital admissions
66
Q

Pharmacological management of COPD

A
  • Influenza vaccinations
  • Steroids (not as responsive as asthma)
  • Bronchodilators (improvement in symptoms, activity levels, QoL, modest changes in FEV1)
  • Supplemental oxygen
67
Q

Surgical management of COPD

A
  • Lung transplant
68
Q

Dental implications of COPD

A

Increased caries risk (1o + 2o dentitions):

  • Medication effects
  • Increased prevalence of mouth breathing
  • Saliva: thick, reduced flow, low saliva /plaque pH due to powder inhalers
  • Lactose in some inhalers
  • 11-fold increase in risk of hypomineralisation
  • Increased m. streptococcus

Increased risk of erosion:

  • Prolonged + frequent use of acidic asthma inhalers
  • Reduced saliva flow + poor quality saliva
  • Increased incidence of GORD

Increased risk of gingivitis:

  • Combination of medication effects, mouth breathing + immunological factors
  • Increased calculus deposits due to altered saliva composition

Increased risk of oral candidiasis (pseudomembranous candidiasis):

  • Associated with long-term use of inhaled corticosteroids
  • Can be avoided by use of puffer spacer devices + oral rinsing after each use

Impact on facial growth (poor quality evidence):

  • Increased upper anterior + total anterior facial height
  • High arched palate
  • Greater overjet
  • Increased incidence of posterior crossbite
69
Q

How does smoking implicate COPD

A

Periodontal disease, nicotine stomatitis, oral cancer

70
Q

Comorbidities of COPD

A
  • Cardiovascular disease
  • Osteoporosis
  • Diabetes
  • GORD
  • Anxiety/depression
71
Q

Medical history for COPD

A
  • Diagnosis including severity of condition
  • Comorbidities
  • Frequency and severity of attacks
  • Length of time since last attack
  • Types of medication being used (number of meds + dose, including changes in meds over time)
  • Common triggers (stress, smells)
  • All previous asthma/COPD-related hospitalisations
72
Q

Dental management local anaesthesia for asthma

A
  • Possible hypersensitivity to methylparabin/sodium metabisulphate that may induce an asthma attack
  • Avoid adrenaline-containing LA + avoid block injections due to potential adrenergic effects if injected intravenously
73
Q

Inhalation sedation in dental management

A
  • N2O is an airway irritant

- In partially controlled/uncontrolled cases, liaise with respiratory physiciain prior to tx

74
Q

General anaesthesia in dental management

A
  • Delay until patient is well- controlled

- Liaise with anaesthetic team

75
Q

Adverse drug reactions in dental management

A
  • Up to 14% of asthmatics have aspirin-exacerbated respiratory disease (cross-sensitivity between aspirin + NSAIDs)
  • Opiates may lead to respiratory depression + histamine release
  • Antibodies: no contraindications unless a known trigger
  • Fluoride varnish: some contain natural resin (e.g. colophony)
76
Q

During dental treatment, any warnings?

A
  • Be aware of postural exacerbation of symptoms. Increased dyspnoea when laid supine = consider moving patient to semi-supine or upright
  • Be aware of triggering factors (such as stress)
  • Use rubber dam to reduce cough reflex (airway compromise?)
  • Use LA judiciously
  • Consider delaying treatment if symptomatic at beginning of visit
77
Q

Less than 50% of people use inhalers properly

A

True

78
Q

Only 10-20% of inhaler dose reaches the lung

A

True

79
Q

OHI in dental management

A
  • Use a spacer
  • Rinse after inhaler use
  • Meticulous oral hygiene
  • Consider a more personalised preventive regime if high risk
80
Q

Emergency management of an acute asthma attack (mild)

A
  • Normal mental state, slightly increased use of accessory muscles, able to talk normally
  • Salbutamol (Ventolin) with spacer (6 puffs if <6yo, 12 puffs if >6yo)
  • Ipratopium (atrovent - 20 mcg/puff) with spacer (4 puffs if <6 yo, 8 puffs if > 6yo)
  • Reassess after 20 minutes
  • If nil improvement, move to moderate protocol
81
Q

Emergency management of an acute asthma attack (moderate)

A
  • Normal mental state, increased use of accessory muscles, tachycardia, limitation of ability to talk normally
  • Give supplemental oxygen if oxygen saturation is <92% (requires admission into hospital)
  • Salbutamol/ipratropium as above, repeat every 20 mins for 1 hour
  • Oral prednisolone (2mg/kg), continue for 1-2 days at 1 mg/kg (only if continuing with salbutamol, otherwise cease)
82
Q

Emergency management of an acute asthma attack (severe)

A
  • Agitated/distressed, moderate use of accessory muscles, retractions, tachycardia, marked limitation of ability to talk
  • Protocol as for moderate + oral aminophylline + IV magnesium sulphate (Requires admission into hospital)
83
Q

Emergency management of an acute asthma attack (Critical)

A
  • Confused/drowsy, maximal use of accessory muscles, retractions, marked tachycardia, unable to talk
  • Protocol as for severe + admission into ICU + change to nebulised continuous dose of salbutamol / ipratropium (risk of salbutamol/ipratropium overdose)

Block 5 Respiratory (4 decks)

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