Respiratory Diseases Flashcards

1
Q

What is asthma?

A

Reversible airflow obstruction, caused by bronchial hypersensitivity to innocuous stimuli.

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2
Q

What is the asthma triad?

A

Bronchial smooth muscle constriction
Bronchial mucosal oedema
Excessive mucous secretion into the airway

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3
Q

Describe the asthma cellular responses.

A

Allergen triggers age production.
Causes a B cell/T cell interaction, which causes degranulation of mast cells.
Leads to the asthma triad- oedema of bronchial wall, narrowing of the airway, mucous secretion.

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4
Q

What are the signs and symptoms of asthma?

A

Cough
Wheeze
Shortness of breath
Diurnal variation- worse overnight and early in the morning
Difficulty breathing out and lungs fill with air.

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5
Q

What does peak expiratory flow rate measure?

A

Airway resistance.

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6
Q

Describe some common asthma triggers.

A

Cold air
Infections- i.e. Chest infections
Dust
Smoke
Chemicals at work
Atopy- allergy to a range of different environmental stimuli.

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7
Q

What investigations might you wish to do if you suspect someone has asthma?

A

PEFR- morning and night
Skin prick test

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8
Q

Describe the biphasic response of asthma.

A

Acute asthma attack occurs- there is an early response caused by mast cell degranulation and with the action of Beta2 agonists, the patient recovers.
But they then develop a more significant attack later on- caused by activation of T cells, interleukin 4 and interleukin 5.
Leads to increased bronchial hyper-responsiveness.

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9
Q

Describe the drugs that may be used in an asthma patient?

A

Intermittent short acting beta-adrenergic agonists
Inhaled corticosteroids- low dose
Inhaled corticosteroids- high does
Regular long acting beta adrenergic agonist
Compound preparations- inhaled steroid with long acting beta agonist.
Adjuvant therapy- regular montelukast, prednisolone, biologic therapy.

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10
Q

What is the action of beta-adrenergic agonists?

A

Relax bronchial smooth muscle
Reduce bronchoconstriction
Reduce resting bronchial tone

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11
Q

What is the difference between a short acting and a long acting beta-adrenergic drug?

A

Short acting is taken as a reliever drug
Long acting is taken as a preventer drug.

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12
Q

Why might someone need a corticosteroid treatment for asthma?

A

If they have to take a short acting beta-adrenergic agonist more than 3 times per week.

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13
Q

What are the possible consequences of inhaled corticosteroid treatment?

A

Candida infections
Adrenal suppression
Osteoporosis

No evidence for adrenal suppression or osteoporosis if the daily dose is less than 1500 micrograms per day.

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14
Q

What drugs impair ventilation and shouldn’t be taken in patients with asthma?

A

Beta-blockers
Opioids
Benxodiazepines.

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15
Q

What drugs improve ventilation?

A

Bronchodilators- beta-adrenergic agonists and anticholinergic drugs.
Anti-inflammatory- corticosteroid
Prevent mast cell degranulation- chromglycate, leukotriene receptor antagonists.

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16
Q

What drug improves gas exchange?

A

Oxygen.

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17
Q

How might some of these asthma drugs be administered?

A

Metred dose inhaler
Nebuliser
Oral tablet

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18
Q

Why might you wish to use a spacer if you have a corticosteroid inhaler?

A

Improves drug delivery, makes it easier to get the full volume of drug into the airway.
Reduces the risk of candida.

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19
Q

Give examples of short acting beta2 agonists.

A

Salbutamol
Terbutaline.

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20
Q

Give examples of long acting beta2 agonists.

A

Salmeterol

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21
Q

What is the onset time, lasting time and purpose of a short acting beta agonist?

A

Onset is 2-3 minutes
Lasts 4-6 hours
Used to treat acute bronchial constriction

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22
Q

What is the onset time, losing time and purpose of a long acting beta agonist?

A

Onset time is 1-2 hours
Lasts 12-15 hours
Used to prevent acute bronchial constriction
Always used with an inhaled steroid- if not, it puts the patient as increased risk of having an acute coronary syndrome.

23
Q

What is the action of anticholinergics?

A

Inhibit muscarinic nerve transmission in autonomic nerves
Additive effect in bronchial with beta agonists and effective in reducing mucous secretion.

24
Q

What is the action of corticosteroids?

A

Reduce inflammation in the bronchial walls.

25
Q

Give examples of corticosteroids in relation to asthma.

A

Beclomethasone
Budesonide
Fluticosone
Mometasone

26
Q

What is an advantage of having a combine preparation of an inhaled steroid with a long acting beta agonist?

A

Combined benefit of long acting prevention with the agonists and steroids.

27
Q

What drug is a mast cell stabiliser?

A

Chromoglycate

28
Q

What drug is a leukotriene inhibitors?

A

Montelukast

29
Q

What questions would you ask to ascertain the severity of their asthma?

A

What medication are you taking for your asthma?
When was the last time you had an asthma attack?
Have you been hospitalised ever with asthma?
Have you ever has to take oral steroids?
What are your asthma triggers?

30
Q

If your patient has a diagnosis of asthma, how might this affect your treatment plan/management of this patient?

A

Avoid any triggers- i.e. cold air
Potentially contraindicate the use of fluoride varnish
Inhalers can cause dry mouth and oral thrush
Inhalers can cause reflux.

31
Q

What is COPD?

A

Chronic Obstructive Pulmonary Disease

Mixed reversible airway obstruction (asthma component) and irreversible destructive lung disease (bronchiectasis and emphysema component).

32
Q

What is Bronchiectasis?

A

Disease of the airways- recurring damage to the airway by chronic infection.
Inflamed tube wall- scarred and thickened airway wall
Widened airway
Excess mucous gathering in the airway

Patchy infection will remain in the the airways for weeks or months- mucous unable to be removed.
Mucous will be green.

33
Q

What is emphysema?

A

Destruction of alveoli- occurs when things get into he alveoli that are not good- i.e. smoke, asbestos, small fibres.

The more damage there is, the less gas exchange occurs.

34
Q

What are the symptoms of COPD?

A

Mucous production
Fatigue
Cough
Dyspnoea
Shortness of breath
Chest discomfort

35
Q

What are the complications of COPD?

A

Pneumonia
Heart failure
Acute respiratory distress

36
Q

What are the risk factors for COPD?

A

SMOKING!
Chronic asthma
Chronic bronchitis

37
Q

How is COPD classified?

A

Based on the risks of exacerbation or death and the symptoms that the patient is experiencing.

ABCD classification
- D is the highest risk with more symptoms

38
Q

What is the management of COPD?

A

Fundamentals are non-drug based
- smoking cessation
- Prevention of flu
- Pulmonary rehabilitation

Inhaled theories only used if the above interventions do not see to of had much benefit.

Long acting bronchodilator
Inhaled steroids
Systemic steroids
Oxygen support

39
Q

What factors can exacerbate COPD?

A

Environmental factors- dust
Noncompliance with medications
Bacterial pathogens
Viral infections
Atypical bacteria

40
Q

COPD can progress to Type 1 and Type 2 respiratory failure, what does this mean?

A

Type 1
- Hypoxia, reduced surface area for gas exchange, thickened alveolar mucosal barrier.
- Often hyperventilate to compensate.
- Problem within the alveoli

Type 2
- Hypercapnia and hypoxia.
- airway narrowingg, restive lung defects.
- Ventilation failure.

41
Q

What factors are there to consider in relation to dentistry, in a patient with COPD?

A

Ability to attend treatment- potentially will need supplemental oxygen during treatment.
Patient may not be able to lay flat.
Candid risk if using inhaled steroid- rinse mouth out after use and use a spacer.
Smokers or ex-smokers- increased risk of oral cancer risk.

42
Q

What is Cystic Fibrosis?

A

Genetic disease caused by an inherited defect in cell chloride channels- CFTR gene on chromosome 7.

43
Q

What are the signs and symptoms of CF?

A

Production of excess sticky mucous
Any secretions affected- mainly th lungs and pancreas
Troublesome cough
Repeated chest infections- eventually leading to bronchitis and bronchiectasis.
Prolonged diarrhoea
Poor weight gain

44
Q

What are the consequences of CF?

A

Liver dysfunction
Osteoporosis
Diabetes symptoms- prolonged pancreas disease
Reduced fertility- mainly male

45
Q

How is CF diagnosed?

A

Prenatal screening
Perinatal testing- blood spot test at day 5.
Sweat test
CFTR gene testing

46
Q

What is the treatment for CF?

A

Physiotherapy to help remove the mucous secretions from the lungs
Bronchodilators to open the airways
Antibiotics to reduce chest infections
Steroids to reduce airway inflammation
Pancreatic enzyme replacement
Nutritional supplements
CFTR modulators
Stem cell transplants
Exercise
Transplantation

47
Q

What are the causes of lung cancer?

A

SMOKING!
Radon gas
Chemicals within work- asbestos
Wood stoves
Genetics
Radiation therapy for some cancers
COPD and pulmonary fibrosis

48
Q

What type of lung cancers are there?

A

Adenocarcinomas
Small-cell carcinomas
Squamous cell carcinoma
Large cell carcinomas

49
Q

What are the signs and symptoms of lung tumours?

A

Persistent cough
Haemoptysis
Pneumonia
Metastasis- bone, liver, brain
Dysphagia
SVC compression
Recurrent laryngeal nerve palsy- hoarse voice

50
Q

In relation to lung cancer, what is the dentists role?

A

Prevention

Smoking cessation advise- ask, advise, act.

51
Q

What is obstructive sleep apnoea?

A

Airway obstruction whilst asleep- airway muscle tone drops which allows the tongue to fall back and blocks the airway.

52
Q

What is central sleep apnoea?

A

Patient’s motivation to breathe from the brain is stopped.

53
Q

How do you test for obstructive sleep apnoea?

A

Hypopnoea index- measures the number of events of airway obstruction per hour.

54
Q

What is the treatment for sleep apnoea?

A

CPAP machine- blows air into the airway, keeps the airway at a specific pressure at all times so that the tongue and pharynx are apart.

Mandibular advancement device- tongue attached tot he mandible and mandible is moved forwards o prevent the tongue obstructing the pharynx.

Positional therapy.