Respiratory Disease Flashcards
Taking a history of patient and examination of pt with respiratory disease in dental clinic
Importance of taking a history of a pt w resp disease
-Assesement begins in waiting room. Check for shortness of breath, wheeze etc.
-History: Generally fit and well Chest problems Shortness of breath Current medications More specific questions as necessary
- Assess pt response to previous dental tx
- Tx may need to be postponed if during an acute exarcebation of disease
- Easy to mistake respiratory disease pt with cardiac disease as the signs and symptoms are non specific
Differentiating between cardiac and respiratory disease
- Signs and symptoms non-specific so sometimes difficult to differentiate
- If you have left sided heart failure, you are more likely to want to sit up during sleep due to orthopnea (shortness of breath while lying flat)
General clinical features of respiratory disease and explanation of each
1) Cough
- Common and non-specific
- May arise as a result of acute or chronic chest disease, cardiac problems or even psychological problems
2) Haemoptysis
- Coughing up blood from the respiratory tract
- Causes include chest infection, inhaled foreign body, pulmonary oedema or lung cancer
3) Chest Pain
- Respiratory or cardiac disease, trauma or physiological
- If related to inspiration then probably respiratory origin
4) Dyspnoea
- Sensation of shortness of breath
- Speed of onset and duration may indicate the cause
- Orthopnea- if dyspnoea when laying flat, indicating a cardiac cause
- Paroxusmal noctural dyspnoea- if pt is awoken by SOB
5) Wheeze
- Small airway noise
- Expiratory
- Commonly asthma
- Can’t get air out
6) Stridor
- Upper airway noise
- Inspiratory harsh sound
- Can’t get air in
Speed of onset of dyspnoea (sudden, hours, days, months)
Sudden:
- Foreign object
- Pulmonary embolism
- Pneumothorax
Hours:
- Asthma
- Pulmonary Oedema
- Pneumonia
Days:
-Pleural effusion
Months:
-Pulmonary fibrosis
How a dentist can look for respiratory disease during examination (after history)
1) General appearance
- After walking from waiting room
- Breathlessness at rest
- Difficulty speaking?
- Wheeze
- Multi-pitch expiratory sound
- May indicate small-airway obstruction, for example asthma
Stridor
- Harsh noise on ispiration
- Indicative of upper airway obstruction such as laryngeal oedema
2) Examination of hands
Finger clubbing
-Doming of nails and loss of skin fold angle
-Possible respiratory aetiology
3) Face and Oral Cavity
Cyanosis
-Blue discolouration of face and mucous membranes
Cervical Lyphadenopathy
Homer’s Syndrome
- Unilateral drooping of the upper eyelid
- Constriction of the pupil
- Lack of facial sweating
- Due to infiltrative spread of a lung tumour to the cervical sympathetic chain
Pulmonary Function Tests. Examples
-Peak Expiratory Flow Rate (PEFR):
Maximum expiratory flow rate during a forced expiration after full inspiration
Measured with a peak flow meter
or
-Spirometry
What is spirometry used for and significance in this for respiratory diseases
- Used to measure FEV (forced expiratory volume) and FVC (forced vital capacity)
- Pt has full inspiration then exhales for as fast and long as possible
- FEV1 is the forced expiratory volume after 1 second
- FEV1/FVC v important
- If <75%, it suggest some sort of airflow limitation
- Something is blocking the airway
- For example asthma
- FVC may be similiar to normal
- If Fev1/FVC is similiar or greater than 75%, then perhaps some restrictive lung disease
- But FVC would be much lower
- Reduced lung capacity
- Pulmonary fibrosis for example
Average PEFR male and female
- Male is 500-700l/min
- Fem is 400-600l/min
Investigations for respiratory disease
-Lung function tests eg PEFR and Spirometry
-Chest X ray
Looking for puddled liquid on opposing sides of the diaphragm
Look through a bronchoscope
If something found, then x ray at right angles to see if it’s in the right place and depth
- CT Scan
- Bronchoscope
Examples of 8 Common Upper Respiratory Tract Infections and definitions of each
1) Common Cold
- Usually viral
- Leads to runny nose, sore throat, malaise, pyrexia
2) Rhinitis
Inflammation of the mucous membranes of the nose
Runny and stuffy nose
Sneezing
If perennial, maybe allergies or asthma
Tx: decongestants, antihistamines and nasal topical steroid sprays
3) Pharyngitis
- Inflammation of the pharynx
- Viral
- Runny nose, cough, headache, hoarse voice
- If bacterial, commonly Strep. pyogenus, or Staph. aures
4) Sinusitis
- Inflammation of the mucous membranes of the sinuses
- Increased pressure and pain
- Antral floor irritation can lead to toothache
- Thick, nasal mucous, plugged nose and facial pain
5) Inhalation of a foreign body
- Typically drunken stupor or kids
- Endo file eg
- Corners clot is when blood clot is left behind nasopharynx post surgery
6) Influenza
- Orthomyxovirus A/B
- Mild-severe symptoms
- High fever, sore throat, muscle pain, headache and fatigue
- Tx: symptomatic and prophylaxis
7) Laryngo-tracheo-bronchitis
- aka Coups
- Respiratory infection
- Usually viral
- Swelling inside the trachea
- Interferes with normal breathing
- Barking cough
- Stridor
- Hoarse voice
- Fever
- Runny nose
- Burning retrosternal pain
- Tx- oxygen and steam inhalations and tracheotomy
8) Epiglottitis
Management of Epiglottitis
A- Airway Inflammation leading to obstruction
I- Increased Pulse
R- Restlessness
R- Retractions
A- Anxiety increased
I- Inspiratory Stridor
D- Drooling
Tx:
- Decrease Anxiety
- Don’t examine throat
- Position for comfort
- Cool mist humidification
- Oxygen
- No oral fluids
Definition and characteristics of Asthma
- Common, chronic reversible airway obstruction
- Airway becomes more narrow and more difficult to breathe through
- Expiratory
- Resolves spontaneously or with tx
- 3 Characteristic Features:
1) Hyper-Responsive Airways
2) Inflammation
3) Excessive mucous production
Epidemiology of Asthma
- Increasing incidence
- Male more likely to be affected than female in children
- Male equal to female in adults
- 0-10 and 20-30 most likely to be diagnosed
Aetiology of Asthma
-Most cases show a degree of atopy (genetic tendency)
- Asthma exacerbation caused by immune cells reacting to a particular stimuli, leading to inflammation of the airway, making them more narrow
- Hypersecretions during asthmatic exacerbations
- Extrinsic precipitants for atopy include house dust mite faeces, pollen and salivary proteins from cat/dog fur
- Intrinsic precipitants include atopy (increased sensitivity to common environmental agents that do not usually trigger an asthmatic response due to raised IgE levels) and bronchial hyper-reactivity (shown by a provocation test-inhaled histamine)
-Additional factors exercise, cold air, pollution, stress, viral infection, drugs eg NSAIDs and diet (tartazine)
Pathogenesis of Asthma
- Triad of oedemia (vascular leakage), bronchoconstriction and increased mucous secretion
- Mediated by mast cells which degranulate after activation of IgE receptors releasing histamine and thromboxanes
- Lymphocytes- IL5 activates eosinophils which release major basic protein, causing shedding of the epithelium
Why does it feel like you can’t breathe in asthma even though it’s an expiratory disease
- Airway is getting smaller
- Filling up of air as you cant exhale it
- Feels like you cant get any more in
Clinical Features of Asthma
- Shortness of Breath
- Wheeze
- Cough
- Symptoms worse in am
- Decreased movement and hyperinflation of the chest
- Increased expiratory time (Decreased FEv1/FVC)
- Quieting of voice and shortening sentences
Investigations of Asthma
- No single satisfactory asthma test
- History: family history
- Clinical Examination- PEFR- most asthmatics show AM dipping
-Lung Function Tests:
PEFR>15% improvement with bronchodilators or steroids if severe-keep peak flow charts
FEV1/FVC: airflow limitation pattern
-Skin Tests:
identifies extrinsic causes
-CXR:
hyperinflation with air trapping
- Allergen Provocation Test
- Exercise Test
- Blood gases in acute phase
Management of Asthma
-Education
Cause, effect and regular med use
-Prevention
Avoid allergens
Household hygeine
Prophylaxis before cold air/exercise
-Therapy, with increasing severity of asthma
Sodium Chromoglycate (Stabilises mast cells)
B2 adrenoreceptor agonist (bronchodilator and smooth muscle relaxation) eg. salbutamol
Used to relieve asthma attacks
Theophylline (bronchodilator)
Anticholinergics (bronchodilator)
Blocks the action of acetylcholine
Steroid metered dose inhalers eg Beclomethasone
Systemic Corticosteroid- Anti-inflammatory
Immunosuppressive drugs such as cyclosporine
Acute Severe Asthma definition and clinical diagnosis
-Acute exacerbation of asthma that does not respond to corticosteroid or bronchodilator therapy
-PEFR<30% normal and quietening voice
Leads to 999 and hospitalisation
Management of Acute Severe Asthmatic in dental chair
PEFR <30% normal and quietened voice
- Terminate all tx and remove all dental materials and instruments from the patients mouth
- Sit pt upright or in a comfortable position
- Administer B2 agonist
- Improvement should improve within 15 seconds, and if none, then repeat 3 times
- If still no improvement, administer oxygen and call for medical assistance
- Administer adrenaline 0.3-0.5mls 1:1000 solution
Dental Relevance of Asthma
-Prevention of asthmatic attacks
-Thorough history required: Assess risk of acute exacerbation How well controlled Severity Time since last serious attack Frequency of attacks Precipitating agents Hospitalised Dose and type of medication Taken most recent dose? Side effects Bronchodilator available
- Administer bronchodilator as premedication
- Ensure pt has inhaler to hand and taken last dose
- Supplementary bronchodilators and oxygen available in case of emergency
- Keep pt anxiety and stress to a minimum
- Sedation with care
- NSAIDs or aspirin may precipitate or worsen an asthmatic attack in a sensitive pt
- Inhaled steroids can cause Candida infection in the palate so pts must rinse after inhaler use
- Postpone tx if necessary
- Use rubber dam to decrease inhalation chance
- Most asthmatics can be treated safely under LA
- Prolonged use of steroids may cause delayed healing
Chronic Obstructive Pulmonary Disease Definition
- Group of lung diseases that lead to damage of the lung tissue with persistent and progressive limitation of air flow
- Chronic bronchitis and emphysema are two of the most common causes of COPD and often co-exist
- Smoking implicated in 95% of cases
- Emphysema is dilatation and destruction of the alveolar wall, distal to the terminal bronchioles
- Decreases the surface area for haseous exchange
- Expiratory airflow limitation and air trapping
- Known as pink puffers as they have difficulty breathing despite being well purfused
- Chronic Bronchitis is defined as a productive cough of sputum on most days for 3 months of 2 successive years
- Obstruction by narrowing airway with mucosal thickening, oedema and excess musous from hypertrophic and hyperplastic glands, so limiting airflow
- Bronchoconstriction
- Epithelial cell layer can ulcerate and heal as squamous epithelium
- Pts with chronic bronchitis are known as blue bloaters
Aetiology of COPD and explanation
-Smoking Persistant mucosal irritation Glands hypertorphy and become infiltrated with polymorphs Protease release Elastic qualities of pulmonary tissue
-Atmospheric pollution
Minor role
-A1 anti-trypsin deficiency
Failure to block proteases before the return to systemic circulation
Accelerated degenerative pulmonary damage
Pulmonary protective protease
-Cystif Fibrosis
Mutation in the CFTR gene
Defective chloride ion exchange system
HEavym thick, sticky mucous production, clogging air way passages and ducts
Pathogenesis of COPD
-In bronchitis, there is damage to the respiratory epithelium
Leading to ulceration, excess mucous production and variable airway narrowing
- In emphysema, there is airspace dilation with loss of elastic tissue within the alveolar walls
- Leads to gas trapping, over inflation and limitation of expiratory outflow
Main clinical features of COPD
- 3 cardinal symptoms include chronic cough, sputum production and dyspnoea
- Less common symptoms include chest tightness and wheezing
- Signs include hyperinflation, hypertrophied accessory muscles, wheezes
Pink Puffers v Blue Bloaters Clinical Features and Explanation
Pink Puffers (Emphysema)
- Increased alveolar ventilation because air still getting to the alveoli unlike in chronic bronchitis
- Normal or low PaCO2
- Normal PaO2
- Breathless but not cyanosed
- May progress to Type I Respiratory failure
- Pink Skin
- Increased minute ventilation
- Pursed lip breathing
- Barrel-chest
- Decreased breath sounds
- Cachectic appearance
- Co2 responsive so compensatory hyperventilation
Blue Bloaters (Chronic Bronchitis)
- Inflammatory change
- Bronchoconstriction
- Mucous hypersecretion leading to cough
- Alveolar hypoxia because the oxygen is not getting through to the alveola
- Decreased alveolar ventilation
- Raised PaCO2
- Low PaO2
- When pt develops alveolar hypoxia, pulmonary arteries vasoconstrict to shunt blood to healthier alveoli, which can result in pulmonary hypertension, which can cause right sided failure or cor pulmonale
- Rely on hypoxic drive (don’t give more than >24% oxygen in emergency)
- Co2 retention leads to warm peripheries, bounding pulse, co2 flap and confusion
- Cyanosis
- Crackles and Wheeze
- Obesity
- Peripheral oedema
- Chronic productive cough
- Sputum
- CO2 retention so insensitive to it
Warning when delivering oxygen to patient with advanced respiratory disease
- Overdelivery of oxygen can dip them into respiratory arrest
- If ever giving oxygen in an emergency make sure you check pt is fine for 5 mins after delivery of oxygen
Investigations for COPD
-CXR shows hyperinflation >6 anterior ribs above diaphragm
-Decreased peripheral lung markings on CXR and bullae
-LFTs show obstruction with air trapping
FEV1/FVC<70% (PEFR v low)
Residual volume high
Total lung capacity high (large volume trapped and useless gas)
-FBC: secondary polycythaemia (absolute increase in RBCs)
