Respiratory Flashcards
(39 cards)
1
Q
What are the functions of the respiratory system?
A
- Gas exchange
- Oxygen is transported from the air to the blood in the pulmonary capillaries
- Carbon dioxide is removed from the blood and exhaled
- Regulation of blood pH
- Defence mechanisms
- Including removal of foreign particles
- Participation in taste, smell etc
- Respiratory tract secretions
- Produced by goblet cells and bronchial glands
- Form a protective mucocilliary blanket and provide surfactant function
2
Q
How do lungs work?
A
- Breathing passive process – using diaphragm
- If we inhale air – diaphragm moves down – low pressure in lungs
- If we exhale air – diaphragm moves up – high pressure in lungs
3
Q
What is the regulation of airway function?
A
- Bronchial smooth muscles innervated by:
- Parasympathetic NS
- Act through ACh
- Sympathetic NS
- Act through A and NA
- Parasympathetic NS
- Causes constriction of airways
- Can also be produced by neuropeptides and other mediators released during inflammatory responses
4
Q
Definition of airway obstruction
A
- Airflow obstruction in asthma is the result of contraction of the airway smooth muscle and swelling of the airway wall due to:
- Smooth muscle hypertrophy and hyperplasia
- Inflammatory cell infiltration
- Oedema
- Goblet cell and mucous gland hyperplasia
- Mucus hypersecretion
- Protein deposition including collagen
- Epithelial desquamation
5
Q
What is the definition and characteristics of asthma?
A
- Chronic inflammatory disorder of the airways in which many cells and cellular elements play a role
- Causes an associated increase in airway hyperesponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing
6
Q
What is the progression of asthma?
A
- Immediate reaction
- Triggers (allergens, infection, smoking etc)
- Bronchospasm
- Triggers (allergens, infection, smoking etc)
- Late or delayed reactions
- Acute inflammation
- Bronchoconstriction, oedema, secretions, cough
- Chronic Inflammation
- Cell recruitment, epithelial damage, early structural changes
- Airway remodelling
- Cellular proliferation, extra-cellular matrix increase
- Acute inflammation
7
Q
What are the triggers of asthma?
A
- Inhaled allergens which include:
- Household dust (mite)
- Animal dander
- Fungal allergens (mould)
- Grass, tree and weed pollens
- Tobacco smoke
- Personal smoking and passive smoking can aggravate asthma
- Occupational factors
- Agents that can cause or aggravate asthma include:
- Allergens
- Small molecules
- Irritants
- Cold air exposure
- Agents that can cause or aggravate asthma include:
- Food and food additives
- Some individuals are allergic to nuts, eggs, fish, shellfish or some seeds
- Colourings
- Flavour enhancers
- Drugs
- Beta-blockers
- Cholinergic agonists and anticholinesterases
- Aspirin and NSAIDs
- Some complementary medicines (e.g. royal jelly and echinacea)
- Exercise-induced bronchoconstriction
8
Q
What is the process of an asthma attack?
A
- Release of chemicals causes muscle in airways to tighten or contract
- Airways becoming narrower
- Develops very rapidly
- Inner lining of the airways swells and becomes red and inflamed
- Mucous is released
- These changes develop more slowly (over several hours or days)
- Can take that long to reverse after the asthma attack has passed
9
Q
What is the proper asthma diagnosis?
A
- Variable symptoms (cough, wheeze etc) as well as a spirometry test which shows significant reversible airflow limitation
10
Q
What is spirometry?
A
- Spirometry measures how much (FEV1) and how quickly (PEF) you can move air out of your lungs
11
Q
Define FEV1 and what is abnormal FEV1?
A
- FEV1: the volume of air expelled in the first second of a forced expiration
- Considered abnormal if FEVI is less than 75% of the normal predicted value
12
Q
Define FEV1%
A
- result of a formula that takes into account the gender, age and height of the person
13
Q
FEV1% value categories
A
- FEV1 60-75% predicted = mild obstruction
- FEV1 50-59% predicted = moderate obstruction
- FEV1 >49% predicted = severe obstruction
14
Q
What is the importance of PEF measurement?
A
- Peak Expiratory Flow: Measures how fast you can breathe out using the greatest effort
- Used in the monitoring and treatment of asthma to determine how well the lungs are functioning
- A decrease in peak flow can show that the bronchial tubes have narrowed even before asthma symptoms develop
15
Q
What are the goals of asthma therapy?
A
- To provide:
- Symptom control and relief
- Protect against exercise-induced asthma
- Prevent acute asthma and death
- Maintain best lung function
- Maintain quality of life
16
Q
Development of Allergic Asthma
A
- Cross-linking of the IgE molecules by the antigen activate adenylate cyclase and opening Ca2+ channels which causes degranulation
- Calcium entry causes:
- Release of secretory granules containing histamine and the production and release of other agents that cause airway SMC contraction
17
Q
Rarely used asthma drugs
A
-
Oral corticosteroids
- Prednisolone
-
Antibiotics
- Reserved for confirmed infections
-
Antihistamines
- For associated nasal and other allergic symptoms
-
Sedatives
- Contraindicated in acute attacks
18
Q
Characteristics of COPD and differences in regard to asthma
A
- Characterised by airflow limitation that isn’t fully reversible
- Airflow limitation is usually both progressive and associated with abnormal inflammatory response of the lungs to noxious particles or gases
- Combination of:
- Emphysema
- Where the lung parenchyma is structurally damaged
- Airway damage
- With airway wall thickening and narrowing off the airway
- Emphysema
19
Q
COPD Risk Factors
A
- Smoking
- Age
- Gender
- Occupation
- Genetic factors
- Air pollution
- Socio-economic status
- Airway hyper responsiveness and allergy
20
Q
Diagnostic tests used in COPD
A
- Blood tests
- FBP, haemoglobin levels and concentration of RBC
- Chest X-ray
- Shows hyper-expansion of the lungs, bulla (dilated airspaces)
- ECG or Echocardiogram
- Detect signs of right heart failure
- Pulmonary/lung function tests
- Spirometry to detect airflow limitation and obstruction – confirms diagnosis
- Blood gases
- Low oxygen and high carbon dioxide levels
- High resolution CT scan
- For detecting emphysema and bulla
21
Q
Health problems associated with COPD
A
- Obstructive sleep apnoea
- Frequent or prolonged pauses in breathing during sleep
- Leads to deterioration of arterial blood gases and a decrease in the saturation of haemoglobin with oxygen
- Acute respiratory failure
- Sudden decrease PaO2 and in
- Cause: exacerbations of bronchitis with increase in volume and viscosity of mucus causing
- Restlessness, confusion, tachycardia, cyanosis, sweating, hypotension and eventual unconsciousness
22
Q
COPD presentation types
- Blue bloater
- Pink puffer
A
- Blue Bloater
- Patients retains CO2 caused by decreased responsiveness of respiratory centre to prolonged hypoxia
- Leads to cyanosis
- Tendency for peripheral edema
- Ability to increase rate and depth of respiration is lost due to persistent hypoxaemia
- As obstruction worsens, hypoxemia worsens – leads to pulmonary hypertension
- Severe cases: barrel chest appearance
- Patients retains CO2 caused by decreased responsiveness of respiratory centre to prolonged hypoxia
- Pink Puffer
- Hyperventilates to compensate for hypoxia by breathing short puffs
- Patients appears pink
- Little retention of CO2
- Eventually the patient is unable to get enough O2 on spite of rapid breathing
23
Q
COPD treatment aims
A
- Stop smoking
- Drug therapy
- Pulmonary rehabilitation
- Oxygen therapy
- Surgery
24
Q
COPD drug classes
A
- Short acting bronchodilators
- Long acting bronchodilators
- Corticosteroids
- Long-acting anticholinergics
- Xanthine drugs
25
Use of short b2 receptor agonists in COPD
* If patients don’t respond adequately to an appropriate dose of one bronchodilator, they should be given a trial of a different bronchodilator
* Trial of a combination of the 2 classes of bronchodilators with objective of monitoring the response
26
Use of long b2 receptor agonists in COPD
* Salmeterol
* Used in patients who remain symptomatic despite treatment with combinations of short-acting bronchodilators
* Useful for those who have a history of frequent exacerbations
* Monotherapy with L.A.B2 agonists – shown to reduce frequency of exacerbations
27
Use of inhaled corticosteroids in COPD treatment
* Reduce exacerbation rates and slow the decline in health status
* Benefits not seek in patients who continue smoking
28
Use of oral corticosteroids in COPD treatment
* Not recommended for maintenance therapy
* May be needed in some patients with advanced COPD where corticosteroids cannot be withdrawn following acute exacerbation
* Dose as low as possible
* Long-term therapy needs monitoring – development of osteoporosis and given appropriate prophylaxis
29
Need for combination therapy in COPD
* For patients who remain symptomatic on monotherapy, different drug class should be added
* Combined therapy to be discontinued if no benefit after 4 weeks
* Patients are best treated with single-ingredient preparations – dose of each drug can be adjusted
30
Need for oxygen therapy in COPD
* Oxygen therapy
* Patients with advanced COPD (FEV1\<50% predicted) who develop chronic hypoxaemia have improved survival when treated with long-term oxygen
* Benefit greatest if taken for at least 15hr/day
31
Need for Surgery in COPD
* Surgery
* Bullectomy (surgical removal of a bulla) if patient is:
* Are breathless
* Have single large bulla on a computerised tomography (CT) scan
* Have an FEV1 less than 50% predicted
* Lung transplantation usually involves replacement of one diseased lung with a normal lung from an organ donor
32
Pathophysiology of allergic rhinitis and symptoms
* Acute or chronic inflammation of the nasal mucosa mediated by IgE
* Results in release of histamine from mast cells
* Increased production of leukotrienes and prostaglandins
* Symptoms:
* Watery rhinorrhoea
* Sneezing
* Itchy eyes, throat
33
Process of mast cell degranulation
* Antigen binds to IgE molecules on mast cell and cross links them
* Create signalling process, opens calcium channels, calcium enters, mast cells degranulates
* Many mediators e.g. histamine in granules
34
Histamine Receptors
* H1
* Mediating allergic and inflammatory reactions
* Contraction of smooth muscle except blood vessels
* H2
* Gastric acid secretion
35
Characteristics of 1st generation antihistamines
* All enter CNS readily
* Alkylamines: chlorpheniramine
* Mod. Sedation, cough and cold preps
* Ethanolamines: diphenhydramine
* Increase sedation, cough suppression
* Phenothiazines: promethazine
* Increase sedation, anticholinergic effects
* Cyproheptadine
* Mod. Sedation, also anti 5-HT and anticholinergic activity
36
Characteristics of 2nd generation antihistamines
* Non-sedating H1 antagonists
* Less lipid soluble and therefore less CNS action
* Few anticholinergic effects
* Some metabolised by CYP3A4 and therefore interact with inhibitors of CYP3A4 e.g. ketoconazole
37
Major ADRs of 1st generation of antihistamines
* Dry mouth and nose
* Urinary retention
* Blurred vision
38
Major ADRs of 2nd generation of antihistamines
* Loratadine
* Avoid in pre-existing arrhythmia
* Reduce dose with hepatic impairment
39
Steroid and sympathomimetic treatment of allergic rhinitis
* Intranasal steroids
* Rhinocort for chronic allergic rhinitis
* Every 24hr in ‘hayfever’ season
* Sympathomimetics (a-1 adrenergic agonist and a-2 partial agonist) are vasoconstrictors of SMC
* Oxymetazoline
* Relieves temporary nasal congestion
* Both can be used in conjunction with H1 antagonists
