Respiratory Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
  • Causes constriction of airways
    • Can also be produced by neuropeptides and other mediators released during inflammatory responses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the progression of asthma?

A
  • Immediate reaction
    • Triggers (allergens, infection, smoking etc)
      • Bronchospasm
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is spirometry?

A
  • Spirometry measures how much (FEV1) and how quickly (PEF) you can move air out of your lungs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Define FEV1%

A
  • result of a formula that takes into account the gender, age and height of the person
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

FEV1% value categories

A
  • FEV1 60-75% predicted = mild obstruction
  • FEV1 50-59% predicted = moderate obstruction
  • FEV1 >49% predicted = severe obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
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
  • 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
Q

Use of short b2 receptor agonists in COPD

A
  • 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
Q

Use of long b2 receptor agonists in COPD

A
  • 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
Q

Use of inhaled corticosteroids in COPD treatment

A
  • Reduce exacerbation rates and slow the decline in health status
  • Benefits not seek in patients who continue smoking
28
Q

Use of oral corticosteroids in COPD treatment

A
  • 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
Q

Need for combination therapy in COPD

A
  • 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
Q

Need for oxygen therapy in COPD

A
  • 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
Q

Need for Surgery in COPD

A
  • 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
Q

Pathophysiology of allergic rhinitis and symptoms

A
  • 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
Q

Process of mast cell degranulation

A
  • 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
Q

Histamine Receptors

A
  • H1
    • Mediating allergic and inflammatory reactions
      • Contraction of smooth muscle except blood vessels
  • H2
    • Gastric acid secretion
35
Q

Characteristics of 1st generation antihistamines

A
  • 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
Q

Characteristics of 2nd generation antihistamines

A
  • 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
Q

Major ADRs of 1st generation of antihistamines

A
  • Dry mouth and nose
  • Urinary retention
  • Blurred vision
38
Q

Major ADRs of 2nd generation of antihistamines

A
  • Loratadine
    • Avoid in pre-existing arrhythmia
    • Reduce dose with hepatic impairment
39
Q

Steroid and sympathomimetic treatment of allergic rhinitis

A
  • 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