Respiratory Flashcards
(197 cards)
1
Q
What is the primary function of the respiratory system?
A
To supply the blood with oxygen in order for the delivery of oxygen to tissues in all parts of the body - via breathing
2
Q
Purpose of upper respiratory tract:
A
Where air is taken into the body and warmed, moistened, and filtered before passing into the lower respiratory tract
3
Q
Why is the air warmed, moistened, and filtered?
A
To enable maximum gaseous exchange and larger molecules of impurities do not penetrate as far as the lungs
4
Q
Purpose of lower respiratory tract:
A
Air comes into close contact with capillary system of the pulmonary circulation and gaseous exchange occurs. Oxygen moves from air into blood and CO2 moves from blood into lungs.
5
Q
What makes up the upper respiratory tract?
A
Nose, pharynx (throat), larynx (voice box), and trachea
6
Q
How is the air moistened and warmed?
A
Nasal cavity of nose has a large surface area lined with a mucous membrane
7
Q
The mucous membrane in the nasal cavity is continued into the pharynx, continuing the filtering
process. What does the pharynx provide a common passage to? (2)
A
Oesophagus & trachea with a mechanism, the epiglottis, to prevent food going down into the lungs
8
Q
Where is lymph tissue found (2) and its role?
A
Lymph tissue present in the tonsils & lymph glands of the neck. Provides moist environment and defence against bacteria.
9
Q
What protects the larynx?
A
Protrusion of cartilage known as the Adam’s apple. The larynx is the channel between the pharynx & trachea
10
Q
Function of larynx:
A
Helps to facilitate speaking. As air flows from the lungs, the vocal cords open and close together and vibrate, creating sounds.
11
Q
What makes up the trachea? (2)
A
Incomplete rings of cartilage & smooth muscle for support
12
Q
Why are the rings of cartilage incomplete?
A
To allow food to be swallowed easily in the oesophagus without squashing the trachea
13
Q
What lines the trachea (2) & why?
A
The trachea is lined with mucus-secreting goblet cells and ciliated epithelium. The mucus traps dust, dirt and pathogens from the air while the cilia beat and move the mucus (including dust and pathogens) away from the lungs.
14
Q
What comes after the trachea?
A
Passes down the neck into the chest until it divides to form the right & left bronchus
15
Q
Structural differences (2) between bronchi and bronchioles & one similarity:
A
Bronchioles are much smaller
They do not have cartilage rings around them
They do contain smooth muscle
16
Q
Why do bronchioles have smooth muscle and what do bronchioles then divide repeatedly into?
A
They do contain smooth muscle which means they can dilate and constrict in response to environmental factors such as the temperature of the air.
Terminal bronchioles (tiny tubule network)
17
Q
Where do the bronchioles end in?
A
Alveoli
18
Q
Alveoli structure: (2)
A
Each alveolus is a tiny air sac with thin walls of flattened epithelial cells.
They have a big surface area
19
Q
What surrounds the alveoli & why?
A
Network of blood capillaries so the distance for gaseous exchange is as short as possible - maintaining a steep concentration gradient
20
Q
What are the anatomical features of the lungs in terms of lobes & pleural membranes?
A
Right lung - upper, middle, lower lobes
Left lung - upper & lower lobe
Pleural membranes - 2 of them. One stuck to lung surface and the other lines inside of the chest wall. There is pleural fluid to reduce friction between the membranes (in thorax (chest cavity)) & make breathing more efficient.
21
Q
5 functions of the respiratory system:
A
- Creating sounds involved in speaking
- Assisting the detection of smell by olfactory receptors in the nasal cavity
- Moving air to and from the lungs, along the respiratory passages
- Providing a broad surface area for gaseous exchange between air & circulating blood
- Protecting respiratory surfaces from dehydration and temperature changes; protecting the respiratory
system and other body tissues by invasion by pathogens
22
Q
The amount of oxygen in the blood depends on…(2)
A
Volume of blood & haemoglobin concentration
23
Q
Which part of the respiratory system do bacterial & viral infections predominate?
A
Viral = upper airways
Bacterial = further down
24
Q
Microorganisms can enter the lungs either by …
A
Inhalation or aspiration
25
What two things does infection by inhalation depend upon?
The virulence of the organism (e.g. tuberculosis) & the dosage of exposure (how much of the organism)
26
Bacteria and viruses are small enough to reside on aerosolised droplets that can be inhaled.
Mechanisms which trap particles in the airways are more effective against dry materials than against liquid droplets.
27
What is pulmonary aspiration and how does it occur?
The entrance of foreign material into the lungs. It may occur when swallowing and breathing are not coordinated, leading to choking.
28
Pulmonary aspiration is not usually a problem as our normal defence mechanisms can eliminate any bacteria or fungi that enter the lungs; however, sometimes these microbes lodge in the upper airways and form larger colonies resulting in
infection – aspiration pneumonia.
29
The respiratory system goes through various changes with age, including anatomical, physiological and
immunological changes. What is an example of this and what does it lead to?
As a person ages, the elastic fibres in a lung decrease, so the lungs are unable to draw air in and out as adequately as that of a younger person.
30
It is estimated that smoking causes around 110,000 premature deaths every year in the UK. What percentage of these are from lung cancer & chronic obstructive pulmonary disease (COPD)?
Lung cancer: 25%
COPD: 20%
31
Cancer of the lungs is often not discovered until it is too late to cure: 93% of lung cancer patients die within five years. 75% die within the first year of diagnosis. There are approximately 4,000 chemicals in cigarette smoke, many of them toxic. They include nicotine, acetone, ammonia and naphthalene.
32
Carbon monoxide, a poisonous gas created when there is insufficient oxygen present for complete combustion, is present in all cigarette smoke. It binds to haemoglobin much more readily than oxygen, causing the blood to carry less oxygen. What does this lead to in heavy smokers?
Heavy smokers may have the oxygen-carrying power of their blood cut by 15%.
33
What three things happen when a lung fills with cigarette smoke?
1. Carbon monoxide binds to haemoglobin in red blood cells, preventing affected cells from carrying a full load of oxygen.
2. Carcinogens in tobacco smoke damage important genes that control the growth of cells, causing them to
grow abnormally or to reproduce too rapidly.
3. Smoking affects the function of the immune system and increases the risk for respiratory and other
infections.
34
What does nicotine stimulate the release of?
Dopamine from the brain. Dopamine is involved in mood, appetite, and other brain functions.
35
Which organs have the greatest risk of developing cancer & why?
Organs with direct contact with smoke - oesophagus, lung, oral cavity
36
Lung cancer is the leading cause of cancer death among both men and women, and 90% of lung cancer in men and 80% of lung cancer in women is directly attributed to smoking.
Smoking increases the chance of developing lung cancer by 22-fold for a male and 12-fold for a female.
37
What is rhinitis and symptoms (4)?
A term used to describe the irritation & inflammation of the mucous membrane inside the nose with at least one of these symptoms present:
- Sneezing
- Rhinorrhoea (nasal cavity with lots of mucus)
- Nasal congestion (stuffiness)
- Nasal itching
38
How is rhinitis classified?
Allergic or non-allergic
39
How is a person classified for allergic rhinitis & how & which antibody mediates it?
Classified as being seasonal or perennial (year-round)
This depends on whether the person is sensitised to cyclic pollens or year-round allergens. IgE.
40
What would happen when an allergen-sensitive person encounters an allergen? (4)
1. B-lymphocytes produce large amounts of IgE antibodies
2. IgE antibodies bind to mast cells found in the lungs, skin, tongue, and linings of the nose and GI tract
3. Next encounter with allergen causes IgE-primed mast cells to release powerful chemicals like histamine
4. Causes symptoms of allergy like sneezing & wheezing & allergic conjunctivitis
41
What is perennial allergic rhinitis commonly associated with and how is it tested to identify the allergens responsible?
Indoor allergens - house dust mites, cockroaches, fur-bearing pets, rodents, and fungi. Diagnosis via medical history & skin testing to identify responsible allergens.
42
What are three examples of non-allergic rhinitis & what does this condition cause?
Causes profuse chronic watery rhinorrhoea with the absence of nasal & ocular itching. It is not a result of IgE-dependent events.
Perennial intrinsic rhinitis
Idiopathic (unknown) non-allergic rhinitis
Infectious rhinitis
43
What characterises perennial intrinsic rhinitis? (3)
An allergic-LIKE condition with increased eosinophils in the lining and secretions of the nose
Symptoms are the same as perennial allergic rhinitis
Nasal polyps growth
44
How to test for perennial intrinsic rhinitis & why?
Nasal smear test. This'll show positive for eosinophils but absence of allergen triggers
45
What does a person with idiopathic non-allergic rhinitis (vasomotor rhinitis) react to?
Temperature & humidity changes, smoke, odours, and emotional upsets
46
Symptoms of idiopathic non-allergic rhinitis: (2)
Postnasal drip & nasal congestion
47
Patients with idiopathic rhinitis have no demonstrable allergy or eosinophils in their nasal secretions. Diagnosis comes after skin tests and nasal smear for eosinophils.
48
What can infectious rhinitis appear as & symptoms?
Acute viral respiratory infection (cold) which may clear rapidly or continue with symptoms for 6 weeks.
Symptoms are an increased amount of coloured & thickened nasal discharge & nasal congestion.
49
Why do some people develop the complication of an acute or chronic bacterial sinus infection?
Usually associated with blocked sinus drainage.
Sinuses are air-filled spaces in the skull. They can get blocked due to swelling, mucus, or inflammation. Mucus gets trapped and cannot drain properly, leading to infection if bacteria is able to grow.
50
What is another type of rhinitis & its cause?
Rhinitis medicamentosa - can occur by overuse of nasal decongestant sprays (meant to unblock nose & reduce swelling of blood vessels in nose)
51
How long do you have to use the nasal decongestant sprays before swelling recurs again?
Used for more than 5-7 days. The temptation is to
use yet more decongestant and a vicious circle can be set up. A person who has taken a decongestant nasal spray for months or years is using this treatment incorrectly as these medications are intended for short-term use only.
52
Symptoms of rhinitis medicamentosa: (2)
Postnasal drip & nasal congestion
53
Rhinitis medicamentosa happens because repeated use of nasal decongestant sprays damages and desensitizes the blood vessels in the nose. At first, the spray shrinks blood vessels and opens the airway, but with continued use, the blood vessels become dependent on the spray to stay constricted. When the spray wears off, the blood vessels rebound by swelling even more than before, causing worse congestion — that’s the rebound effect
54
Three managements for allergic rhinitis:
Allergen avoidance
Pharmacotherapy
Allergen immunotherapy (when appropriate)
Many of the medications used to treat allergic rhinitis are also used in the management of non-allergic rhinitis.
55
What do antihistamines do?
Inhibit the effects of histamine on H1 receptors in blood vessels, peripheral nerves, and skin receptors, which are the receptor which cause inflammation.
56
Why are second generation antihistamines preferred over first generation antihistamines for the treatment of allergic rhinitis? (4)
1. First generation are associated with sedation & anticholinergic side effects (dry mouth, blurred vision, constipation, and urinary retention)
2. Less sedating and better tolerated
3. First generation are short-acting
4. Second generation antihistamines have once-daily dosing
57
What form do corticosteroids usually come in & when are they typically used?
Nasal spray. Highly effective treatment for rhinitis but are only used short term in severe cases
58
Why are they only used short term in severe cases?
Serious adverse effects associated with long term use of systemic steroids (osteoperosis, growth retardation, diabetes, oedema)
59
Why is the amount used insufficient to cause systemic effects?
Doses used in topical preparations (e.g. nasal spray) are much smaller than those used in oral treatment. The effect is primarily anti-inflammatory.
60
What treatments would a person with mild or episodic symptoms often use?
A second generation oral antihistamine administered regularly or as needed, with the addition of a glucocorticoid nasal spray if needed.
61
Glucocorticoid nasal sprays are the most effective single pharmacologic therapy for allergic rhinitis and may be the best initial therapy for those with persistent or moderate-to-severe symptoms, with add-on second-generation antihistamine as a nasal spray. Decongestant sprays are different a type - which are the ones leading to rhinitis medicamentosa.
62
For young children (under 2 years of age), it is important to exclude other disorders first before initiating treatment with second-generation antihistamines available in liquid formulations.
63
Where does asthma affect & when does it develop?
Affects the large & small airways developing typically in childhood
64
Patients with asthma have episodes of breathlessness (dyspnoea), chest tightness, wheezing and coughing that are due to generalised airway obstruction, caused predominantly by...
Smooth muscle spasm - muscles around airways suddenly tighten & squeeze
65
A central feature of asthma is airway hyper-responsiveness, which is an enhanced bronchoconstrictor response (the lung airways
become smaller) brought on by a variety of inhaled stimuli. What are these? (6)
Cold air
House dust mites
Pollen
Tobacco smoke
Exercise
Upper respiratory infections
66
Where are each IgG, IgA, and IgE found in the body?
IgG = bodily fluids
IgA = mucous secretions like saliva
IgE = surface membranes such as those found in the airways, often high in people with allergies
67
What is the term used to describe the tendency to produce allergic reactions resulting in allergic rhinitis / eczema / asthma?
Atopy
68
Explain the IgE process for inflammation:
The IgE antibodies bind to mast cells which are a class of inflammatory cell present in the airway mucosa that have surface receptors specific for IgE antibodies.
When the allergen binds to the antibody on the mast cell, the mast cell is stimulated to release mediators of inflammation. These include histamine, kinins, cytokines and metabolites of arachidonic acid that act on the blood vessels, smooth muscle, connective tissue, mucus glands and inflammatory cells
69
Which two classes can inflammation be divided into?
Acute inflammation & chronic inflammation
70
What does acute inflammation involve?
Dilation of blood vessels and increases in their permeability
71
What does this lead to? (3)
White blood cells migrating from blood vessels into the tissues.
They attempt to digest and destroy infectious microorganisms.
This leads to the redness, pain, swelling, and heat associated with tissue damage & inflammation
72
What causes chronic inflammation?
Extensive exposure to the provoking stimulus
73
What does this lead to? (4)
This may involve permanent changes such as
- Destruction of tissue
- Local cell proliferation
- Proliferation of connective tissue
- Formation of fibrous tissue.
74
Three benefits of drugs being delivered as dry powders or metered-dose aerosols directly into the lungs via an inhaler:
1. First-pass metabolism of the liver is avoided (drug isn't destroyed by liver)
2. Much lower doses required
3. Side effects minimised
75
However, even with good inhalation technique, only
around 10% to 15% of the contents is inhaled deep into the lungs, up to 85% is deposited on the wall of the pharynx and ultimately swallowed. Many asthmatic patients find an inhaler difficult to use effectively, especially children. In such cases a spacer device can be useful.
76
How are asthma medications classified & what are they?
Classified according to their roles in overall management. Those that offer quick relief or those that contribute to long-term control.
Relievers & preventers
77
The guidelines recommend prescribing which type of short-term reliever therapy for all patients with symptomatic asthma & why?
inhaled Short Acting B2 Adrenoceptor Agonist (SABA) as they work faster and/or with fewer side effects than the alternatives. SABA = bronchodilator
78
Other bronchodilators like inhaled ipratropium bromide (a short-acting muscarinic antagonist, or SAMA), β2 agonist tablets or syrup, and theophyllines are recognised treatment options for the management of asthma as well. High-dose inhaled β2 agonists are also recommended as first-line agents in patients with acute asthma.
79
4 positive effects of B2 agonists:
1. Selective for respiratory tract & do not stimulate B1 adrenoceptors of the myocardium
2. They inhibit mediator (inflammatory chemicals) release from mast cells
3. May increase mucus clearance through action on cilia
4. Cause relaxation of bronchial smooth muscle
80
Two examples of SABAs normally prescribed for short-acting relief of asthma:
Salbutamol & terbutaline
81
When does the maximum effect occur and how long is the duration of action for both salbutamol & terbutaline?
Maximum effect occurs within 30-60 mins and then lasts for 3 to 5 hours. Both treatments have the same efficacy.
82
Ipratropium bromide is a SAMA. Other than SABAs acting faster, why are they preferred? (2)
Ipratropium bromide is not well absorbed into the circulation & does not have much action on the muscarinic receptors other than those found within the bronchi. SABAs only target B2 adrenoceptors on airway smooth muscle.
83
What is the regular preventer drug for adults & children?
Inhaled corticosteroids (ICS). Treatment starts at a dose appropriate to the severity of the disease.
84
What two positive & powerful effects do ICS have when given therapeutically?
Anti-inflammatory & immunosuppressive effects
85
Which is the most widely used inhaled steroids?
Beclometasone dispropionate
Others include mometasone furoate, fluticasone propionate and budesonide
86
How are they administered & when are the full local pulmonary effects achieved?
Via a pressurised metered-dose inhaler (pMDI). Only after several days of treatment.
87
Where is the main site of action for ICS?
Inflamed lower airways
88
What two other locations can ICS reach?
Small amounts of the medicine reaches the systemic circulation directly through the bronchial circulation (Bronchial circulation – part of the systemic circulation; supplies oxygenated blood to the lung tissue itself)
Swallowed steroid is absorbed and passes to the liver where it is metabolised and inactivated before being excreted.
89
These ICS are treatments for prophylaxis of asthma (indication)
Prophylaxis = prevention of disease
90
Which two other preventer treatments are considered less effective in patients taking SABAs alone:
Theophyllines & Leukotriene Receptor Antagonists (LTRAs). Not as effective as ICS when only used in combination with SABAs.
91
How do theophyllines & LTRAs work?
Theophyllines are a xanthine medication with bronchodilator action (relaxing smooth airway muscle). GI symptoms common. Given orally in sustained-release preparations.
LTRAs are a class of anti-asthma therapy that target one of the principal asthma mediators by inhibiting the cysteinyl leukotriene receptor in the airways. In young children under 5 years of age unable to take ICS, LTRAs are a useful alternative.
Both orally taken.
92
Two examples of LTRAs and their indication:
Montelukast - prophylaxis of asthma & symptomatic relief of seasonal allergic rhinitis
Zafirlukast - prophylaxis of asthma
93
Sodium cromoglicate and nedocromil sodium are a separate class of medicines which are also effective in
patients with...
Milder forms of asthma. They belong to the Mast Cell Stabiliser class
94
What is the basic mode of action for sodium cromoglicate?
Stabilise membranes of mast cells & other inflammatory cells, preventing release of mediators
95
Why is sodium cromoglicate not used as much anymore? (2)
1. The onset of action is slow, four to seven days or more
2. The efficacy of cromoglicate is considered to be less than that of topical steroids and topical antihistamines
96
Sodium cromoglicate does not pass through cell membranes and is not metabolised. Therefore, systemic effects and systemic side effects are absent.
97
Some patients with asthma will not be adequately controlled on regular preventer treatment and add-on therapy will be required. NICE guidelines currently suggest that, if an add-on to ICS therapy is required,
the first choice should be...
LTRA such as montelukast, taken orally
98
If further add-on therapy is needed, what can be added to the ICS & LTRA therapy?
Long-Acting B2 Agonist (LABA)
99
Examples of LABAs include formoterol and salmeterol. LABAs are only started in patients already treated with ICS, and so often combination inhalers (LABA & ICS in one inhaler) are used to ensure LABA is not given without ICS and to improve adherence. LABAs mask symptoms and don't directly treat inflammation like ICS do.
100
What is Chronic Obstructive Pulmonary Disease (COPD)?
A progressive, disabling and complex obstructive lung disease which is a collection of conditions that share the features of chronic obstruction of expiratory flow
101
What usually causes the long-term damage to the lungs?
Struggle to breathe in & out commonly caused by smoking
102
Average age of onset for COPD & why is it that 3mill are affected, and 2mill remain undiagnosed?
67 years old. Symptoms are often dismissed as 'smoker's cough'. COPD affects more men than women.
103
Two examples of COPD:
Chronic bronchitis
Emphysema
104
What characterises chronic bronchitis?
Chronic productive cough (phlegm production) for at least 3 months in each of two successive years when other causes like infection with mycobacterium tuberculosis, carcinoma of the lung, or chronic heart failure have been excluded.
105
What is the most consistent pathological finding in chronic bronchitis?
Hypertrophy of the mucus-secreting glands of the bronchial tree with an increase in the number of mucus-secreting goblet cells
106
What does this lead to? (2)
1. Increased mucus production
2. Regular expectoration of sputum
107
Cause of emphysema:
Often caused by smoking
108
What happens to cause emphysema?
Destruction of lung tissue around the alveoli leads to loss of elastic recoil & collapse of small airways during expiration. Leads to expiratory airflow limitation & air trapping, resulting in decreased gas transfer.
109
Patients who have features of chronic bronchitis or emphysema without airflow obstruction have one
or both of those diseases but not COPD. Most patients with COPD, who by definition have airflow
obstruction, have features of both chronic bronchitis and emphysema.
110
Smoking is the main cause of COPD. Around three in 20 people who smoke 20 cigarettes a day and one
in four people who smoke 40 cigarettes will develop COPD if they carry on smoking. For smokers overall
there is a one in four to one in ten chance of developing COPD. It is very rare for non-smokers to develop COPD.
111
Air pollution and polluted working conditions may cause or exacerbate COPD.
There are also a very small number of people who have a genetic risk of developing COPD. This is due
to deficiency of a protein called alpha-1-antitrypsin which leads to liver, lung and blood disorders. It only
affects less than one in 100 cases of COPD.
112
5 symptoms of COPD:
Cough (smoker's cough)
Breathlessness
Green/yellow sputum production
Chest infections (due to bacteria or viruses)
Less common symptoms include weight loss, tiredness, and ankle swelling
113
Chest pain and haemoptysis (coughing up blood) are not typical markers of COPD, but should be
investigated if these occur, as they could be symptoms of lung cancer.
114
Why are some patients with asthma considered to have a form of COPD and those not have a form of COPD?
People whose asthma is characterised by incomplete reversibility of airway obstruction - form of COPD as they cannot be distinguished from those who have chronic bronchitis / emphysema
Those with completely reversible airflow obstruction without features of chronic bronchitis / emphysema have asthma but not COPD
115
Some asthma treatments only partially treat the narrowing and airway obstruction. Therefore, harder to tell if it is irreversible COPD or asthma.
116
What is the most common way of diagnosing COPD?
Spirometry
117
What is a common spirometry test?
Peak flow meter - measure how much air you can blow into a peak flow meter (the peak flow expiratory flow rate (PEFR))
118
Another spirometry test measures how much air you can exhale (blow out) in one second. What does this produce?
A value called FEV1 – forced expiratory volume in one second.
119
Spirometry also determines the forced vital capacity, or FVC. What is this?
Total volume of air which can be expelled from your lungs after taking a deep breath
120
PEFR = Peak Expiratory Flow Rate. The maximum speed at which air can be exhaled after a full breath.
FEV = (forced expiratory) volume of air exhaled in first second in forced expiration
FVC = Forced Vital Capacity. The total volume of air exhaled during a full forced expiration.
121
FEV1/FVC ratios of 0.7 or less are diagnostic of
COPD, but the actual FEV1 value expressed as a percentage of the predicted value is then used to stratify the severity of disease.
122
COPD is divided into mild, moderate and severe groups. How are they determined?
Mild: FEV1 is at least 80% of predicted value
Moderate: FEV1 measure is between 50%–79% of predicted value
Severe: FEV1 measure is between 30%–49% of predicted value
Very severe: FEV1 measure is less than 30% of predicted value
123
What are other tests used (3)?
X-ray
High resolution CT scan
Blood test to determine changes in [rbc in blood] & whether oxygen levels are low
124
COPD is not diagnosed or diagnosed too late. What are reasons for this? (5)
1. Early COPD is difficult to diagnose because of the lack of symptoms in the early stages.
2. Currently, routine annual spirometry is the best method to detect early disease, but because of the major resource requirement, it is routinely only provided for those at high risk, eg those with proven risk factors.
3. Patients may present late, often regarding it as normal to cough and be short of breath because they smoke.
4. Doctors may misdiagnose, especially in patients with milder symptoms who usually turn up for emergency consultations with presumed bronchitis.
5. Confusion between COPD and asthma may lead to misdiagnosis. This is because of similarities between COPD and asthma and because the two syndromes may overlap, with some COPD patients also suffering from asthma, and a proportion of chronic asthma sufferers going on to develop COPD.
125
Why is it detrimental that misdiagnosis can occur?
COPD patients may receive inappropriate treatments like too much inhaled steroid and a lack of anti-cholinergic therapy
126
Other than smoking cessation, what lifestyle change should occur & why?
Dietary advice is also important:
Overweight - sensible weight-reducing diet & exercise
Underweight - dietary supplementation may be considered in late-stage COPD if patient has become severely underweight due to massive hyperventilation
127
What is the final stage of COPD and what occurs from this?
Respiratory failure. Lungs are damaged, levels of oxygen are low, CO2 builds up in bloodstream. Patients need palliative care to make them more comfortable in the end stages of the disease.
128
What are first-line maintenance treatment for stable COPD and how do they help?
Inhaled bronchodilators (relievers) as they 'open' the airways, improving the degree of obstruction to some extent and help lungs to empty on expiration
129
Which treatments do NICE recommend starting with as an as-needed basis for the relief of breathlessness and exercise limitation?
Either a SABA or SAMA
130
What is used when patients remain breathless or have exacerbations despite using short-acting bronchodilators like SABAs or SAMAs?
Maintenance therapies (LAMA or LABA) with long-acting bronchodilators & potentially ICS
131
Airway obstruction treatments for mild & moderate to severe obstruction:
Mild - LABA or LAMA
Moderate to severe - LABA/LAMA combination
132
What happens if symptoms like breathlessness & have exacerbations continue on LABA?
LABA/ICS combination therapy
133
What happens if LABA/ICS is not tolerated by the patient (ICS declined or not tolerated)?
LABA/LAMA combination (e.g. indaceterol / glycopyrronium)
134
What happens for those who remain breathless or have exacerbations despite maintenance therapy with a LAMA or LABA/ICS?
Triple therapy with the addition of a LABA/ICS combination inhaler should be considered
135
As therapy is escalated, patients may continue to use a SABA for symptom relief alongside all inhalers, but SAMAs should not be continued when other muscarinic antagonists are prescribed.
136
When should theophylline (oral bronchodilator) be used & importance of this?
After a trial of short-acting bronchodilators and long-acting bronchodilators, or in patients who are unable to use inhaled therapy, as there is a need to monitor plasma levels and interactions. This is important as the toxic level of theophylline is only just
above the dose that is needed for it to work effectively.
137
What is another treatment option for patients with severe COPD & hypoxaemia?
Long-term oxygen therapy (LTOT). Breathing supplemental oxygen for 15hrs a day, but 20hrs has greater benefits.
138
When does respiratory failure occur?
When it fails in one or both of its gas exchange functions: oxygenation or carbon dioxide removal
139
While acute respiratory failure is characterised by life-
threatening changes in arterial blood gases and acid alkali status, the signs of chronic respiratory failure are less dramatic and may not be as obviously apparent.
140
How can respiratory failure be characterised?
Hypoxaemic (Type 1) (low blood oxygen concentration) or hypercapnic (Type 2) (too much CO2 in blood). May either be acute or chronic.
141
Which is the most common type of respiratory failure & what do they generally all involve & example?
Hypoxaemic - T1
Generally involves fluid in the lungs
Pneumonia
142
Hypercapnic respiratory failure (type II) is also known as hypercapnic acidosis as carbon dioxide is acidic. Hypoxaemia is common in patients with hypercapnic respiratory failure who are breathing normal air. The pH depends on the level of bicarbonate which, in turn, is dependent on the length of time that the hypercapnia lasts. What are common causes?
Drug overdose & severe airway disorders (e.g. COPD)
143
What is the treatment for respiratory failure? (2)
Correcting blood gas balance followed by treatment for the underlying condition which led to the respiratory failure
144
Acute hypercapnic respiratory failure develops over minutes to hours; the high level of carbon dioxide
in the blood leads to a pH that is less than 7.4. Chronic respiratory failure develops over several days or longer; this allows for the kidneys to compensate for the pH which is usually only slightly decreased.
145
What is meant by interstitial lung disease (ILD)?
Also known as diffuse parenchymal lung disease (DPLD). A collective term that covers a heterogenous group of lung diseases affecting the interstitium.
146
Interstitium:
The tissue and space around the air sacs of the lungs
147
Prolonged ILD results in...what is this as well?
Pulmonary fibrosis - lungs become less efficient at taking up oxygen into the bloodstream from air breathed in
148
Common symptoms of pulmonary fibrosis: (2)
Breathlessness & persistent cough
149
Two tests to determine ILD:
CT scan & X-ray
150
For most types of ILD the cause is unknown or idiopathic, but for some cases a specific cause can be identified. But, what is one of the most common identifiable causes of ILD & what are these known as?
Exposure to occupational and environmental agents, especially to inorganic or organic dusts.
Pneumoconioses
151
As we breathe in, particles of dust in the air are filtered off by the nasal hairs. Others, which enter through the mouth, are deposited in the upper respiratory tract. Smaller particles tend to settle in the mucus covering the bronchi and bronchioles and are then wafted upward by tiny hairs (cilia) towards the throat. They are then coughed or spat out, though some may be swallowed. Very small particles are more likely to reach the lung tissue.
152
Respirable dust is the dust in the air which on inhalation may be retained by the lungs. It is capable of penetrating deep into the alveoli because of the fine dust particle size. The amount of dust deposited depends on the duration of exposure, the concentration of dust in the respired air, the volume of air inhaled per minute and the nature of the breathing. Slow, deep breaths are likely to deposit more dust than rapid, shallow breathing.
153
What are two causes of pneumoconiosis?
Benign - inhalation of metal dusts like iron, tin, and barium. Causes small structural changes in lungs. Detected by X-ray.
Symptomatic - coal dust, silica, and asbestos. Symptoms of a cough and breathlessness develop usually after many years of exposure, but only in the later stages of disease.
154
Common cold is probably the most common respiratory infection. Most colds caused by viruses like rhinoviruses. When do symptoms appear?
48hr-72hr after initial viral exposure
155
Two complications of common cold:
Sinusitis
Otitis media (middle ear infection)
156
Treatments of common cold: (4)
Paracetamol
Fluids
Decongestants
Bed rest
157
Sinusitis is an accute inflammatory condition as a result of another infection or allergen. What can both these be?
Quite often the common cold or in some cases, allergic rhinitis (hayfever)
158
Common bacteria involved in sinusitis:
Haemophilus influenza. Viruses can also cause the condition.
159
Which sinuses are commonly involved?
Paranasal sinuses like the maxillary sinuses, and the ethmoid sinuses
160
Symptoms of sinusitis & why:
Pain, pressure, and tenderness over affected sinuses. Due to increased mucous secretion.
Increased mucus secretion → blocked sinus drainage → mucus buildup → increased pressure inside sinuses + inflamed, sensitive sinus lining → pain, pressure, and tenderness over affected areas.
161
Treatment for sinus pain and treatment for mucus flow:
Analgesics (something to cause pain-relief) & decongestants
162
What treatment can be used if a bacterial infection is involved?
An antibiotic like amoxicillin
163
How long does acute sinusitis last and what happens if it does not clear up?
Develops quickly and lasts 1-3 weeks. Severe sinusitis is uncommon.
Becomes a chronic condition if uncleared & symptoms may continue even after infection has gone.
164
What is diagnosis based on?
Symptoms.
There may be an underlying problem such as nasal polyps or dental infection in people who suffer from chronic sinusitis.
165
Who are most commonly affected by otitis externa/media (outer/middle)?
Young children
166
Which is a bacteria commonly associated with otitis externa & cause of development?
Staphylococcus aureus
Trauma, high temperatures, humidity, and allergy play a role in development
167
Effective treatment for otitis externa:
Topical antibiotics in the form of ear drops
168
Two common bacteria involved in otitis media:
Streptococcus pneumonia and Haemophilus influenza
169
Otitis media will commonly follow a cold, and will cause severe pain as the pressure builds up behind the eardrum. Topical and oral painkillers are used to ease the pain and amoxicillin is an effective antibiotic
treatment.
170
What is pharyngitis & cause?
Inflammation of the pharynx caused by bacterial or viral infection. Most cases are due to viral infections, accompanying a cold.
171
Symptoms of pharyngitis: (3)
Malaise or headache
Exudate covering tonsils
Sore throat (described as scratchy)
172
Treatment for pharyngitis:
Depends on bacteria involved, but, penicillin is commonly used
173
Most common cause of epiglottitis:
Haemophilus influenza - causes inflammation of epiglottis
174
Symptoms of epiglottitis: (4)
Sudden fever
Sore throat
Dysphagia (difficulty swallowing)
Drooling
175
It is considered a medical emergency as the inflammation causes airways to become blocked. Treatment for epiglottitis:
Hospitalisation and treated with adrenaline as well as antibiotic therapy
176
Bronchitis (and bronchiolitis involve inflammation of the bronchial tree) is the result of:
An upper respiratory infection and can result from other diseases like flu, rubella, and scarlet fever
177
Chronic bronchitis with a continuing and persistent cough and excessive, virulent sputum production can be due to a combination of factors, such as...(2)
Smoking
Bacterial infections such as Haemophilus influenzae
178
Treatment for bronchitis: (3)
Corticosteroids
Bronchodilators
Antibiotics
179
What causes bronchiolitis, common in infants and children, the viral respiratory disease?
Respiratory Syncytial Virus (RSV). Common cold & cough precede the onset of bronchiolitis usually.
180
Symptoms of bronchiolitis:
Fever, wheezing, or an actual lack of breathing sounds may occur. Can lead to respiratory failure and death.
181
What is pneumonia & its cause:
An inflammatory disease which can affect either/both the lungs. Normally caused by an infection.
182
Terms such as lobar pneumonia, bronchopneumonia and double pneumonia – all referring to the same condition – are used. The causes and treatments are the same.
183
What occurs on an anatomical level?
Alveoli become inflamed & fill up with fluid
184
Symptoms of pneumonia:
Coughing, fever, breathing difficulty
185
Diagnosis can sometimes be difficult as there are other conditions which it shares symptoms with, eg asthma, bronchitis and the common cold. A chest X-ray will show how much the lungs are affected.
186
Which bacterium most commonly causes pneumonia?
Streptococcus pneumonia
However, there are many different types of bacteria and viruses that can lead to pneumonia, including
Haemophilus influenza and Mycoplasma pneumonia.
187
Which individuals are more likely to be hospitalised?
Babies, young children, the elderly, smokers, and people with immunocompromised systems like AIDS sufferers
188
How can mild pneumonia be treated?
Normally at home with fluids, rest, and antibiotics
189
How can severe pneumonia be treated & why?
Patients are hospitalised as complications can occur including septicaemia, lung abscesses, and respiratory failure
190
Which bacterium causes tuberculosis (TB) & its transmission?
Mycobacterium tuberculosis through inhaling tiny droplets from the coughs or sneezes of an infected person
191
Where does TB mainly affect but which other two parts can it also affect?
Lungs. Bones & nervous system.
192
TB that affects the lungs is the only form of the condition that is contagious and usually only spreads after prolonged exposure to someone with the illness.
193
Symptoms of TB:
Fever
Weight loss
Loss of appetite
Tiredness & fatigue
Night sweats
Persistent cough for more than three weeks that brings up phlegm, this may be bloody
194
If the immune system fails to kill or contain the infection, it can spread to the lungs or other parts of the body, and symptoms will develop within a few weeks or months. Patients are described as having active TB.
195
What is meant by having latent TB & why is it still dangerous?
Latent TB = the immune system cannot kill the bacteria but manages to prevent it from spreading in the body, no symptoms will develop.
Latent TB can still develop into active TB infection at a later date. Estimated 1/3 of global population is infected with latent TB. 10% of these develop active TB.
196
Treatment for TB:
Course of antibiotics for 6-18 months. Several antibiotics may be required as some forms of TB are resistant to certain antibiotics.
197
Prevention of TB:
BCG vaccine. Effective for 8/10 people who are given it. BCG vaccine only recommended for people at a greater risk of developing TB.
