RESP Flashcards
1
Q
What is pneumonia?
A
Inflammation of lung parenchyma
2
Q
Who is most at risk of developing pneumonia?
A
- Infants and the elderly
- COPD and certain other chronic lung diseases
- Immunocompromised
- Nursing home residents
- Impaired swallow (neurological conditions etc.)
- Diabetes
- Congestive heart disease
- Alcoholics and intravenous drug users
3
Q
What viruses can cause pneumonia?
A
Adenoviruses, influenza A and B, measles, VZV.
4
Q
Describe in 3 steps the pathogenesis of pneumonia.
A
- Bacteria translocate to normally sterile distal airway.
- Resident host defence is overwhelmed.
- Macrophages, chemokines and neutrophils produce an inflammatory response.
5
Q
Describe the process of pneumonia resolution?
A
Bacteria are cleared and inflammatory cells are removed by apoptosis.
6
Q
What can cause pneumonia to be severe?
A
- Excessive inflammation.
- Lung injury.
- Resolution failure.
7
Q
What protective features does the respiratory tract have against pathogens?
A
Teeth, commensal bacteria, swallowing reflex - epiglottis closes respiratory tract, mucociliary escalator, coughing and sneezing etc.
8
Q
What symptoms might you see in someone with pneumonia?
A
- Fever/sweats/rigors (infecion)
- Cough w/ rusty sputum (s. pneumoniae)
- SOB and pleuritic chest pain
- weakness/malaise
9
Q
What signs might you see in someone with pneumonia?
A
- Signs of infection
- raised heart rate,
- raised respiratory rate,
- low blood pressure
- fever
- dehydration - Signs of lung consolidation on percussion and auscultation
- Dull to percussion
- Decreased air entry
- Bronchial breath sounds
- Crackles ± wheeze
- Increased vocal resonance
± Hypoxia and signs of respiratory failure especially if chronic lung disease or severe pneumonia
10
Q
What investigations would you perform on someone with suspected pneumonia?
A
- CXR - look for air bronchogram in consolidated area.
- FBC (look at WBC’s).
- U+E.
- Liver function tests.
- CRP (marker of inflammation).
- Pulse oximetry
- Microbiology: sputum culture, blood culture, serology etc.
11
Q
What is CURB65 used for?
A
It is a way of assessing the severity of community acquired pneumonia. It predicts mortality.
12
Q
What does CURB65 stand for?
A
Confusion. Urea >7mmol/L. RR >30/min. BP reduced - systolic <90mmHg, diastolic <60mmHg. Age >65.
13
Q
Why is CRB65 often used in the community?
A
Because facilities to measure urea are often not available.
14
Q
Name 2 bacteria that are common causes of pneumonia?
A
- Streptococcus pneumoniae.
- Haemophilus influenzae.
(Legionella’s - back from spain with CI)
15
Q
Describe s.pneumoniae.
A
Gram positive cocci chain. Alpha haemolytic and optochin sensitive.
16
Q
Describe haemophilus influenzae.
A
Gram negative bacilli.
17
Q
What antibiotic would you give to someone with haemophilus influenzae?
A
Co-amoxiclav or doxycycline.
18
Q
What groups of people may develop pneumonia caused by klebsiella pneumoniae?
A
- Homeless people.
- Alcoholics.
- People in hospital.
19
Q
What kind of bacteria is klebsiella pneumoniae?
A
Gram negative bacilli.
20
Q
Name 3 groups of people who might be at risk of hospital acquired pneumonia.
A
- Elderly.
- Ventilator associated.
- Post operative patients.
21
Q
What is the treatment for someone with mild pneumonia (a CURB65 score of 0-1)?
A
PO amoxicillin.
22
Q
Where should someone with mild pneumonia (a CURB65 score of 0-1) be treated?
A
In the community.
23
Q
What is the treatment for someone with moderate pneumonia (a CURB65 score of 2)?
A
PO amoxicillin and clarithromyocin.
24
Q
Where should someone with moderate pneumonia (a CURB65 score of 2) be treated?
A
In hospital.
25
What is the treatment for someone with severe pneumonia (a CURB65 score of >3)?
IV co-amoxiclav and clarithromyocin.
26
A 66 y/o patient presents to you with fever and a productive cough. On examination you notice they are their confused. Their vital signs are: RR - 35; BP - 80/55 and HR: 130. You measure their urea and it comes back at 8mmol/L.
a) What is this patients CURB65 score?
b) Where should they be treated?
c) Describe the treatment for this patient.
a) Their CURB65 score is 5.
b) This patient should be treated in hospital and admitted to critical care.
c) The patient should be given IV clarithromyocin and co-amoxiclav.
27
Give 2 potential complications of pneumonia.
1. Empyema.
| 2. Lung abscess.
28
Who would be eligible for having the vaccine for pneumonia? What is the vaccine?
Polysaccharide Pneumococcal Vaccine
- >65 years
- splenic dysfunction,
- immunocompromised
- chronic medical condition
29
How do you differntiate between HAP and CAP?
Acquired at least 48 hours after hosp. admission
30
How is Hospital Aqcuired Pneumonia diagnosed?
1. new fever
2. purulent secretions
3. New radiological infiltrates
4. New leukocytosis / CRP increase
5. plus increasing O2 requirements
31
A lady who has recently had pneumonia presents to you with SOB and chronic cough. She is producing copious amounts of purulent sputum. What is the likely diagnosis?
Bronchiectasis.
32
What antibiotic might be used against less common 'atypical' pathogens responsible for causing pneumonia?
Macrolides like clarithromyocin as they are often resistant to beta lactams.
33
How can less common 'atypical' pathogens responsible for causing pneumonia be identified?
They are hard to grow in culture and so serology and antigen tests are often used.
34
Name 3 less common 'atypical' pathogens that can be responsible for causing pneumonia.
1. Mycoplasma pneumoniae.
2. Chlamydia psittaci/pneumoniae.
3. Coxiella burnetti.
4. Legionella pneumophilia.
35
Aside from antibiotics, what else would you prescribe to patients admitted to the hospital with pneumonia?
ANALGESICS
| LMWH if inpatient >12hrs
36
A patient comes in with bilateral lymphadenopathy. Give 3 conditions that you would include in your differential diagnosis?
1. Local infection e.g. tonsilitis/TB.
2. Lymphoma.
3. Sarcoidosis.
37
Where are a high proportion of cases of TB found?
The indian sub continent e.g. India, Bangladesh, Pakistan etc.
38
Give 5 risk factors for TB.
1. If you live in a high prevalence area.
2. IVDU.
3. Homeless.
4. Alcoholic.
5. HIV+.
39
How is TB transmitted?
Aerosol transmission - mycobacterium TB bacilli are inhaled and enter the lung.
40
Describe pulmonary infection of TB.
Bacilli settle in lung apex. Macrophages and lymphocytes mount an effective immune response that encapsulates and contains the organism forever. (granuloma formation)
41
Why are mycobacteria resistant to gram staining?
High lipid content with mycolic acids in cell wall
42
Describe the microorganism that causes TB?
MYCObacteria, gram negative acid fast bacilli
43
Describe the pathogenesis of pulmonary TB disease.
1. Bacilli and macrophages form primary focus (ghon focus).
2. Mediastinal lymph nodes enlarge.
3. Primary focus and enlarged lymph nodes = primary complex. (ghon complex)
4. Granuloma develops into a cavity.
5. The cavity is filled with TB bacilli - these are expelled when the patient coughs.
44
TB disease: Where in the lung is a granuloma cavity most likely to develop?
Most likely to develop in the apex of the lung as there is more air and less blood supply/immune cells.
45
Presentation of TB: what systemic symptoms might you see?
1. Weight loss.
2. Night sweats.
3. Anorexia.
4. Malaise.
46
Presentation of TB: what pulmonary TB symptoms might you see?
1. Cough.
2. Chest pain.
3. Breathlessness.
4. Haemoptysis.
47
What might you see on a CXR taken from someone with TB?
1. Consolidation.
2. Collapse.
3. Pleural effusion.
48
Name 6 places where TB might spread to?
1. Bone and joints - pain and swelling.
2. Lymph nodes - swelling and discharge.
3. CNS - TB meningitis.
4. Miliary TB - disseminated.
5. Abdominal TB - ascites, malabsorption.
6. GU TB - sterile pyuria, WBC in GU tract.
49
What test might you do to diagnose latent TB?
Mantoux test - stimulates type 4 hypersensitivity reaction.
50
How can TB be prevented?
1. Active case finding - reduce infectivity.
2. Detect and treat latent TB.
3. Vaccination - BCG.
51
What is the gold standard for diagnosing TB?
SPUTUM TEST
(has to be repeated 3 times)
- would also see gohn complex on x ray
52
What are the different stages of TB?
Initially ACTIVE phase: bacterium are multiplying, not everyone has symptoms but can be fever, night sweats, weight loss, bloody sputum
LATENT phase: bacterium are no longer multiplying - 90% of people will remain asympotmatic
53
What is a gohn complex?
Combination of gohn focus (bacteria and macrophages forming a granuloma) and mediastinal enlarged lymph nodes
54
What happens if the bacteria do not stay contained within the gohn focus?
bacteria disseminate throughout the body causing MILIARY TB
55
What is the treatment for TB? How long do you need to take the medication for?
```
RIPE
R- rifampicin (6 months)
I - isoniazid (6 m)
P -pyrazinamide (2 m)
E -ethambutol (2 m)
```
56
What are the problems associated with drug resistance in TB treatment?
1. TB becomes more difficult to treat.
2. Medication course > 20 months.
3. Increased risk of side effects.
4. Increased relapse rate.
57
Why does TB treatment need to last for 6 months?
TB treatment lasts for at least 6 months to ensure all the dormant bacteria have 'woken up' and been killed.
58
Compliance in taking TB medication is critical. Why?
Resistance and relapse may be likely if the patient is non-compliant
59
Give side effects for each of the TB medications
Rifampicin - red urine/sweat/tears
Isoniazid - peripheral neuropathy
Pyrazinamide - hepatitis
Ethambutamol - optic neuritis
60
Name 2 upper respiratory tract infections.
1. Common cold: caused by rhinovirus.
| 2. Sore throat: caused by adenoviruses, EBV.
61
What is the centor criteria?
The likelihood of a sore throat being due to bacterial infection. If 3 or 4 of Centor criteria are met, the positive predictive value is 40% to 60%
- Tonsillar exudate
- Tender anterior cervical adenopathy
- Fever over 38°C (100.5°F) by history
- Absence of cough.
62
Are URTI more likely to be bacterial or viral?
Viral
63
What is cystic fibrosis?
An autosomal recessive disorder in which CFTR channels are faulty leading to thick mucus clogging ducts.
64
State why cystic fibrosis increases the viscosity and tenacity of the bronchial mucus?
Failure to excrete Cl- leads to Na+ retention. This then leads to H2O retention.
65
Describe the pathogenesis of cystic fibrosis.
There is a defect in chromosome 7 coding CFTR protein. Cl- transport is affected and there is production of thickened mucus secretions.
66
When does CF present?
In childhood
67
What are the signs and symptoms of CF?
Signs: steatorrhea, children with a failure to thrive, finger clubbing, rectal prolapse
Symptoms: heavy mucus production, cough
68
How would you test for CF?
1. FAECAL ELASTASE in newborns (marker of pancreatic damage caused by CF).
2. Sweat test: measure the amount of salt collected from the skin.
Genetics testing
69
Give 4 potential complications of CF
1. Infertility
2. Pancreatitis
3. RTI
4. Bronchiectasis
5. Malnutrition
6. DM
70
How do you manage CF?
1. Prevention of infection e.g. vaccination.
2. Segregation to prevent spread.
3. Surveillance - monitor FEV1.
4. Enzyme supplements for pancreatic insufficiency.
5. Anti-pseudomonal antibiotic therapy.
6. Physical therapies e.g. airway clearance and exercise.
7. Supporting therapies e.g. ensure a good diet.
71
Define inspiratory reserve volume (IRV).
The additional volume of air that can be forcibly inhaled after a tidal volume inspiration.
72
Define expiratory reserve volume (ERV).
The additional volume of air that can be forcibly exhaled after a tidal volume expiration.
73
Define forced vital capacity (FVC).
The maximum volume of air that can be forcibly exhaled after maximal inhalation.
74
Define total lung capacity.
The vital capacity plus the residual volume. It is the maximum amount the lungs can hold.
75
Define residual volume (RV).
The volume of air remaining in the lungs after a maximal exhalation.
76
Define functional residual capacity (FRC).
The volume of air remaining in the lungs after a tidal volume exhalation.
77
Define tidal volume (TV).
The volume of air moved in and out of the lungs during a normal breath.
78
Define FEV1.
The volume of air that can be forcibly exhaled in 1 second.
79
What 2 equations can be used to work out TLC?
1. TLC = VC + RV.
| 2. TLC = TV + FRC + IRV.
80
What is a normal tidal volume?
500ml.
81
What equation can be used to work out FRC?
FRC = ERV + RV.
82
Define peak expiratory flow (PEF).
The greatest rate of airflow that can be obtained during forced expiration. Age, sex and height can all affect PEF.
83
What is the transfer coefficient?
The ability of O2 to diffuse across the alveolar membrane
84
How can you find the transfer coefficient?
Low dose CO is inspired, the patient is asked to hold their breath for 10s at TLC, the amount of gas transferred is measured.
85
Name 3 diseases that might have a low transfer coefficient.
1. Emphysema.
2. Anaemia.
3. Fibrosing alveolitis.
86
Name a disease that might have a high transfer coefficient.
1. Pulmonary haemorrhage.
87
How is airway obstruction defined by spirometry?
- FEV1 < 80% predicted.
| - FEV1/FVC < 0.7.
88
What happens to the FVC and FEV1/FVC ratio in a restrictive lung disease?
- FVC reduced.
| - FEV1/FVC ratio normal.
89
How would you describe the PEF for asthma.
variable
90
What factors can commonly exacerbate asthma?
1. Allergens.
2. Viral infections.
3. Cold air.
4. Exercise.
5. Stress.
6. Cigarette smoke.
7. Drugs e.g. aspirin.
91
How would you describe the airways in asthma?
Hyper-reactive. This leads to inflammation.
92
What is allergic asthma?
When an innocuous allergen triggers an IgE mediated response. The immune recognition processes are faulty and so there is increased IgE, IL-3,4 and 5 production.
93
What is non-allergic asthma?
Airway obstruction induced by exercise, cold air and stress.
94
Describe the process of IgE binding to and activating mast cells.
IgE binds to the high affinity receptor on the mast cell surface. There is cross-linking and biochemical cascades. The mast cells are sensitised and there is degranulation.
95
What might be released on mast cell degranulation?
1. Pre-formed histamine.
2. Newly synthesised eicosanoids e.g. cysteinyl leukotrienes (cys LTs) and prostaglandin D2.
3. Cytokines e.g. IL-3,4,5.
96
Give 3 reasons why the airways hyper-reactive in asthmatics?
1. Inflammatory infiltrate.
2. Eosinophils.
3. Epithelium destruction gives easier access to bronchoconstrictors.
97
What are the 2 principles of asthma treatment?
1. Alleviate symptoms.
| 2. Target inflammation.
98
What are the main cells responsible for inflammation in asthma?
Mast cells and eosinophils.
99
What is the advantage of having inhaled medications in the management of asthma?
Inhaled medications are more likely to reach the target sites and there is reduced chance of side effects.
100
A young person presents to you with breathlessness, wheeze and cough. There appears to be inflammation of the airways. When you do a spirometry test the results are variable. You ask the patient to do a peak flow diary and the results of this show diurnal variation. Is the patient likely to have asthma or COPD?
They are likely to have asthma!
Although breathlessness, wheeze and cough are symptoms of both asthma and COPD the fact that the spirometry results are variable is a large indication that this person has asthma!
The patient is also young and COPD tends to be more common in older people.
101
What 2 types can asthma be divided into?
1. Allergic asthma (extrinsic); atopic. IgE and mast cell involvement.
2. Non allergic asthma (intrinsic).
102
Describe asthma.
An inflammatory disease characterized by hyper-responsive airways. Airway obstruction is reversible. There is inappropriate smooth muscle contraction.
103
Extrinsic asthma: what happens when IgE binds to mast cells?
Vasoactive substances are released causing bronchoconstriction, oedema, bronchial inflammation and mucus hyper-secretion.
104
What occupations may be associated with an increased risk of developing asthma?
1. Paint sprayers - exposure to fumes.
2. Animal breeders.
3. Bakers.
4. Laundry workers.
105
What are the symptoms of asthma?
1. Breathlessness.
2. Diurnal variation - often worse in the morning.
3. Cough.
4. Episodic wheeze.
5. Chest tightness.
106
What investigations might you do on someone to determine whether they have asthma?
1. PEFR.
2. Spirometry should show an obstructive pattern; FEV1 < 80%, FEV1/FVC < 0.7, PEFR - variable.
3. Test for atopy; RAST, skin prick test.
3. CXR.
4. Eosinophil count.
5. O2 saturation.
107
How can reversibility be tested in asthma?
When given a beta agonist there will be a 400ml increases in FEV1 OR a 20% improvement in PEFR.
108
What tool can be used to assess the severity of asthma?
RCP3
- Recent nocturnal waking?
- Usual asthma symptoms during the day?
- Interference with ADL's?
May also want to ask about whether the patient has used any rescue medications.
109
What is the function of RCP3?
It is used to assess the severity of asthma.
110
Describe the management/treatment of asthma.
- Improve control and avoid triggers!
- Smoking cessation is important.
- Beta agonists provide symptomatic relief.
- ICS are anti-inflammatory.
- Sometimes a short course of systemic steroids might be used.
111
Give 5 side effects of systemic steroids.
1. Diabetes.
2. Osteoporosis.
3. Hypertension.
4. Oral candida (oral steroids).
5. Skin thinning.
112
What 4 measurements can be used to diagnose acute severe asthma?
1. RR > 25.
2. HR > 110.
3. PEFR 35-50% predicted.
4. Unable to complete a sentence in one breath
113
What is the first line treatment for acute severe asthma?
Nebulised salbutamol with oxygen.
IV corticosteorids and abx if evidence of infection
114
What percentage of asthma is thought to be caused by occupational factors?
10%
115
What type of T lymphocyte is involved in asthma?
CD4+
116
What are the 3 characteristic features of asthma?
1. Airflow obstruction.
2. Hyper-responsive airways to a range of stimuli.
3. Bronchial inflammation.
117
Describe the process of airway remodelling in asthma.
1. Hypertrophy and hyperplasia of smooth muscle cells narrow the airway lumen.
2. Deposition of collagen below the BM thicken the airway wall.
3. Eosinophils also play a role in remodelling.
118
Give 3 histo-pathological changes that occur in asthma.
1. Basement membrane thickening.
2. Epithelium metaplasia; increased no. of goblet cells leads to mucus hypersecretion.
3. Increase in inflammatory gene expression on many cell types.
119
What are the signs of asthma?
1. Secretions.
2. Obstructive spirometry.
3. Variable PEFR.
4. Reversibility when given beta-2-agonist, FEV1 > 20%.
5. Diurnal variation.
120
What are the exacerbating factors for asthma?
```
Infection
Allergens
Pollution
Smoking
Stress
Some medications (ACE I, beta blockers, NSAID’s)
Cold weather
Exercise
Being overweight
```
121
What is the gold standard test for asthma? How is it differentiated from COPD?
SPIROMETRY = FEV1/FVC<70%
To distinguish this from COPD reversibility testing is performed – the patient is given a bronchodilator to take and their peakflow is taken again 20 minutes later. The FEV1 will improve by more than 15% in a patient with asthma
122
What is the treatment for asthma?
1. SABA e.g. salbutamol
2. Corticosteroid
3. Corticosteroid + LABA
4. Higher dose CS
123
What is atopy?
Atopy is the tendency to develop IgE mediated reactions to common aeroallergens
124
What symptoms do asthma and COPD patients have in common?
Wheezing
Chest tightness
SOB
125
How does an asthmatics cough differ from a COPD cough?
COPD - productive in the morning
| Asthma - dry at night
126
How does SOB differ between asthma and COPD?
COPD more of a relentless progressive SOB with
| wheeze whereas asthma has epsiodic attacks with exposure to allergen
127
Who is at risk of asthma death?
* ≥3 classes of treatment
* recent admission/ frequent attender
* previous near-fatal disease
* brittle disease
* psychosocial factors
128
Give 4 DdX for asthma
1. Bronchiectasis
2. CF
3. COPD
4. PE
129
Give an example of an occupational asthma.
Baker's asthma; flour being the harmful allergen.
130
How might you diagnose someone with having occupational asthma?
1. Do a PEFR test at their place at work and take a history to determine whether their symptoms are worse at work.
2. Serum immunology looking for IgE to a particular workplace allergen.
131
What is COPD?
An irreversible obstructive lung disease
132
What 3 diseases does COPD describe?
1. Emphysema
2. Chronic bronchitis
3. Chronic Obstructive Airway Disease
133
Why is COPD an example of type 2 resp failure?
It results in REDUCED O2 and INCREASED CO2 in the blood
| 2 things go wrong
134
What is the affect of COPD on residual volume and total lung capacity?
RV and TLC are increased.
135
What are the main cells responsible for inflammation in COPD?
Neutrophils and macrophages.
136
What are the main causes of COPD?
SMOKING!
Also alpha 1 trypsin deficiency, cystic fibrosis, IV drug use (particularly cocaine), industrial exposure to irritants e.g. mining.
137
What is chronic bronchitis?
Exposure to irritants and chemicals e.g. smoke -> hypertrophy and hyperplasia of mucus secreting glands -> increased mucus -> airway obstruction. Neutrophil and macrophage involvement -> bronchi become inflamed.
138
How is airway obstruction defined by spirometry?
- FEV1 < 80% predicted.
| - FEV1/FVC < 0.7.
139
Would a patient with emphysema be a 'pink puffer' or a 'blue bloater'?
They would be a 'pink puffer'.
These patients often present with symptoms of weight loss; breathlessness; barrel chest; pursed lip breathing; CO2 retention.
140
Would a patient with chronic bronchitis be a 'pink puffer' or a 'blue bloater'?
They would be a 'blue bloater'.
These patients often present with symptoms of chronic cough, phlegm, cor pulmonale, hypoxia and hypercapnia, wheeze, crackles and cyanosis
141
What scale might be used to assess breathlessness?
MRC dyspnoea scale; scored from 1-5.
| 5 statements that describe the entire range of respiratory disability from none to almost complete incapacity
142
Aside from COPD, what might be a differential diagnosis for breathlessness?
1. Heart failure.
2. PE.
3. Pneumonia.
4. Lung cancer.
143
Shortness of breath can lead to exercise limitation. Give 3 potential consequences of this.
1. Muscle wasting.
2. Depression and anxiety.
3. Disability
144
Give 3 advantages and 1 disadvantage of using ICS in the treatment of COPD?
Advantages:
1. Improve Q.O.L.
2. Improve lung function.
3. Reduce the likelihood of exacerbations.
Disadvantages:
1. There is an increased risk of pneumonia.
145
Define exacerbation.
An acute event characterised by worsening symptoms beyond normal day to day variation. It often leads to a change in medication.
146
Give 5 potential consequences of exacerbations of COPD/asthma.
1. Worsened symptoms.
2. Decreased lung function.
3. Negative impact on Q.O.L.
4. Increased mortality.
5. Huge economic cost.
147
What is the treatment for an exacerbation of COPD?
1. Oxygen.
2. Bronchodilators.
3. Systemic steroids.
4. Antibiotics if there is breathlessness and sputum production.
148
What are the aims of treatment for exacerbations of COPD?
1. Minimise the impact of the current exacerbation.
| 2. Prevent subsequent exacerbations.
149
Give 3 ways in which subsequent exacerbations be prevented.
1. Smoking cessation.
2. Vaccination.
3. LABA/LAMA/ICS.
150
How would you distinguish the cause for COPD as being an alpha 1 trypsin deficiency?
- the individual will be young
- have a family history of COPD (again in young individuals)
- have liver disease
- in A1ATD the lower acinar of the lungs are affected, whereas those at the top are affected in COPD (as the irritants don’t get as far down through the lungs).
151
What symptoms would a COPD patient have?
1. Asymptomatic for many years, usually until its too late
2. SOB
3. Lack of energy/ tired (this is because the cells are not getting the oxygen that they need for energy)
4. chronic cough
5. wheezing
152
What signs would a COPD patient have?
1. Barrel shaped chest
2. Ankle swelling
3. Sputum and a chronic cough (is this sputum is any colour other than clear or white it means the individual has got an infection – need to get some antibiotics)
4. Cyanosis – blue lips and skin
153
Why would a COPD patient have ankle swelling?
Caused by resulting heart failure
(pulmonary arteries constrict creating pulmonary hypertension – more effort for the heart to pump blood through the lungs leading to strain on the heart and eventually permanent damage. The heart is also beating faster to try and deliver oxygen around the body as there is less of it).
154
What investigations would you do to diagnose COPD?
1. Spirometry - GOLD STANDARD (FEV1/FVC <70%)
2. CXR - hyperinflation of the lungs, a flattened diaphragm, and a barrel shaped chest.
3. DLCO - patient inhales a fixed amount of CO2 and the amount of CO2 exhaled is measured after a certain time period (reduced in people with COPD as the exchange pathway is impaired)
155
How do you treat COPD?
```
Lifestyle - stop smoking
Pharma
1. SABA (salbutamol)
2. LABA (salmeterol)
3. LABA + corticosteroid
4. LABA + corticosteroid + LAMA
Iatrogenic
O2 therapy (aim for sats 88 - 92%)
```
156
Why do you aim for oxygen therapy of 88-92% saturation?
1. In COPD, patients optimise their gas exchange by HYPOXIC VASOCONSTRICTION leading to altered alveolar ventilation-perfusion (Va/Q) ratios
2. Excessive oxygen administration overcomes this, leading to increased blood flow to poorly ventilated alveoli, and thus increased Va/Q mismatch and increased physiological deadspace
157
What is occupational lung disease?
Caused by inhaling harmful substance in the workplace NOT when present lung condition is worsened by work conditions.
158
Give some common causes of occupational asthma
wood
flour
metalworking fluids
isocyanate paint
159
What are some of the consequences of occupational asthma?
1. ⅓ of OA patients unemployed
2. loss of earnings
3. depression
4. chronic resp ill health
5. compensation
160
Give examples of 4 asbestos related diseases
1. pleural disease/pulmonary fibrosis/cancer
2. pleural plaques (harmless marker of exposure)
3. diffuse pleural thickening (obliteration of costophrenic angle)
4. Asbestosis
5. Mesothelioma
161
What is hypersensitivity pneumonia?
Also known as extrinsic allergic alveolitis
- type 3 or 4 hypersensitivity
- inflammatory response in lungs due to innocuous substances, which tend to be associated to jobs or hobbies
162
What is the management for OLD/ hypersensitivity pneumonia?
AVOID ANTIGEN
| acute = corticosteroids
163
Give 4 ways in which occupational lung disorders can be prevented
1. Risk assessment.
2. Legal requirement under COSHH.
3. Prevent and minimise exposure to harmful substances.
4. Monitor worker's health so health problems can be identified early.
164
What is the epidemiology of lung cancer?
male female 2:1
| 1/3 of all cancer deaths
165
List 4 of the potential causes for lung cancer
1. Cigarettes
2. Occupational
3. asbestos, radon, nickel, chromate, arsenic, uranium….
4. Lung fibrosis
166
Give 2 early symptoms and 2 late symptoms of lung cancer.
1. Early: change in cough, wheeze, hemoptysis.
| 2. Later: weight loss, lethargy.
167
What signs would you see in a patient with lung cancer?
Weight loss, Anaemia, Clubbing, Supraclavicular or axillary nodes
168
What are the two different types of lung carcinoma?
1. Small cell (10-15%)
| 2. Non-small cell (85%)
169
Which type of malignant bronchial tumour tends to have a worse prognosis?
Small cell (late onset and more commonly associated with smoking)
170
Give 3 main cell types that make up non small cell lung cancer?
1. Squamous cell (20%).
2. Adenocarcinoma (40%).
3. Large cell.
171
What does TNM stand for?
1. T: tumour (T1-4).
2. N: nodal involvement (N0-3).
3. M: metastases (M0-1).
- Increased staging = decreased survival.
172
Name 5 places that lung cancer might metastasise to.
1. Bone.
2. Brain.
3. Liver.
4. Lymph nodes.
5. Adrenal glands.
173
What are paraneoplastic syndromes?
Disorders triggered by immune response to a neoplasm.
174
Give 5 examples of paraneoplastic syndromes.
1. Finger clubbing.
2. Anorexia.
3. Weight loss.
4. Hypercalcemia.
5. Hypernatremia.
175
What investigations might you do on someone to determine whether they have lung cancer?
- CXR.
- CT scan.
- Bronchoscopy.
- Surgical and percutaneous biopsy.
- Bloods.
176
It is important to ask a patient if they've had any previous cancers. Name 5 cancers that can spread to the lung.
1. Breast.
2. Prostate.
3. Kidney.
4. Melanoma.
5. Lymphoma.
177
Give an example of a malignant pleural tumour.
Mesothelioma.
178
What can cause pleural tumours?
Occupational - asbestos exposure!
179
What are signs and symptoms of mesothelioma?
1. Breathlessness.
2. Chest pain.
3. Weight loss.
4. Sweating.
5. Abdominal pain.
180
What investigations might you do on someone to determine whether they have mesothelioma?
- CXR.
- CT scan.
- Pleural biopsy.
181
What is the treatment for mesothelioma?
1. Symptom control.
2. Palliative chemotherapy or radiotherapy.
3. Radical surgery (removal of tumour blood supply).
182
How does the treatment differ between local and systemic lung cancer?
- Local: surgery and radiotherapy.
| - Systemic: chemotherapy.
183
Why do lung cancers metastasize quickly?
Due to proximity of medistinum and hilar lymph nodes
184
What are the characteristics of a squamous cell carcinoma?
1. Releases PTH
| 2. Increased production of keratin -> pneumonia
185
What is the characteristic feature of adenocarcinoma?
Generates mucin due to increase in glandular tissue
186
What cell proliferates in small cell carcinoma of lung?
Immature neuroendocrine cells -> secrete ACTH
- > paraneoplastic syndrome
- > cushings- like symptoms
187
How are stage 1/2 lung tumours managed?
Stage I/II -> surgical excision and radical deep x-ray therapy
188
How are stage 3/4 lung tumours managed?
stage III/IV -> Palliative chemotherapy, chemotherapy and radiotherapy, palliative care
189
Define bronchiectasis.
Irreversible and abnormal dilation of the bronchi with chronic inflammatory and fibrotic changes.
190
Why is there an increased risk of infection in bronchiectasis?
1. Excess mucus secretion
2. Loss of cilia so less mucus clearance
3. Difficulty breathing and build up of bacteria
191
Describe the pathogenesis of bronchiectasis.
1. Failed mucocilliary clearance + impaired immune function
2. microbe can easily invade and cause infection.
3. inflammation and progressive lung damage.
4. Bronchitis -> bronchiectasis -> fibrosis.
192
What can cause bronchiectasis?
1. Often post-infective e.g. previous pneumonia, TB or whooping cough infection.
2. Congenital causes e.g. primary ciliary dyskinesia.
3. 50% idiopathic.
4. End stage/ complication of COPD/CF etc
193
Which bacteria might cause bronchiectasis?
1. Haemophilus influenzae.
2. Pseudomonas aeruginosa.
3. Staphylococcus aureus.
194
Give 6 symptoms of bronchiectasis.
1. Chronic productive cough.
2. Recurrent chest infections.
3. Dyspnoea and wheeze.
4. Recurrent exacerbations.
5. Chest pain.
6. Haemoptysis.
195
What investigations might you do on someone to determine whether they have bronchiectasis?
- High resolution CT scan (wide bronchi)
- Spirometry - would be obstructive.
- Sputum culture.
- CXR.
196
What is the treatment/management for bronchiectasis?
1. Education.
2. Smoking cessation.
3. Annual influenza and pneumococcal vaccinations.
4. Antibiotics.
5. Anti-inflammatories.
6. Bronchodilators.
7. Improved mucus clearance e.g. physiotherapy.
197
Bronchiectasis is a disease characterised by irreversible dilation of the bronchi. True or False: spirometry shows an obstruction pattern.
True!
Even though bronchi are dilated there is chronic inflammation, scarring and thickening of the bronchi wall which result in airway obstruction.
198
A lady who has recently had pneumonia presents to you with SOB and chronic cough. She is producing copious amounts of purulent sputum. What is the likely diagnosis?
Bronchiectasis.
199
What is the function of the pleura?
It allows movement of the lung and lung expansion against the chest wall.
200
What produces and reabsorbs pleural fluid?
The parietal pleura. ('attached' to the chest wall)
201
Name 3 diseases associated with the pleura.
1. Pleural effusions.
2. Pleural plaques.
3. Pneumothorax.
202
What is pleural effusion?
Build up of fluid in the pleural space. It limits how much the lungs can expand and therefore impairs breathing.
203
What are the two ways fluid can enter the pleural space?
Transudate and exudate
204
What is transudate and what conditions cause it to enter pleural space?
Excessive Production of Pleural fluid or Resorption is Reduced.
E.g. heart failure, cirrhosis, nephrotic syndrome
205
What is exudate and what conditions cause it to enter pleural space?
Result from damaged pleura.
| E.g. PE, bacterial pneumonia, cancer, viral infection, pancreatitis
206
How might you diagnose pleural effusion?
1. Take a good history.
2. Imaging.
3. Thoracentesis - can tell you transudates v exudates.
207
What signs and symptoms would you observe in pleural effusion?
Signs: reduced chest movement on affected side, reduced breath sounds, dull to percussion
Symptoms: SOB, cough, chest pain
208
How would you distinguish between transudate and exudate in thorancentesis?
```
Transudate = clear
Exudate = cloudy ( >29g/L protein)
```
209
How do you treat pleural effusion?
Aspirate or pleurodesis
210
What is a pneumothorax?
Air in the pleural space which can lead to partial of complete lung collapse.
211
What are the three main types of pneumothorax?
1. Traumatic e.g. stab wound.
2. Spontaneous: can be primary (PSP) or secondary (SSP).
3. Iatrogenic.
212
What is the treatment for a traumatic pneumothorax?
Drainage
213
What are the S&S for pneumothorax?
Signs: low blood pressure, low oxygen levels, diminished breath sounds on the affected side
Symptoms: SOB, sharp, ONE SIDED chest pain, altered consciousness
214
What is a tension pneumothorax?
MEDICAL EMERGENCY
- air moves into pleural space but not out
- trachea deviated towards negative pressure on CXR (away from affected lung)
- insert chest drain
215
Pulmonary embolism: where might an emboli arise from?
Emboli often arise from a dislodged DVT - from ILIOFEMORAL veins.
216
What is the consequence of a small, peripheral PE?
Infarction!
| There is ventilation but no perfusion; dead space.
217
What is the consequence of a large, central PE?
Ischaemia!
| There is resistance to flow which can also result in RHF.
218
What are symptoms of a small, peripheral PE?
- Breathlessness.
| - Pleuritic chest pain.
219
What are symptoms of a large, central PE?
- Severe central chest pain.
| - Pale and sweaty.
220
What investigations might you do in someone to determine whether they have PE?
- CXR.
- ECG.
- D-dimer.
- V/Q lung scan - shows ventilated areas with perfusion defects.
- CTPA - can detect emboli.
221
What is D dimer?
A small protein fragment found after a blood clot is degraded by fibrinolysis.
222
The Wells scoring system is used to work out the probability of a person having a PE. Name 5 factors that the scoring system uses.
1. Clinical signs/symptoms of DVT.
2. HR > 100bpm.
3. Recent immobilisation.
4. Previous DVT/PE.
5. Haemoptysis.
6. Malignancy.
Score >4 - PE likely.
223
Describe the treatment for PE.
1. Thrombolysis is used for a large PE.
2. LMWH (anti-coagulant) and oral warfarin.
3. NOAC (anticoagulant).
4. Analgesia for pain relief.
224
What diseases might be in the differential diagnosis of PE?
1. Asthma.
2. COPD.
3. Pneumonia.
4. MI.
225
Give examples of diseases that lead to V/Q mismatch and so could cause type 1 respiratory failure.
1. Cardiac failure.
2. PE (dead space, V/Q = ∞)
3. Shunt (V/Q = 0)
4. Pulmonary hypertension.
226
Define pulmonary hypertension.
- mPAP > 25mmHg.
| - Secondary RV failure
227
What can cause an increase in mPAP?
Increased resistance to flow.
| Increased flow rate.
228
Give 5 causes of pulmonary hypertension.
1. Hereditary.
2. Idiopathic.
3. Drug use.
4. HIV infection.
5. Pulmonary hypertension secondary to left heart disease (valvular, systolic/diastolic dysfunction).
229
Give 5 symptoms of pulmonary hypertension.
```
Initial symptoms:
1. Dyspnoea on exertion.
2. Lethargy.
3. Fatigue.
4. Syncope.
Symptoms as RV failure develops:
1. Pulmonary oedema.
2. Abdominal pain.
```
230
What investigations might you do in someone to determine whether they have pulmonary hypertension?
1. ECG - see if there's RV hypertrophy.
2. Spirometry.
3. CXR - enlarged proximal pulmonary arteries.
4. Echocardiography.
231
What might you notice in the ECG take from someone with pulmonary hypertension?
There might be signs of RV hypertrophy.
232
What might you notice in a CXR take from someone with pulmonary hypertension?
There might be enlarged proximal pulmonary arteries which taper distally
233
Describe the usual treatment for someone with pulmonary hypertension.
1. Initial treatment is O2.
2. Warfarin (due to risk of thrombosis).
3. Diuretics (for oedema).
4. Ca2+ blockers (pulmonary vasodilators).
5. Treat underlying cause.
234
Why might someone with pulmonary hypertension experience peripheral oedema?
1. Blood accumulates in the pulmonary artery.
2. The RV experiences a greater AFTERLOAD and works harder to get blood out of the ventricle and into the pulmonary artery.
3. There is RV hypertrophy and right heart failure. (COR PULMONALE) This results in peripheral oedema.
235
Why does someone with chronic bronchitis develop cor pulmonale?
There is pulmonary vasoconstriction in the lungs in an attempt to shunt blood to better ventilated alveoli -> pulmonary hypertension -> RHF -> cor pulmonale.
236
What are the 5 major categories of interstitial lung disease?
1. Associated with systemic diseases e.g. rheumatological.
2. Environmental aetiology e.g. fungal, dusts.
3. Granulomatous disease e.g. sarcoidosis.
4. Idiopathic e.g. IPF.
5. Other.
237
Give 4 major signs and symptoms of interstitial lung disease.
1. Cough.
2. Breathlessness.
3. Finger clubbing.
4. Evidence of systemic disease.
238
Would pulmonary function tests taken from someone with interstitial lung disease show a restrictive or obstructive pattern?
They would be restrictive!
| There is decreased gas transfer and a reduction in PaO2.
239
What kind of disease is sarcoidosis?
It is a granulomatous disease!
| It can affect any organ system but typically affects the lungs/lymph nodes.
240
What is the usual treatment for sarcoidosis?
Steroids
241
Give 5 signs of sarcoidosis.
1. Bi-lateral hilar lymphadeonopathy (BHL).
2. Erythema nodosum.
3. Uveitis.
4. Non productive cough, SOB, wheeze.
5. Metabolic affect of sarcoidosis = hyperacalcaemia -> nephrocalcinosis.
6. Arthalgia.
7. Hepatosplenomegaly.
8. Neurological: inflammation of the meninges and seizures.
9. Heart block.
10. Lung fibrosis.
11. Finger clubbing is rare!
242
What is the effect of sarcoidosis on the skin?
Erythema nodosum
243
What is the effect of sarcoidosis on the eyes?
Uveitis.
244
Give a metabolic effect of sarcoidosis.
Hypercalcaemia.
245
What is the effect of sarcoidosis on bone?
Arthralgia.
246
What is the effect of sarcoidosis on the liver?
Hepatosplenomegaly.
247
Give a neurological effect of sarcoidosis.
- Inflammation of the meninges.
| - Seizures.
248
Give 2 diseases that might be in the differential diagnosis of sarcoidosis.
1. Lymphoma.
| 2. Pulmonary TB.
249
Why does TB cause hypercalcaemia?
Granulomatous diseases -> increased vitamin D production and so increased bone resorption, increased absorption from gut and increased re-absorption from kidney.
This is also seen in sarcoidosis.
250
What is Wegener's granulomatosis?
Vasculitis of unknown aetiology. It commonly involves the upper airway and endo-bronchi.
251
What are the symptoms of wegener's granulomatosis?
1. Rhinorrhoea.
2. Nasal mucosa ulceration.
3. Cough.
4. Haemoptysis.
5. Pleuritic chest pain.
252
What would serum tests for someone with Wegener's granulomatosis show?
- C-ANCA and anti-PR3 positive.
