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Respiratory Flashcards

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1
Q

Define inspiratory reserve volume (IRV).

A

The additional volume of air that can be forcibly inhaled after a tidal volume inspiration.

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2
Q

Define expiratory reserve volume (ERV).

A

The additional volume of air that can be forcibly exhaled after a tidal volume expiration.

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3
Q

Define forced vital capacity (FVC).

A

The maximum volume of air that can be forcibly exhaled after maximal inhalation.

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4
Q

Define total lung capacity.

A

The vital capacity plus the residual volume. It is the maximum amount the lungs can hold.

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5
Q

Define residual volume (RV).

A

The volume of air remaining in the lungs after a maximal exhalation.

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6
Q

Define functional residual capacity (FRC).

A

The volume of air remaining in the lungs after a tidal volume exhalation.

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7
Q

Define tidal volume (TV).

A

The volume of air moved in and out of the lungs during a normal breath.

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8
Q

Define FEV1.

A

The volume of air that can be forcibly exhaled in 1 second.

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9
Q

When is FEV1 abnormal

A

When FEV1 is less than 80% if the predicted value = obstruction

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10
Q

Define forced vital capacity

A

Total amount of air a person can exhale after full exhalation

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11
Q

When is FVC abnormal

A

When is is less than 80% of the predicted value

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12
Q

When is obstructive lung disease diagnosed in terms of lung function tests

A

FEV1/FVC <0.7
FEV1 lower than FVC
Suggests that there is some obstruction slowing the passage of air getting out of the lungs

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13
Q

What are the two main obstructive lung diseases

A

Asthma - narrowed airway due to bronchoconstriction

COPD - Chronic airway and lung damage causing obstruction

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14
Q

Describe the lung function test results for restrictive lung diseases

A

FEV1/FVC above 0.7
FVC and FEV1 equally reduced below 80% predicted volume
Restriction to the ability of the lungs to expand and take in air

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15
Q

Define peak expiratory flow (PEF).

A

The greatest rate of airflow that can be obtained during forced expiration. Age, sex and height can all affect PEF.

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16
Q

What is the transfer coefficient?

A

The ability of O2 to diffuse across the alveolar membrane.

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17
Q

How can you find the transfer coefficient?

A

Low dose CO is inspired, the patient is asked to hold their breath for 10s at TLC, the amount of gas transferred is measured.

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18
Q

Name 3 diseases that might have a low transfer coefficient.

A
  1. Emphysema.
  2. Anaemia.
  3. Fibrosing alveolitis.
  4. Pulmonary hypertension
  5. Idiopathic pulmonary fibrosis
  6. COPD
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19
Q

Name a disease that might have a high transfer coefficient.

A
  1. Pulmonary haemorrhage.
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20
Q

What happens in respiratory acidosis

A

Fail to get rid of CO2 resulting in a decrease in pH

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21
Q

What are the causes of respiratory acidosis

A 
Hyperventilation 
COPD
Any cause of respiratory failure 
 - Type 1 = PE 
 - Type 2 = hypoventilation
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22
Q

Describe the renal compensation to respiratory acidosis

A

Kidneys increase H+ secretion in form of NH4+ and will release more HCO3- into the plasma which increases pH

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23
Q

Define respiratory alkalosis

A

Too much CO2 lost resulting in an increased pH as CO2 is lost

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24
Q

What are the causes of respiratory alkalosis

A

CO2 depletion due to hyperventilation
Hypoxia
T1 respiratory failure due to PE

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25
What is the renal compensation for respiratory alkalosis
Kidneys decrease H+ secretion thereby retaining H+ and helping the pH return to normal Decrease in H+ secretion will result in a decrease in HCO3- reabsorption resulting in HCO3- excretion and thus a fall in plasma HCO3-
26
What is metabolic acidosis
Excess acid production resulting in a decrease in pH
27
What are the causes of metabolic acidosis
Renal failure GI HCO3- loss Dilution of the blood Failure of H+ excretion - hypoaldosteornism
28
What is the respiratory compensation to metabolic acidosis
Decrease in pH will stimulate chemoreceptors of the lung resulting in enhanced respiration resulting in a fall in CO2 resulting in a increase in pH
29
What are the causes of a metabolic alkalosis
``` Increase in pH Vomiting (Due to loss of gastric secretions) Volume depletion Alkali ingestion Hyperaldosteronism Hyperkalaemia ```
30
What is the respiratory compensation for metabolic alkalosis
Increase in pH inhibits chemoreceptors of the lung thereby reducing respiration thereby increasing CO2 resulting in a decrease in pH
31
What are the natural defences of the upper respiratory tract against pathogens
Mucosal defences - Cough reflex - Mucus barrier and respiratory cilia - Surface secretions (Defensins and complement) Innate immunity - macrophages - neutrophils Adaptive immunity - B-cells - T cells
32
Name 2 upper respiratory tract infections.
``` Rhinovirus = cold, bronchitis, sinusitis Influenza = flu Coronavirus = colds but sometimes severe respiratory illness Adenovirus = URTI, pharyngitis, bronchitis, pneumonia ```
33
Name some emergency respiratory infections
Severe acute respiratory distress syndromes (SARS) Middle East respiratory syndrome novel coronavirus Avian influenza
34
What viruses can cause pneumonia?
Adenoviruses, influenza A and B, measles, VZV.
35
What are the causative agents of the common cold
Rhinovirus and coronavirus
36
What are the symptoms of rhinitis or sinusitis
``` Blocked/runny nose Sore throat Cough Sneezing Pain, swelling and tendernesss around sinuses Facial pain Fever ```
37
What is the management of rhinitis and sinusitis
Nasal decongestants = xylometazoline Broad spectrum antibiotics = Co-amoxiclav
38
Is sinusitis usually bacterial or viral?
Viral.
39
What are the causative agents of bacterial sinusitis
Streptococcus pneumoniae | Haemophilus influenzae
40
What are the symptoms of bacterial sinusitis
Unilateral pain Purulent discharge Fever
41
What are the complications of sinusitis
Brain abscess, sinus vein thrombosis, orbital cellulitis
42
Is pharyngitis normally caused by bacterial or viral infection?
Viral e.g. rhinovirus, adenovirus etc. | Rarer causes = EBV and acute HIV
43
What bacteria might sometimes cause pharyngitis?
Streptococcus pyogenes. | Rare = mycoplasma pneumoniae, N. gonorrhoea, C.diptheriae
44
What are the symptoms of pharyngitis
``` Painful throat Dry/scratchy throat Pharyngeal erythema Dry cough lymphadenopathy Fever Tonsils inflamed and swollen ```
45
What is the Centor criteria used for?
It determines the likelihood that a sore throat is bacterial or viral
46
What signs make up the Centor criteria?
1. Tonsillar exudate. 2. Tender/enlarged anterior cervical lymph nodes. 3. Fever (>38°C). 4. Absence of cough. (3 or 4 of these = 50% chance of bacterial infection). (0-2 = viral infection)
47
What is the management of pharyngitis
Self limiting disease Symptomatic treatment No antibiotics Persistent and severe tonsillitis treated with phenoxylmethylpenicillin
48
What is the causative agent of acute epiglottis
Haemophilus Influenza B
49
What are the symptoms of acute epiglottis
Odynophagia (Pain on swallowing) Sore throat Inspiratory stridor (High pitched wheezing noise when she breathes it in) Febrile
50
What is the management of acute epiglottis
``` Prevention = HiB vaccine Treatment = amoxicillin --> Doxycycline or co-amoxiclav ```
51
What is the causative agent of whooping cough
Bordatella pertussis - childhood disease with 90% cases below the age of 5
52
What type of bacteria is Bordetella pertussis?
Gram negative bacilli.
53
What is the disease course of whooping cough
7-10 day incubation 1-2 wk catarrhal stage 1-6wk paroxysmal stage
54
What are the symptoms of whooping cough in adults?
- Chronic paroxysmal cough = sudden and severe | - Inspiratory 'whoop' posttussive vomiting (Vomiting after cough)
55
What are the complications of whooping cough
Pneumonia Encephalopathy Sub-conjunctival haemorrhage
56
What antibiotics might you use in someone with bordetella pertussis infection?
Clarithromyocin.
57
What agar would you culture bordetella pertussis on?
Bordet Gengou agar.
58
When is someone vaccinated against bordatella pertussis?
A child is vaccinated at 8, 12 and 16 weeks and at 3 years 4 months with dTaP vaccine.
59
What is the causative agent in influenza
``` Influenza A (Severe outbreaks) Influenza B and C ```
60
What are the main antigens on influenza A?
- Hemagglutinin (H). | - Neuraminidase (N).
61
What is the function of hemagglutinin?
'Grappling hook'; grabs onto cells.
62
What is the function of neuraminidase?
'Bolt cutters'; cuts newly formed virus loose from infected cells.
63
Which influenza pathogen is commonly behind severe and extensive outbreaks? Why?
Influenza A; it replicates a lot and mutations are common.
64
What are the two types of genetic variability in influenza
Antigenic drift | Antigenic shift
65
Define antigenic drift.
When there are small mutations and minor antigenic variation. Antigenic drift can cause seasonal epidemics.
66
Define antigenic shift.
When there are larger mutations and major antigenic variation. Antigenic shift can cause pandemics!
67
How can influenza virus be transmitted?
- Aerosol: coughing and sneezing, inhale particles. | - Droplet: hand to hand.
68
What is the reproduction number?
The average number of secondary cases generated from a primary case.
69
What are the symptoms of influenza
URT infections = cough, sore throat, runny nose | Systemic symptoms = fever, headache and myalgia
70
What are the complications of influenza
Bacterial pneumonia
71
What is the treatment for influenza?
Supportive care! Antiviral medications might be used to reduce the risk of transmission.
72
Define outbreak.
>2 linked cases.
73
Define epidemic.
More cases in a region/country.
74
Define pandemic.
Epidemics that span international boundaries.
75
What are the possible consequences of pandemics?
1. High morbidity. 2. Excess mortality. 3. Social disruption. 4. Economic disruption.
76
What factors are there to suggest that future pandemics may be likely?
1. More travel. 2. Increasing world population. 3. Rise in intensive farming.
77
What factors are there to suggest that future pandemics may be unlikely?
1. Healthier population due to medical advances. 2. Better healthcare. 3. Vaccination. 4. Antivirals.
78
Where are a high proportion of cases of TB found?
The indian sub continent e.g. India, Bangladesh, Pakistan etc.
79
What are the 4 main mycobacterial species
Mycobacterium tuberculosis Mycobacterium bovis Mycobacterium africanum Mycobacterium microti
80
Describe mycobacterium tuberculosis.
1. Acid fast bacilli. 2. Has a waxy capsule. 3. It grows slowly and therefore is hard to culture in a lab. 4. It can resist phagolysosomal killing resulting in granulomatous disease.
81
What mycobacterium can cause abdominal tuberculosis?
Mycobacterium bovis. | - Can be found in unpasteurised milk.
82
Give 5 risk factors for TB.
1. If you live in a high prevalence area. 2. IVDU. 3. Homeless. 4. Alcoholic. 5. HIV+. 6. smoking 7. Prisons and malnutrition
83
How is TB transmitted?
Aerosol transmission - mycobacterium TB bacilli are inhaled and enter the lung.
84
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.
85
Describe the pathogenesis of pulmonary TB disease.
1. Bacilli and macrophages form primary focus. 2. Mediastinal lymph nodes enlarge. 3. Primary focus and enlarged lymph nodes = primary complex. 4. Granuloma develops into a cavity. 5. The cavity is filled with TB bacilli - these are expelled when the patient coughs.
86
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.
87
Presentation of TB: what systemic symptoms might you see?
1. Weight loss. 2. Night sweats. 3. Anorexia. 4. Malaise. 5. Fever
88
Presentation of TB: what pulmonary TB symptoms might you see?
1. Cough for more than 3 weeks in a year 2. Chest pain. 3. Breathlessness. 4. Haemoptysis.
89
What are the extra pulmonary symptoms of TB
Lymph node TB with swelling and discharge Bone pain and swelling in the joint Abdominal TB = ascites and abdominal lymph nodes
90
What tests might you do in someone with suspected TB
Inflammatory markers = raised CRP, hyperalbuminaemia, thrombocytosis Microbiology = Ziehl neelsen on sputum/biopsy Tuberculin skin test (Mantoux test for latent TB) = stimulates T4 hypersensitivity reaction CXR
91
What might you see on a CXR taken from someone with TB?
1. Consolidation. 2. Collapse. 3. Pleural effusion.
92
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.
93
What test might you do to diagnose latent TB?
Mantoux test - stimulates type 4 hypersensitivity reaction.
94
What drugs are given in the treatment of TB?
Rifampicin (6 months). Isoniazid (6 months). Pyrazinamide (2 months). Ethambutol (2 months).
95
TB treatment: which 2 drugs are taken for the entire 6 months in active TB?
1. Rifampicin. | 2. Isoniazid.
96
TB treatment: which 2 drugs are taken for only the first 2 months for active TB?
1. Pyrazinamide. | 2. Ethambutol.
97
Which drug is taken for 6 months for latent TB
Isoniazid
98
Which drug is taken for 3 months for latent TB
Rifampicin
99
Give 3 potential side effects of Rifampicin.
1. Red urine. 2. Hepatitis. 3. Drug interactions; rifampicin is an enzyme inducer.
100
Give 2 potential side effects of Isoniazid.
1. Hepatitis. | 2. Neuropathy.
101
Give 3 potential side effects of Pyrazinamide.
1. Hepatitis. 2. Gout. 3. Rash.
102
Give 1 potential side effect of Ethambutol.
1. Optic neuritis.
103
Compliance in taking TB medication is critical. Why?
Resistance and relapse may be likely if the patient is non-compliant.
104
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.
105
What is the acronym commonly used for the drugs taken in TB treatment? HRZE.
``` HR = 6 months. ZE = 2 months. - H - isoniazid. - R - rifampicin. - Z - pyrazinamide. - E - ethambutol. ```
106
TB treatment: Give 4 factors that can increase the risk of drug resistance?
1. If the patient has had previous treatment. 2. If they live in a high risk area. 3. If they have contact with resistant TB. 4. If they have a poor response to therapy.
107
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.
108
How can TB be prevented?
1. Active case finding - reduce infectivity. 2. Detect and treat latent TB. 3. Vaccination - BCG.
109
A special culture medium is needed to grow TB. What is the medium called?
Lowenstein Jensen Slope.
110
Lowenstein Jensen Slope is a medium used to grow TB. What is special about this medium?
1. It contains growth factors that promote mycobacterial growth. 2. It contains small amounts of penicillin that prevent pyogenic bacteria growth.
111
What might a lymph node biopsy from someone with TB show?
Caseating granuloma.
112
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.
113
State the name of the pathological lesion that characterises primary tuberculosis?
Ghon complex.
114
State two socioeconomic factors that are associated with an increased prevalence of tuberculosis.
1. Overcrowding. 2. Poverty. 3. Lower socio-economic class.
115
Define pneumonia
Infection of the lung tissue | = acute lower respiratory chest infection
116
Name 5 groups of people who might be at increased risk on pneumonia.
1. The elderly. 2. Children. 3. People with COPD. 4. Immunocompromised people. 5. Nursing home residents.
117
What are the two anatomical classifications of pneumonia
Bronchopneumonia = patchy consolidation of different lobes Lobar pneumonia = Fibrosuppurative consolidation of a single lobe
118
Describe in 3 steps the pathogenesis of pneumonia.
1. Bacteria translocate to normally sterile distal airway - alveolar macrophage response 2. Resident host defence is overwhelmed. 3. Macrophages, chemokines and neutrophils produce an inflammatory response leading to airway exudate and parenchyma damage
119
What intrinsic factors can affect pneumonia?
Cold temperature, infection, stress, exercise, various pollutants.
120
Describe the process of pneumonia resolution?
Bacteria are cleared and inflammatory cells are removed by apoptosis.
121
What are different etiological classifications of pneumonia
Community acquired pneumonia Hospital acquired pneumonia Aspiration pneumonia Immunocompromised pneumonia
122
What are the three main causes of community acquired pneumonia
Streptococcus pneumococcus Mycoplasma pneumoniae Haemophilus influenzae
123
What are the atypical causes of community acquired pneumonia
S.aureus Moraxella cattarrhalis Chlamydia pneumoniae Legionella pneumonphilia
124
What are the main causative agents of hospital acquired pneumonia
>48 hours since hospital admission S.aureus Pseudomonas Aeruginosa Klebsiella pneumoniae
125
Which groups are at greater risk of aspiration pneumoniae
Patients with stroke, bulbar palsy, decreased GCS, GORD
126
What causes of immunocompromised pneumonia
S.pneumococcus M.pneumoniae H. Influenza Rarer causes - Pneumocystis Jirevecii - TB - Aspergillus - CMV/HSV
127
What symptoms might you see in someone with pneumonia?
- Productive cough with purulent sputum (Rusty) and haemoptysis - Sweats and rigor - Fever. - Breathlessness. - Pleuritic chest pain. - Anorexia, malaise - Myalgia, headache, arthralgia suggests atypical pneumonia.
128
What signs might you see in someone with pneumonia?
``` Tachycardia + Tachypnoea Cyanosis Confusion Consolidation - Dull percussion due to lung collapse - Bronchial breathing (Harsh breathing on insp and exp due to consolidation) - Crackles (Air passing through sputum) ```
129
What investigations might you do on someone to determine whether or not they have pneumonia?
- CXR - look for air bronchogram in consolidated area, infiltrates, cavities - FBC (look at WBC's). - U+E. - ABG - Liver function tests. - CRP (marker of inflammation). - Microbiology: sputum culture, blood culture, serology etc - Sera Abs for atypicals ie mycoplasma, chlamydia and legionella
130
How can pneumonia be prevented?
How can pneumonia be prevented? - Children are given PCV. - Smoking cessation is encouraged. - Influenza vaccines are given to children and the elderly.
131
What is CURB65 used for?
It is a way of assessing the severity of community acquired pneumonia. It predicts mortality.
132
What does CURB65 stand for?
``` Confusion. Urea >7mmol/L. RR >30/min. BP reduced - systolic <90mmHg, diastolic <60mmHg. Age >65. ``` 1 point for each 0-1 = home Mx 2 = hospital Mx >3 = consider ICU
133
Why is CRB65 often used in the community?
Because facilities to measure urea are often not available.
134
What is the treatment for pneumonia
Abx O2 Analgesia if pleurisy Chest physio
135
Which antibiotics are used for mild pneumonia
Amoxicillin OR clarithromycin
136
What antibiotics are used for moderate pneumonia
Amoxicillin AND Clarithromycin
137
What antibiotics are used for severe pneumonia
Co-amoxiclav/cefuroxime AND clarithromycin
138
What antibiotics are used for atypical pneumonia
``` Chlamydia = tetracycline PCP = Co-trimoxazole Legionella = Clarithro + Rifampicin ```
139
What groups of people may develop pneumonia caused by klebsiella pneumoniae?
- Homeless people. - Alcoholics. - People in hospital.
140
What are the complications of pneumonia
``` Respiratory failure Hypotension (Due to dehydration and septic vasodilatation) Atrial fibrillation pleural effusion Empyema Lung abscesses Sepsis Myocarditis/pericarditis Jaundice ```
141
What is empyema?
Pockets of pus that have collected in a body cavity e.g. in the pleural cavity
142
What bacteria can cause empyema
Anaerobes Staph Gm -ve Associated with recurrent aspiration
143
Give 3 signs of empyema.
1. WBC/CRP don't settle with antibiotics. 2. Pain on deep inspiration. 3. Pleural collection.
144
What is the usual treatment for empyema?
Drainage.
145
What might you see in tap of someone with empyema
Turbid pH <7.2 Decrease glucose Yellow
146
What are lung abscesses
Severe localised suppuration within the lung associated with cavity formation
147
What are the causes of lung abscesses
Aspiration Bronchial obstruction by tumour or foreign body Septic emboli
148
What are the features of lung abscesses
``` Swinging fever Cough, foul purulent sputum and haemoptysis Malaise and wt loss Pleuritic pain Clubbing Empyema ```
149
What is the management of lung abscesses
Aspiration Abx Surgical excision
150
Name 3 groups of people who might be at risk of hospital acquired pneumonia.
1. Elderly. 2. Ventilator associated. 3. Post operative patients.
151
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.
152
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.
153
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.
154
What can cause acute airway obstruction?
Tumour or foreign bodies with distal collapse of the lung.
155
If the trachea, bronchi and bronchioles are involved in a disease process, is this likely to be an obstructive or a restrictive disease?
Obstructive.
156
If the lung parenchyma are involved in a disease process, is this likely to be an obstructive or a restrictive disease?
Restrictive.
157
If the chest wall is involved in a disease process, is this likely to be an obstructive or a restrictive disease?
Restrictive.
158
What happens to the FEV1, FVC and FEV1/FVC ratio in an obstructive lung disease?
- FEV1 is < 80% predicted. - FVC is normal. - FEV1/FVC ratio < 0.7.
159
What happens to the FVC and FEV1/FVC ratio in a restrictive lung disease?
- FVC reduced. | - FEV1/FVC ratio normal or increased
160
Give an example of a reversible obstructive lung disease.
Asthma.
161
Give an example of an irreversible obstructive lung disease.
COPD.
162
What is the affect of COPD on residual volume and total lung capacity?
RV and TLC are increased.
163
Give an example of a restrictive lung disease.
Pulmonary fibrosis.
164
What is bronchiectasis?
chronic infection of the bronchi/bronchioles leading to Permanent dilation of bronchi leading to a build-up of excess mucus and predisposes someone to chest infections.
165
Describe the pathogenesis of bronchiectasis.
Failed mucocilliary clearance and impaired immune function mean that a microbe can easily invade and cause infection. This leads to inflammation and therefore progressive lung damage. Bronchitis -> bronchiectasis -> fibrosis.
166
What can cause bronchiectasis?
1. Often post-infective e.g. previous pneumonia, TB or whooping cough, measles 2. Congenital causes e.g. primary ciliary dyskinesia/CF/Kartenger's 3. 50% idiopathic. 4. Hypogammaglobinaemia 5. Bronchial obstruction (Tumour, foreign body) 6. Ulcerative colitis and Rheumatoid arthritis
167
Which bacteria might cause bronchiectasis?
1. Haemophilus influenzae. 2. Streptococcus Pneumococcus 2. Pseudomonas aeruginosa. 3. Staphylococcus aureus.
168
Give 6 symptoms of bronchiectasis.
1. Chronic productive cough with purulent sputum 2. Recurrent chest infections. 3. Fever and wt loss 3. Dyspnoea and wheeze. 4. Recurrent exacerbations. 5. Chest pain. 6. Haemoptysis.
169
What are the signs of Bronchiectasis
Clubbbing coarse inspiratory wheeze (Crackles) Wheeze Purulent sputum
170
Complications of bronchiectasis
Pneumonia Pleural effusion Pneumothorax Pulmonary HTN
171
What investigations might you do on someone to determine whether they have bronchiectasis?
- High resolution CT scan showing dilated and thickened airways - Spirometry - would be obstructive. - Sputum culture. - CXR showing thickened bronchial walls (Tramlines and rings) - Bloods (Serum Abs for aspergillus, RF, a1-AT) - Bronchoscopy
172
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 - salbutamol 7. Improved mucus clearance e.g. physiotherapy = postural drainage 8. Treat underlying cause - Mucus = DNAse - Immune deficiency = IVIg 9. Surgical lung resection
173
What antibiotic is used for P.aeruginosa
Ciprofloxacin
174
What antibiotic is used for H.influenza
Amoxicillin Co-amoxiclav Cephalosporin
175
The airways in a person with bronchiectasis often become chronically colonised. What is the airway of a neonate likely to be colonised with?
s.aureus.
176
The airways in a person with bronchiectasis often become chronically colonised. What is the airway of a child likely to be colonised with?
h.influenzae.
177
The airways in a person with bronchiectasis often become chronically colonised. What is the airway of an adult likely to be colonised with?
pseudomonas aeruginosa.
178
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.
179
Define CF.
An autosomal recessive disease resulting in abnormal exocrine gland function.
180
Which chromosome codes or CFTR?
Chromosome 7.
181
Describe the pathogenesis of cystic fibrosis.
There is a defect in chromosome 7 coding CFTR protein leading to increased Na+ reabsorption and decreased luminal Cl- secretion. there is production of thickened mucus secretions due to increased water reabsorption
182
How is cystic fibrosis passed on?
It is an autosomal recessive condition. | 1 in 25 people are carriers.
183
A common mutation in which gene can cause CF?
A mutation in ∆F508.
184
Why do patients with CF have salty sweat
Because in the sweat glands there is decreased Cl and Na+ reabsorption
185
What are the clinical features of CF in neonates
Failure to thrive Meconium ileus (Sticky intestine) Rectal prolapse
186
What are the respiratory clinical features of CF in children and young adults
``` Nasal polyps and sinusitis Resp - Cough - Wheeze - Recurrent infections - Bronchiectasis - Haemoptysis - Pneumothorax - Cor pulmonale ```
187
What are the gastrointestinal clinical features of CF in children and young adults
``` Pancreatic insufficiency = DM and steatorrhea Distal intestinal obstruction syndrome Gallstones Cirrhosis male infertility Osteoporosis Vasculitis Arthritis ```
188
What are the signs of CF
Clubbing Hypertrophic pulmonary osteoarthropathy Cyanosis Bilateral coarse crepitus
189
What are the common causative respiratory agents in early CF
S.aureus | H.Infleunza
190
What are the common causative respiratory agents in late CF
P.aeruginosa | B.cepacia
191
How is CF diagnosed
Sweat test = Na+ and Cl- >60mM Genetic screening for common mutations Faecal elastase test for pancreatic exocrine function
192
What investigations might you do In someone with CF
Bloods Sputum MCs CXR shows bronchiectasis + hyperinflation Abdo US shows fatty liver, cirrhosis and pancreatitis Spirometry shows obstructive defect
193
What is the management of CF
Physio = postural drainage and forced expiratory technique Abx = acute infections and prophylaxis Mucolytics = DNAse Bronchodilators Vaccinate Pancreatic enzyme replacement ADEK supplements Insulin Ursodeoxycholic acid for impaired hepatic function
194
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.
195
Malignant bronchial tumours can be divided into two groups; what are they?
1. Non small cell cancer (Squamous cell carcinoma, adenocarcinoma, large cell) 2. Small cell cancer.
196
Which type of malignant bronchial tumour tends to have a worse prognosis?
Small cell cancer.
197
Give 5 causes of lung cancer.
1. SMOKING! - Occupational: 2. Asbestos exposure. 3. Radon exposure. 4. Coal tar exposure. 5. Chromium exposure.
198
Which type of NSCC is most common in smokers?
Squamous cell carcinoma.
199
Describe the pathology of squamous cell carcinoma
Central located | Evidence of squamous differentiation with keritanisation
200
Which type of NSCC is most common with non smokers
Adenocarcinoma
201
Describe the pathology of adenocarcinoma
Peripherally located with glandular differentiation leading to gland formation and mucus production with mets to the pleura, lymph nodes, brain, bone and adrenal glands
202
From what cells are Small Cell Cancers derived from and what is the significance of this?
Neuroendocrine cells centrally located near bronchi | Can secrete peptide hormones such as ACTH, PTHrP, ADH and HCG.
203
What are three rare lung tumour types
Adenoma Hamartoma Mesothelioma
204
The 5 year lung cancer survival rate is 8-10%. Why is this?
People often present very late with lung cancer and so treatment is much harder.
205
Give 3 main cell types that make up non small cell lung cancer?
1. Squamous cell (20%). 2. Adenocarcinoma (40%). 3. Large cell.
206
Give 6 symptoms of local disease lung cancer.
1. Chest pain. 2. Wheeze. 3. Breathlessness. 4. Cough. 5. Haemoptysis. 6. Recurrent chest infections - pneumonia 7. Anorexia and wt loss 8. Hoarseness
207
What are the signs of lung cancer
Chest consolidation, collapse and pleural effusion Cachexia Anaemia Clubbing and hypertrophic pulmonary osteoarthropathy
208
Give 6 symptoms of lung cancer that has metastasised.
1. Bone pain, especially waking up in the night from pain. 2. Headache and confusion 3. Seizures. 4. Neurological deficit. 5. Hepatic and/or abdominal pain - hepatomegaly 6. Weight loss.
209
Name 5 places that lung cancer might metastasise to.
1. Bone. 2. Brain. 3. Liver. 4. Lymph nodes. 5. Adrenal glands.
210
Name 5 places that cancer might metastasise to the lung from
Brain, prostate, kidney, thyroid , melanoma, lymphoma
211
What are paraneoplastic syndromes?
Disorders triggered by immune response to a neoplasm.
212
Give 5 examples of paraneoplastic syndromes.
1. Finger clubbing. 2. Anorexia. 3. Weight loss. 4. Hypercalcemia. 5. Hypernatremia.
213
Endocrine paraneoplastic syndromes include
ADH = SIADH ACTH = Cushing's syndrome Serotonin = Carcinoid (Flushing and diarrhoea) PTHrP
214
Rheumatoid paraneoplastic syndromes include
Dermatomyositis/polymyositis
215
Neuronal paraneoplastic syndromes include
Purkinje cells leading to cerebellar degeneration | Peripheral neuropaty
216
What are the complications of lung cancer
``` Recurrent laryngeal N palsy Phrenic nerve palsy SVC obstruction Horner's Atrial fibrillation ```
217
What investigations might you do on someone to determine whether they have lung cancer?
- CXR (Coin lesion, hilar enlargement, consolidation, collapse, effusion) - CT scan for staging - Bronchoscopy. - Surgical and percutaneous biopsy. - Bloods.
218
What does TNM stand for?
1. T: tumour (T1-4). Tis = carcinoma in situ T0 = none evident T1 = <3cm in lobar or more distal airway T2 = >3cm and >2cm from carina or pleural involvement T3 = <2cm from carina and involves chest wall and diaphragm T4 = Involves mediastinum or malignant effusion is present 2. N: nodal involvement (N0-3). N0 = none involved N1 = Peribronchial or ipsilateral hilum N2 = Ipsilateral mediastinum N3 = Contralateral hilum or mediastinum or supraclavicular 3. M: metastases (M0-1). M0 = non M1 = distant metastasis - Increased staging = decreased survival.
219
What tests might you do on a patient to determine whether they're fit for operation?
1. ECG. 2. Lung function tests. 3. Determine performance status.
220
What are the treatment options for NSCLC
1. Surgical resection for peripheral lesions with no mestastatic spread 2. Curative radiotherapy 3. Chemo and radiotherapy for more advanced disease
221
What is the treatment for SCLC
Typically disseminated @ presentation and may respond to chemo
222
What are the palliation options for lung cancer
``` Radiotherapy for bronchial obstruction, haemoptysis, bone and CNS mets Stenting and radio for SVC obstruction Endobrachial therapy Pleural drainage Analgesia ```
223
Secretion of which hormones might result in paraneoplastic changes?
1. PTH. | 2. Increased ADH (SIADH).
224
Why is the prognosis for small cell lung cancer normally very poor?
Small cell cancers often metastasise and so prognosis is poor.
225
What does the medulla detect?
The pH (H+ conc) of the CSF.
226
What do carotid and aortic bodies detect?
Chemoreceptors respond to increased CO2 and decreased O2.
227
What is type 1 respiratory failure?
Hypoxia - decreased PaO2. | PaCO2 is normal or slightly low due to hyperventilation.
228
What is type 2 respiratory failure?
Hypoxia and hypercapnia - decreased PaO2 and increased PaCO2. There is alveolar hypoventilation.
229
Give 3 signs of hypercapnia.
1. Bounding pulse. 2. Flapping tremor. 3. Confusion 4. Headache 5. Flushing and peripheral vasodilation
230
What are the signs of acute hypoxia
Dyspnoea Agitation Confusion Cyanosis
231
What are the chronic signs of hypoxia
Polycythaemia PHT Cor pulmonale
232
What can cause type 1 respiratory failure?
1. Airway obstruction. 2. Failure of O2 to diffuse into the blood. 3. V/Q mismatch. 4. Alveolar hypoventilation.
233
What can cause type 2 respiratory failure?
Alveolar hypoventilation.
234
Give examples of diseases that obstruct the airway and so could lead to type 1 respiratory failure.
1. COPD. 2. Obstructive sleep apnoea. 3. Asthma. (Can't get O2 in but can get CO2 out).
235
What are the obstructive causes of alveolar hypoventilation
COPD Asthma Bronchiectasis Bronchiolitis
236
What are the restrictive causes of alveolar hypoventilation
Decreased respiratory drive due to sedation, trauma or tumour Neuromuscular disease ie. MND, GBS, Myasthenia gravis Chest wall deformity ie. kyphoscoliosis, obesity
237
Give examples of diseases that lead to a failure of O2 to diffuse into the blood and so could cause type 1 respiratory failure.
1. Emphysema. | 2. ILD e.g. IPF, sarcoidosis.
238
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.
239
What is the management of T1 respiratory failure
Give O2 to maintain SpO2 94-98% | Assisted ventilation if PaO2 <8Kpa
240
What is the management of T2 respiratory failure
Controlled O2 therapy
241
What treatments might be given for V/Q mismatch?
Ventilation support e.g. CPAP and BIPAP.
242
What is continuous positive airway pressure (CPAP)? When might it be used?
Ventilation support often given to people with Obstructive Sleep Apnoea. It improves gaseous exchange by providing a continuous positive airway pressure.
243
What is bilevel positive airway pressure (BIPAP)? When might it be used?
Ventilation support often given to people who have had acute exacerbations of COPD. It causes pressure to decrease when you breathe out and increase when you breathe in therefore improving ventilation to perfused alveoli.
244
Define asthma
Episodic reversible airway obstruction causing dyspnoea, cough and wheeze due to bronchial hyper-reactivity to a variety of stimuli
245
What are the three processes that aid bronchial constriction
Bronchial muscle contraction Mucosal swelling and inflammation Increased mucus production
246
Describe the epidemiology of asthma
Peaks at 5yrs and most outgrow by adolescence
247
What 2 categories can asthma be divided into?
1. Allergic asthma (extrinsic); atopic. IgE and mast cell involvement. 2. Non allergic asthma (intrinsic).
248
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.
249
What is non-allergic asthma?
Airway obstruction induced by exercise, cold air and stress.
250
What factors can commonly exacerbate asthma?
1.Cold weather. 2. Exertion. 3. Fumes. 4. Often worse at night 5. Allergens 6. Stress. viral infections 7. Cigarette smoke 8. Drugs
251
Extrinsic asthma: what happens when IgE binds to mast cells?
Vasoactive substances are released causing bronchoconstriction, oedema, bronchial inflammation and mucus hyper-secretion.
252
Describe the pathophysiology of acute asthma
Mast cell and allergen interaction leading to histamine release, bronchoconstriction, mucus plugs and mucosal swelling
253
Describe the pathophysiology of chronic asthma (12hr)
Th2 cells release IL-3,4,5 causing mast cells, eosinophil and B cell recruitment leading to airway remodelling
254
What are the causes of asthma
1. Atopy = T1 hypersensitivity to variety of antigens (Dust mites, pollen, food, animals, fungus) 2. Stress = Cold air, Viral URTI, Exercise, emotion 3. Toxins = smoking, pollution, Drugs (NSAIDs and beta blockers
255
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.
256
What are the symptoms of asthma?
1. Breathlessness. 2. Diurnal variation - often worse in the morning. 3. Cough with sputum 4. Episodic wheeze. 5. Chest tightness.
257
What are the signs of asthma
Tachycardia and tachypnoea Widespread polyphonic wheeze Hyperinflated chest decreased air entry
258
What investigations might you do on someone to determine whether they have asthma?
1. PEFR (Dinural variation and morning dipping) 2. Spirometry should show an obstructive pattern; FEV1 < 80%, FEV1/FVC < 0.7, PEFR - variable. - >15% improvement in FEV1 with Beta agonist 3. Test for atopy; RAST, skin prick test. 3. CXR - hyperinflation 4. Eosinophil count. 5. O2 saturation 6. Bloods - FBC - Increased IgE - Aspergillus serology
259
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.
260
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. ```
261
What is the function of RCP3?
It is used to assess the severity of asthma.
262
What are the 2 principles of asthma treatment?
1. Alleviate symptoms. | 2. Target inflammation.
263
What are the general measures used in the treatment of asthma
Technique for inhaler use Avoidane: allergens, smoking, dust Monitor (Peak flow diary) Educate
264
What is the first pharmacological option for chronic asthma
Short acting beta agonist ie. Salbutamol for symptomatic relief
265
What is the second pharmacological option for chronic asthma
Low dose inhaled corticosteroid ie beclometasone or budesonide
266
What is the third pharmacological option for chronic asthma
Long acting beta agonist ie. Salmeterol or formoterol
267
What are the fourth pharmacological options for chronic asthma
Increase inhaled steroid dose Leukotriene receptor antagonist (Montelukast/zafirlukast) Theophylline
268
what is the 5th pharmacological option for chronic asthma
Prednisolone
269
How to B2 agonists work
SABA or LABA Stimulate the B2 adrenergic receptors in the smooth muscle of the airway which increases cAMP production which decreases intracellular calcium leading to smooth muscle relaxation and bronchodilation
270
What are the side effects of B2 agonists
``` Fine tremor increases HR and Palpitations Anxiety Headache muscle cramps Decreased K+ ```
271
Name two SABA
Salbutamol | Terbutaline
272
Name 2 LABA
Salmeterol | Formoterol
273
Name some corticosteroids used in the treatment of asthma
``` Hydrocortisone (Cortisol) Prednisolone (Longer lasting cortisol) Dexamethasone Beclometasone Budesonide ```
274
How do corticosteroids work in the treatment of asthma
Lipophilic molecule which passes through the phospholipid bilayer and binds to nuclear glucocorticoid or mineralocorticoid receptor causes altered protein synth Leads to altered anti-inflammatory effects due to increased lipocortin-1 which decreases phospholipase A2 which decreases eicosanoid production including prostaglandins, thromboxanes and leukotrienes
275
What are the side effects of inhaled corticosteroids
Oral candidiasis | Dysphonia
276
What are the side effects of oral glucocorticoids
``` Cushing's Increased appetite Increased weight GI ulcers and acute pancreatitis Osteoporotic fractures Skin thinning Hypertension Diabetes ```
277
Describe how theophylline works
Phosphodiesterase inhibitor that causes decreases intracellular calcium leading to airway smooth muscle relaxation
278
What are the SE of theophylline
Nausea and vomiting Arrhythmias Seizures Decreases K+
279
Name a short acting muscarininc antagonist
Ipratropium
280
Name a long acting muscarinic antagonist
Tiotropium
281
Describe how muscariininc antagonists work in the treatment of asthma
Acting on M3 receptors by preventing ACh from binding the M3 receptor and preventing phospholipase C conversion to DAG which stops protein kinase C activation and prevents smooth muscle contraction
282
What is the first line treatment for acute severe asthma?
Nebulised salbutamol with oxygen. | IV corticosteorids and abx if evidence of infection.
283
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.
284
What are the 3 characteristic features of asthma?
1. Airflow obstruction. 2. Hyper-responsive airways to a range of stimuli. 3. Bronchial inflammation.
285
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.
286
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.
287
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.
288
What can chronic obstructive pulmonary disease be sub-divided into?
1. Chronic bronchitis. | 2. Emphysema.
289
Is chronic bronchitis reversible?
Chronic bronchitis is irreversible.
290
Define COPD
Airway obstruction FEV1 <80% FEV1:FVC <0.70
291
Define chronic bronchitis
Cough and sputum production on most days for 3 months o 2 successive years
292
Define emphysema
Histological diagnosis of enlarged air spaces distal to the terminal bronchioles leading to destruction of alveolar walls
293
Describe the pathophysiology of 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.
294
How is airway obstruction defined by spirometry?
- FEV1 < 80% predicted. | - FEV1/FVC < 0.7.
295
What are the main causes of COPD?
Occupational factors (Dust/chemicals) Smoking Pollution Alpha1 Anti trypsin deficiency
296
Deficiency of what protease inhibitor can cause emphysema?
Alpha 1 anti-trypsin deficiency.
297
What is the function of alpha 1 anti-trypsin?
It inhibits neutrophil elastase
298
What can cause chronic bronchitis?
It is often tobacco smoking induced and can be aggravated by pollution and infections.
299
What can happen over time in a patient with chronic bronchitis?
The patient might become hypercapnic, hypoxic and have progressive right sided cardiac failure (cor pulmonale) due to pulmonary vasoconstriction. There is fibrosis and tissue destruction.
300
What is the pathology of emphysema?
Irritants and chemicals trigger inflammatory mediators to release matrix destructive enzymes -> elastin destruction and enlargement of alveolar air spaces -> air trapping.
301
What can cause emphysema?
It is often tobacco smoking induced. It can also be associated with alpha-1-antitrypsin deficiency and coal dust exposure.
302
What are the symptoms of COPD?
1. Breathlessness. 2. Wheeze. 3. Chronic cough. 4. Sputum (White/clear) 5. Wt loss
303
Give 5 signs of emphysema.
1. Tachypnoea 2. Prolonged expiratory phase 3. Barrel chest (Hyperinflation) 4. Early inspiratory crackles 5. Cyanosis 6. Cor pulmonale/ increased jugular venous pressure
304
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.
305
Describe the pathology of pink puffer emphysema
Increased ventilation so they are breathless but not cyanosed Means PaO2 is normal PaCO2 is normal or low Progresses to T1 respiratory failure
306
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.
307
Describe the pathology of blue bloater in chronic bronchitis
Decreased alveolar ventilation so they are cyanosed by not breathless so there is decreased PaO2 but increased PaCO2 leading to T2 respiratory failure and cor pulmonale
308
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). 1. Dyspnoea worse only on vigorous exercise 2. SOB on hurrying or walking up stairs 3. Walks slowly or has to stop for breath 4. Stops for breath after <10m 5. Too breathless to leave house or SOB upon dressing
309
What are the complications of COPD
Cor pulmonale Acute exacerbations and infection Polycythaemia Pneumothorax
310
Give 3 factors that can be used to establish a diagnosis of COPD?
1. Progressive airflow obstruction. 2. FEV1/FVC ratio < 0.7. 3. Lack of reversibility.
311
Aside from COPD, what might be a differential diagnosis for breathlessness?
1. Heart failure. 2. PE. 3. Pneumonia. 4. Lung cancer.
312
What investigations might you do in someone with suspected COPD
Bloods (Polycythaemia, a1-AT level, ABG) CXR (Hyperinflation and prominent pulmonary arteries and bullae) ECG (RVH, RAH) Spirometry where FEV1 <80% and FEV1:FVC <0.70
313
Describe the classification system for COPD severity
Mild = FEV1 <80% but FEV1/FVC <0.7 and symptomatic Moderate = FEV1 50-79% Severe = FEV1 30-49% Very severe = FEV1 <30%
314
What are the treatments for COPD?
1. Smoking cessation! 2. Pulmonary rehabilitation. 3. SABA/LABA for symptom relief. 4. Mucolytics 4. Inhaled Corticosteroid. 5. Long term oxygen therapy 5. Lung volume reduction surgery - quite rare.
315
Define exacerbation.
An acute event characterised by worsening symptoms beyond normal day to day variation. It often leads to a change in medication.
316
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.
317
What is the likely cause for an exacerbation of COPD?
Viral infection e.g. RSV, influenza, parainfluenza, rhino and coronaviruses.
318
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.
319
What are the aims of treatment for exacerbations of COPD?
1. Minimise the impact of the current exacerbation. | 2. Prevent subsequent exacerbations.
320
Give 3 ways in which subsequent exacerbations be prevented.
1. Smoking cessation. 2. Vaccination. 3. LABA/LAMA/ICS.
321
What broad class of drugs are commonly used to alleviate symptoms?
Bronchodilators.
322
What broad class of drugs are commonly used to target inflammation?
Steroids.
323
Name 3 types of bronchodilators that are commonly used.
1. Beta agonists. 2. Muscarinic antagonists. 3. Methylxanthines.
324
What makes LABA long acting?
They have increased lipophilicity.
325
What type of beta adrenergic receptors are found in the lungs?
Beta 2.
326
Where are beta 1 adrenergic receptors found?
In the heart.
327
Where are beta 3 adrenergic receptors found?
In adipose tissue.
328
Describe the process of PKA synthesis from beta 2 receptor activation.
Beta 2 interacts with Gs. This activates adenylate cyclase. Adenylate cyclase converts ATP to cyclic AMP, this then leads to PKA synthesis -> bronchodilation.
329
Give 2 functions of cAMP.
1. Stabilisation of mast cells, inhibits mast cell mediator release. 2. Relaxes airway smooth muscle.
330
What happens following activation of the M3 receptor?
M3 interacts with Gq. Phospholipase C is activated, this leads to DAG and IP3 production which further leads onto Ca2+ and PKC production = bronchoconstriction
331
How do muscarinic antagonists work?
They prevent M3 receptor activation and so there is a reduction in Ca2+ activation. This means less MLC kinase is produced and you have reduced muscle contraction.
332
How do methylxanthines work?
They are PDE inhibitors. They increase cAMP production and therefore PKA production. PKA inhibits MLC kinase and you have reduced muscle contraction.
333
Where is PDE4 found?
In the airways and inflammatory cells.
334
What is the function of MLC kinase?
MLC kinase phosphorylates MLC which causes muscle contraction.
335
What inhibits Myosin Light Chain kinase?
PKA.
336
What activates MLC kinase?
Calmodium. | Calmodium is produced from Ca2+
337
Using the myosin light chain, explain how beta agonists and methyxanthines work to alleviate symptoms.
Beta agonists and methylxanthines result in increased cAMP and therefor PKA. MLC kinase is inhibited and you have less smooth muscle contraction in the airway -> bronchodilation.
338
Using the myosin light chain, explain how muscarinic antagonists work to alleviate symptoms.
Muscarinic antagonists block M3 receptor activation and so you have a reduction in Ca2+ production. Less MLC is activated and so you have less smooth muscle contraction in the airway -> bronchodilation.
339
Where are anti-inflammatory steroids produced?
Adrenal cortex.
340
Where in the adrenal cortex are mineralocorticoids produced and give an example of one.
- Zona glomerulosa. | - Aldosterone.
341
Where in the adrenal cortex are glucocorticoids produced and give an example of one.
- Zona fasciculata. | - Hydrocortisone.
342
Give 3 potential side effects of prolonged hydrocortisone use.
- Muscle wasting. - Osteoporosis. - Increased risk of infection.
343
What are the main cells responsible for inflammation in asthma?
Mast cells and eosinophils.
344
What are the main cells responsible for inflammation in COPD?
Neutrophils and macrophages.
345
How does anti IgE therapy work?
Ab binds to and neutralises free IgE; this prevents IgE binding and results in decreased mast cell sensitisation. Allergens are unable to activate mast cells.
346
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.
347
What is the function of inositol trisphosphate?
Inositol trisphosphate (IP3) increases free cytosolic Ca2+ by releasing Ca2+ from intracellular compartments. Ca2+ activates MLC kinase = bronchial smooth muscle contraction.
348
What does activation of the M3 receptor cause?
1. Bronchoconstriction. 2. Vasodilation. 3. Glandular secretions.
349
Pulmonary embolism: where might an emboli arise from?
Emboli often arise from a dislodged DVT - from iliofemoral veins.
350
What is the consequence of a small, peripheral PE?
Infarction! | There is ventilation but no perfusion; dead space.
351
What is the consequence of a large, central PE?
Ischaemia! | There is resistance to flow which can also result in RHF.
352
Give 5 risk factors for PE. | Spasmodical
``` Sex: F Pregnancy Age (Increased) Surgery Malignancy Oestrogen (OCP) DVT/PE previous history Immobility Colossal size (Obesity) Antiphospholipid Abs Lupus Anticoagulant ```
353
What are the symptoms of PE
Dyspnoea Pleuritic chest pain Haemoptysis Syncope and dizziness
354
What are the signs of PE
``` Fever Cyanosis Tachycardia Tachypnoea Hypotension Increased JVP ```
355
What are symptoms of a small, peripheral PE?
- Breathlessness. | - Pleuritic chest pain.
356
What are symptoms of a large, central PE?
- Severe central chest pain. | - Pale and sweaty.
357
What investigations might you do in someone to determine whether they have PE?
- CXR = dilated PA, linear atelectasis and oligaemia - ECG = sinus tachycardia and RBBB - D-dimer. - ABG = decreased PaO2 and decreased PaCO2 - V/Q lung scan - shows ventilated areas with perfusion defects. - CTPA - can detect emboli.
358
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.
359
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.
360
How long is the treatment for an idiopathic pulmonary embolism?
At least 6 months.
361
Give 4 signs of a large PE.
1. Shocked. 2. Central cyanosis. 3. Raised JVP. 4. Accentuation of second heart sound.
362
Define Pneumothorax
Accumulation of air in the pleural space secondary to lung collapse A defect in the visceral pleura causes air to enter the pleural space from the lungs. The elastic recoil of the lungs then causes them to deflate
363
What are the three main types of pneumothorax?
Closed = Intact chest wall and air leaks from the lung into the pleural cavity Open = Defect in the chest wall allows communication patient and exterior Tension = air in the pleural cavity through one way valve that cannot escape leading to mediastinal compression
364
What are the causes of pneumothorax
Spontaneous Primary - No underlying lung disease and often occurs in young thin men who are smokers Secondary - Underlying lung disease including COPD, TB, pneumonia Traumatic (Penetrating Iatrogenic
365
What are the symptoms of pneumothorax
``` Acute sudden onset SOB Dyspnoea Pleuritic chest pain Can be asymptomatic Tension = respiratory distress and cardiac arrest ```
366
What are the signs of pneumothorax
``` Decreased chest expansion Resonant percussion Decreased breath sounds Decreased vocal resonance Tension = increased JVP, mediastinal shift, increased HR ```
367
What investigations would you do in someone with pneumothorax
CXR but skip in someone with suspected tension pneumothorax Ultrasound ABG
368
What is the management for primary pneumothorac
usually self resolve otherwise needle aspiration
369
What is the management for secondary pneumothorax
Conservative treatment if <1cm Needle aspirate if 1-2cm Chest drain if >2cm or SOB
370
What is the management for tension pneumothorax
Resuscitate patient No CXR 100% O2 Needle aspiration for instant relief then proceed to chest drain
371
Describe the pathophysiology of a tension pneumothorax.
A pleural tear creates a 1-way valve through which air passes in inspiration -> increased intra-pleural pressure -> respiratory distress, shock and cardiac rest.
372
What does pleural fluid contain?
Proteins e.g. albumin, globulin.
373
What is the function of the pleura?
It allows movement of the lung and lung expansion against the chest wall.
374
What produces and reabsorbs pleural fluid?
The parietal pleura.
375
Name 3 diseases associated with the pleura.
1. Pleural effusions. 2. Pleural plaques. 3. Pneumothorax.
376
Define pleural effusion
Excess fluid in the pleural space
377
What are the different classifications of pleural effusion
Transudate = <25g/L of protein and caused by organ failure Exudate = >35g/L of protein and are due to the 4 I's
378
What are the causes of transudate pleural effusion
Increased venous pressure - Congestive cardiac failure - Constrictive pericarditis Hypoproteinaemia Renal failure Meig's syndrome Hypothyroidism
379
What are the causes of exudate pleural effusion
``` Infection = pneumonia and TB Infiltration = cancer of lung, breast, lymphoma, malignant mesothelioma Infarction = PE and MI Inflammation = RA and SLE ```
380
What are the symptoms of pleural effusion
SOB Cough Pleuritic chest pain
381
What are the signs of pleural effusion
``` Stony dull percussion Decreased breath sounds Decreased chest expansion Mediastinal shift Decreased vocal resonance Clubbing in lung cancer increased jugular venous pressure in HF ```
382
What investigations would you do in someone that has suspected pleural effusion
Bloods CXR = Blunt costophrenic margins, mediastinal shift Diagnostic tap Pleural biopsy
383
What is the management of pleural effusions
Treat underlying cause Use drainage or aspiration if symptomatic May require a chest drain
384
What is pleural fibroma?
Fibrous tumour of the pleura.
385
What are the consequences of pleural fibroma?
Pleural fibromas can grow to a massive size and compress on lung tissue. Occasionally they can secrete insulin related factors and so produce hypoglycaemic symptoms.
386
Define sarcoidosis
Non-caseating granulomatous disease that most commonly affects lung and lymph nodes
387
What is the epidemiology of sarcoidosis
20-40yrs F>M Afro caribbean HLA-DRB1 and DQB1 alleles
388
What are the symptoms of sarcoidosis
20-40% disease presents incidentally on CXR 1. Bi-lateral hilar lymphadeonopathy (BHL). 2. Erythema nodosum. 3. Uveitis, Keratoconjunctivitis and Sicca 4. Non productive cough, SOB, wheeze., chest pain 5. Metabolic affect of sarcoidosis = hyperacalcaemia -> nephrocalcinosis. 6. polyArthalgia and dactylitis 7. Hepatosplenomegaly. 8. Neurological: inflammation of the meninges and seizures. 9. Heart block. 10. Lung fibrosis. 11. Finger clubbing is rare! 12. Fever, anorexia, wt loss
389
What is the staging system for the respiratory symptoms of sarcoidosis
Stage 1 = bilateral hilar lymphadenopathy Stage 2 = BHL + peripheral infiltrates Stage 3 = Peripheral infiltrates alone Stage 4 = Progressive mid zone fibrosis
390
What investigations in sarcoidosis
Bloods = increased ESR, Ca, ACE and lymphopenia CXR for staging LFT's = restrictive pattern Tissue biopsy = non caveating granulomas
391
What is the management for sarcoidosis
Patients with asymptomatic BHL don't require Rx Acute sarcoidosis = bed rest and NSAIDs Chronic = Prednisolone
392
Define interstitial lung disease
Disease affecting the lung interstitium = connective tissue between the alveolar epithethelium and the capillary endothelium = increased fibrous tissue within the lung parenchyma resulting in increased stiffness and decreased expansion
393
What are the causes of interstitial lung disease
``` Idiopathic pulmonary fibrosis Pneumoconiosis Hypersensitivity pneumonitis Infection = TB Sarcoidosis Connective tissue disease ie. SLE, RA, systemic sclerosis and ankylosing spondylitis ```
394
Which drugs can cause interstitial lung disease
``` Bleomycin Amiodarone Radiation Methotrexate Aspirin and ACEi Nitrofurantoin ```
395
What are symptoms of ILD
Progressive SOB Drug cough Failure to respond to treatment of other conditions
396
What are the signs of ILD
``` Crackles - end inspiratory Tachypnoea Clubbing Peripheral cyanosis Decreased chest expansion ```
397
What is the commonest cause of ILD
Idiopathic pulmonary fibrosis
398
What is IPF characterised by
Dysregulated fibroblasts and myofibroblasts
399
What is IPF
A disease characterised by chronic inflammation and permanent scarring in the alveoli. Respiratory ability is affected. Chest infection and hypoxic damage are likely.
400
Give 4 risk factors for IPF.
1. Smoking. 2. Dust exposure. 3. Exposure to infectious agents. 4. Long term antidepressant use.
401
What are the symptoms of IPF
Dry cough Dyspnoea Malaise and Wt loss Arthralgia
402
What are the signs of IPF
Cyanosis Clubbing Crackles - fine, end inspiratory
403
What investigations would you do in someone with suspected IPF
``` Bloods = increased CRP ABG = decreased PaO2 and increased PaCO2 CXR = decreased lung volume, honeycomb lung Lung biopsy Spiro = Restrictive BAL = Lymphocytes increased ```
404
What is the management for someone with IPF
Stop smoking Pulmonary rehabilitation Steroids
405
What is the effect of interstitial lung disease on lung volumes?
Reduced TCO, VC and FEV1. FEV1/FVC ratio and PEFR is normal.
406
What is the treatment for interstitial lung disease?
Steroids and immunosuppressive agents. Lung transplantation may be required.
407
When looking to diagnose IPF, what 3 findings would you look for on pulmonary function
1. Reduced TLCO. 2. Restrictive spiromerty: low FEV1 and FVC but normal ratio. 3. Low/normal PaO2.
408
What is hypersensitivity pneumonitis (EAA)?
Inhalation of allergen in sensitised patients leads to a type 3 hypersensitivity reaction; there is an inflammatory response in the alveoli and small airways Chronic exposure leads to granuloma formation and obliterative bronchiolitis
409
Name a cause of hypersensitivity pneumonitis (EAA).
1. Farmer's lung; due to mouldy hay and aspergillus spores. 2. Bird fancier's lung; due to proteins present in bird faeces 3. Malt workers lung due to aspergillus clavatus
410
What are the clinical features of EAA 4-6hr post exposure
Fevers, rigors, malaise Dry cough and dyspnoea Crackles (no wheeze) Resolution 24-48 hours following antigen removal
411
What are the clinical features of chronic EAA
Increasing dyspnoea Wt loss T1 respiratory failure Cor pulmonale
412
What investigations would you do in someone with EAA
Bloods = increased ESR, neutrophilia CXR = honey comb lung Spirometry = restrictive defect Bronchoalveolar enlargement = increased lymphocytes and mast cells
413
What is the management for EAA
Remove allergen/avoid exposure | Steroids (Hydrocortisone/prednisolone)
414
What are occupational lung disorders?
Lung disorders due to a response to inhaling something at work e.g. fumes, dust, gas, aerosol.
415
Give 5 damage mechanisms of occupational lung disorders.
1. Direct injury. 2. Infection. 3. Allergy e.g. EAA. 4. Chronic inflammation e.g. COPD. 5. Destruction of lung tissue e.g. emphysema. 6. Lung fibrosis. 7. Carcinogenesis.
416
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.
417
What are the potential consequences of occupational lung disorders?
1. Increased morbidity and mortality. 2. Loss of income. Occupational lung disorders are avoidable and easily missed! It is important to balance health and employment and seek advice as soon as you notice any signs of lung problems.
418
What is the name of the lung disorder group that reflects inhaled dust/toxins?
Pneumoconiosis.
419
Give an example of a pneumoconiosis?
Coal worker's pneumoconiosis, silicosis, asbestos exposure, extrinsic allergic alveolitis.
420
What is asbestosis
Due to inhalation of asbestos for a period >10years
421
Pneumoconiosis: What might be the consequences of asbestos exposure?
- Lung cancer. - Persistent pleural effusion. - Diffuse pleural fibrosis. - Diffuse interstitial lung fibrosis.
422
What are the symptoms of asbestosis
Chest pain, wt loss, clubbing, dyspnoea
423
What is silicosis
Inhalation of silica particles from quarrying and sand blasting
424
What is coal workers pneumoconiosis
Inhalation of coal and dust particles which is ingested by macrophages which die and release enzymes causing fibrosis
425
What can silicosis and coal workers pneumoconiosis lead to
Massive fibrosis in the upper lobe
426
What does someone with silicosis have an increased risk of developing?
TB. | There is a borderline increased risk of cancer.
427
Define mesothelioma
Cancer arising from the mesothelium, the epithelial layer of the serosa
428
What is the major cause of mesothelioma
Asbestos
429
What is the epidemiology of mesothelioma
M>W Present between 40-70 Latent periods between exposure and development of tumour may be 45 years
430
What are the signs and symptoms of mesothelioma
``` SOB Dull chest pain Weight loss Fever Fatigue Clubbing Lymphadenopathy Hepatomegaly ```
431
What investigations might you do on someone to determine whether they have mesothelioma?
- CXR = show pleural thickening - CT scan. - Pleural biopsy.
432
What is the treatment for mesothelioma?
1. Symptom control. 2. Palliative chemotherapy or radiotherapy. 3. Radical surgery (removal of tumour blood supply).
433
What is the difference between radical radiotherapy and palliative radiotherapy?
1. Radical: daily treatments for 4-6 weeks. | 2. Palliative: the patient attends the minimum number of visits possible to control symptoms.
434
Give one advantage and one disadvantage of adding chemotherapy to radiotherapy.
- Advantage: survival advantage. | - Disadvantage: increased risk of toxicity.
435
Give 5 side effects of radiotherapy.
1. Fatigue. 2. Anorexia. 3. Cough. 4. Oesophagitis. 5. Systemic symptoms.
436
What are the 3 main aims of palliative chemotherapy?
1. Relieve symptoms. 2. Improve quality of life. 3. Shrink tumours.
437
Give 4 side effects of chemotherapy.
1. Alopecia. 2. Nausea/vomiting. 3. Peripheral neuropathy (nerve damage in extremities). 4. Constipation or diarrhoea.
438
Why is treatment of mesothelioma so difficult?
Mesothelioma is incurable as it is resistant to surgery, chemotherapy and radiotherapy. The average time from diagnosis to death is about 8 months.
439
Define pulmonary hypertension.
- mPAP > 25mmHg. | - Secondary RV failure.
440
What can cause an increase in mPAP?
Increased resistance to flow. | Increased flow rate.
441
Give 5 causes of pulmonary hypertension.
1. Left heart disease (Mitral stenosis, mitral regurgitation) 2. Lung parenchymal disease as chronic hypoxia leads to hypoxic vasoconstriction (COPD, asthma ILD, CF) 3. Pulmonary vascular disease (Idiopathic pulmonary hypertension, pulmonary vasculitis, Pulmonary embolism) 4. Hypoventilation (Kyphosis, scoliosis, MND, Myasthaenia gravis)
442
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.
443
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.
444
What might you notice in the ECG take from someone with pulmonary hypertension?
There might be signs of RV hypertrophy.
445
What might you notice in a CXR take from someone with pulmonary hypertension?
There might be enlarged proximal pulmonary arteries which taper distally.
446
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.
447
Why might someone with pulmonary hypertension experience peripheral oedema?
Blood accumulates in the pulmonary artery. The RV experiences a greater afterload and works harder to get blood out of the ventricle and into the pulmonary artery. There is RV hypertrophy and right heart failure. This results in peripheral oedema.
448
Give 5 signs of pulmonary hypertension.
1. RV hypertrophy (ECG). 2. Loud pulmonary secondary sound. 3. Right parasternal heave. 4. Enlarged proximal pulmonary arteries (CXR). 5. In advanced disease there are signs of RHF, elevated JVP, hepatomegaly and pleural effusion etc.

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