10. Respiratory Flashcards
(117 cards)
1
Q
What is decompression sickness?
A
Increased partial pressure at below sea level leads to diffusion of nitrogen from lungs into blood so if the diver ascends too quickly the rapid change in pressure causes bubble formation leading to tissue damage and pain.
2
Q
What is respiratory distress syndrome?
A
Loss of surfactant upsets Laplace’s law and surface tension of small alveoli isn’t kept low so there is alveolar collapse due to pressure differences in different sized alveoli. Less surface area for gas exchange and respiratory failure.
3
Q
How is respiratory distress syndrome in premature babies managed?
A
Mum is given steroid injections to stimulate surfactant generation if anticipated.
4
Q
How is carbon monoxide poisonous?
A
CO binds to haemoglobin and forms carboxyhaemoglobin so haemoglobin has less space to bind to O2 and also has greater affinity so won’t deliver O2.
5
Q
What are the results of acute and chronic carbon monoxide poisoning?
A
Acute - death.
Chronic - headaches, confusion, nausea etc.
6
Q
How is carbon monoxide treated?
A
Hyperbaric O2 therapy - O2 concentration high enough to displace CO and restore haemoglobin function.
7
Q
What is pulmonary embolism?
A
Thrombus from a site other than the lungs lodges in one of the arteries of the pulmonary tree.
8
Q
What are the effects of pulmonary embolism?
A
V/Q mismatch in the section of lung the artery supplies so pO2 of the blood leaving that section is normal but pCO2 is low as no new blood enters so has longer to equilibrate with alveolar air. The health lung is overloaded due to blood being redirected there. Too much blood means inefficient exchange of pO2 - blood has low pO2 and normal pCO2. Overall, there is type I respiratory respiratory failure.
9
Q
What is the fatal danger of a pulmonary embolism?
A
Sudden pulmonary hypertension causes mechanical shock from RV failure in the heart.
10
Q
How is hypercapnia from V/Q mismatch in pulmonary emboli corrected?
A
Increased respiratory rate.
11
Q
What are the types of respiratory failure?
A
Type I - pO2 low, pCO2 normal or low.
Type II - pO2 low, pCO2 high.
12
Q
What is type I respiratory failure caused by?
A
Diffusion defect or V/Q mismatch.
13
Q
What diffusion defects can cause type I respiratory failure?
A
Pulmonary oedema - fluid in alveoli so increased diffusion distance.
Emphysema - decreased compliance of lungs causing hyperexpansion and reduced surface area for gas exchange.
Pulmonary fibrosis - fibrous deposits between alveolus and capillary basement membrane so increased diffusion distance.
14
Q
What is type II respiratory failure caused by?
A
Decreased respiratory effort, chest wall defects, decreased compliance, extremely high airway resistance.
15
Q
What can decrease respiratory effort and hence cause type II respiratory failure?
A
Narcotics/head injuries/neurological deficits impact ability of respiratory centre. Muscular dysfunction anywhere from the brain to the NMJ (MS, Duchenne’s muscular dystrophy etc).
16
Q
What chest wall defects can cause type II respiratory failure?
A
Rigid structure means it’s harder to move and inflate the lungs. Severe scoliosis/kyphosis, severe pectum excavatum/carranatum, flail chest (multi-rib fracture), tension pneumothorax.
17
Q
What can cause decreased compliance that causes type II respiratory failure?
A
Severe pulmonary fibrosis.
18
Q
What causes increased airway resistance that leads to type II respiratory failure?
A
Severe life threatening asthma attack, acute exacerbation of late-stage COPD.
19
Q
What is asthma?
A
A reversible airway obstruction.
20
Q
What is the pathophysiology of asthma?
A
Airway remodelling: increased airway smooth muscle thickness; damaged epithelia/basement membrane from chronic inflammation from reaction to allergens. Contraction of smooth muscles, due to histamine and prostaglandin release in response to stimuli, increase airway resistance so less air is expired initially.
21
Q
What is a hypothesis that could explain why asthma is so prevalent in the Western world?
A
Hygiene hypothesis - overuse of cleaning chemicals means immune system is less trained for harmless bacteria so hyperactive.
22
Q
What are the types of asthma?
A
Allergic, viral - disappears by 5 years, occupational asthma.
23
Q
What are the features of a history leading to an asthma diagnosis?
A
Expiratory, polyphonic wheeze; dry cough with diurnal variation (worse at night) - induced by exercise; breathlessness; chest tightness; reversed with B2 agonists.
24
Q
What are the features of examination leading to an asthma diagnosis?
A
Eczema; lethargy and uncomfortable at rest; below heigh for age and underweight; laboured breathing signs - Harrison’s sulcus (indrawing of costal cartilages), tracheal tug, subcostal recession, obvious use of accessory muscles of inspiration.
25
What are the features of investigation leading to an asthma diagnosis?
Primary - PEFR reduces, single breath spirometry FEV1:FVC >70% but reversed with salbutamol.
Supportive (optional) - FENO high levels of NO, skin prick sensitivity to allergens, chest X ray excludes other causes.
26
What is the long term treatment for asthma?
Lifestyle - minimise exposure to allergens, exercise, fresh air.
Pharmacological - relievers: B2 agonists salbutamol and M3 antagonists ipratropium, preventers: low dose corticosteroids to suppress local immune function.
27
How is an asthma attack recognised?
Poor respiratory effort/loud wheeze/silent chest; panicked, agitated, sympathetic features - sweating, dry mouth, dilated pupils, nausea; altered GCS (cerebral hypoxia); O2 saturation <92% with peripheral cyanosis; pO2 low and pCO2 normal or rising.
28
How is an asthma attack managed?
High flow 100% O2, nebulised salbutamol and ipratropium continuously, IV salbutamol, aminophylline (smooth muscle relaxation in airways), and magnesium sulphate (no smooth muscle contraction in airways).
29
What is chronic obstructive pulmonary disease?
Progressive, worsening airway obstruction. An umbrella for chronic bronchitis and emphysema.
30
What is chronic bronchitis?
Mucus hypersecretion and inflammation due to cigarette smoke.
31
What are the features of chronic bronchitis?
Cough chronically productive with frequent infections. Airway remodelling to increase arterial smooth muscle.
32
What is emphysema?
Pathological destruction of terminal bronchioles and walls between alveoli.
33
What is the pathophysiology of emphysema?
Inflammatory response to chronic irritation from cigarette smoke causes macrophages to release elastase and other proteolytic enzymes so breaks down elastin. Redundant bullae form and collapse on expiration due to loss of supportive tissue so obstruct.
34
What are the features of emphysema?
Fick's law - less surface area for diffusion so impaired gas exchange. Less elastin lowers compliance so there is hyperinflation of lungs, causing barrel chest.
35
What are the causes of COPD?
Smoking mainly, a1-antitrypsin deficiency (hereditary leading to overactivity of elastase causing emphysema), pollution, occupational.
36
How do the stages of COPD present?
Early - productive cough, dyspnoea, tachypnea.
Middle - purse lip breathing, use of accessory muscles to inspire, barrel chesting.
Late - compensated respiratory acidosis (CO2 retention), wheeze, peripheral and central cyanosis, flapping tremor, pulmonary hypertension.
37
How is COPD diagnosed?
History used primarily but single breath spirometry and other tests can support diagnosis.
38
What single breath spirometry results support COPD diagnoses?
FEV1:FVC ratio affected without reversibility.
Mild 50-80%
Moderate 30-49%
Severe <30%
39
What tests support diagnosis of COPD?
CXR excludes other differential, CT assesses bullae in emphysema, ABG checks acid/base status, a1-antitrypsin blood test in young non-smoker.
40
What assesses COPD prognosis?
```
MRC dyspnoea score assesses amount of exertion that causes breathlessness:
1 - strenuous exercise
2 - hurrying or walking up hill
3 - walking at own pace
4 - 100m walking
5 - getting dressed
```
41
What lifestyle modifications are made to manage COPD?
Stop smoking (KEY), moderate exercise if MRC allows it, manage other co-morbidities.
42
What are the pharmacological interventions that are used to manage COPD?
B2 agonists, e.g. salbutamol, for bronchodilation but also causes systemic effects like tachycardia.
M3 antagonists, e.g. ipratropium, for bronchodilation but side effects like dry mouth and nausea.
Aminophylline for bronchodilation from inhibits phosphodiesterase so more cAMP and PKA so MLCK phosphorylated. Also increases respiratory drive and power.
Oral corticosteroids to reduce inflammation to improve chronic bronchitis.
Mucolytics thin the mucus so easier airway clearance.
43
What are some non-pharmacological interventions used in COPD management?
Pulmonary rehab - breaks cycle of breathlessness.
Long term O2 therapy - need 16 hours a day, no smoking around it due to flamability.
Pneumonectomy - remove damaged lung lobe so FEV1 increased and V/Q mismatch is corrected but less surface area for gas exchange.
44
What are the investigation performed in acute exacerbations of COPD?
Pulse oximetry, ABG, sputum culture, CRP, U&Es, FBC, CXR.
45
What is the management of acute exacerbations of COPD?
Titrated O2 therapy to get O2 sats above 88%.
Salbutamol, atrovent, aminophylline.
High dose steroids if non-infectious.
Non-invasive ventilation if conscious.
46
What are upper respiratory tract infections?
Acute inflammation of the middle airways, nothing sinister in most cases and usually viral.
47
What is the presentation of URTIs?
Dyspnoea, productive cough, fever, malaise. Associated with sinusitis and otitis media due to connections to nasal cavity.
48
What is the CXR of URTIs?
Clear as only middle airways affected.
49
What is pneumonia?
A lower respiratory tract infection with inflammation of the lung alveoli. It impairs gas exchange and causes type I respiratory failure if unchecked.
50
How is pneumonia classified?
Place of acquiring - community or hospital.
Presentation - acute or chronic.
Organism - bacterial, viral, or fungal.
Pathology - lobar, broncho, or interstitial.
51
What are the symptoms of pneumonia?
Productive cough, fever, malaise, rigors, pleuritic chest pain, nausea and vomiting.
52
What are the signs of pneumonia?
Pyrexia, tachycardia, tachypnea, cyanosis, dullness to percussion, bronchial breathing, pulmonary crackles.
53
What are the investigations for pneumonia?
```
Bloods - FBC, CRP, U&Es, lactate, culture.
Erect CXR (shows consolidation in affected lobe), sputum culture.
```
54
How is the management plan for pneumonia decided?
Using CURB-65 score: confusion, urea >7mmol/L, respiratory rate >30/min, BP <90/60, age >65 years.
If score over 1 - severe and needs hospital admission.
If score 1 or 0 - moderate pneumonia so care in the community.
55
How are hospital admitted pneumonia patients treated?
Co-amoxiclav and clarithromycin given. B2 agonists/M2 antagonists particularly in asthmatics. High flow O2.
56
How are community cared for pneumonia patients treated?
Amoxicillin as probably streptococcus pneumoniae.
57
What are the sequelae of pneumonia?
Resolution with minimal scarring so normal lung function. Lung abscess formation that ruptures and cause empyema. Bronchiectasis (permanent dilation of bronchioles). Septicaemia or meningitis. Death from type I respiratory failure.
58
What are the atypical causes of pneumonia with their treatment?
Gram negative bacteria: legionella, chlamydia.
| Treat with macrolides (clarithromycin) or tetracyclines (doxycycline).
59
What are the viral causes of pneumonia?
Adenovirus, respiratory synctial virus, influenza.
60
What is the presentation of viral pneumonia?
Severe, haemorrhage into lung parenchyma, patchy diffuse ground glass appearance on CXR.
61
How is hospital acquired pneumonia treated?
Co-amoxiclav as normally staph. aureus, tazocin if no improvement.
62
What is aspiration pneumonia?
Contents of the GI tract end up in the lungs due to compromise to epiglottis/larynx as protective mechanisms.
63
What is the normal cause and treatment for aspiration pneumonia?
Viridans streptococci and other anaerobes. Co-amoxiclav as first line.
64
What are the causes of immunosuppressive pneumonia?
PCP, TB, other mcyobacteria, aspergillus, cytomegalovirus.
65
How do splenectomies affect risk of pneumonia?
Patient at increased risk of colonisation by strep. pneumonia, H.influenzae etc. so have immunosuppressive pneumonia but with normal pathogens.
66
What is tuberculosis?
Bacterial infection of the lungs by mycobacterium tuberculosis, or M. bovis, or other mycobacteria.
67
What are the features of mycobacterium tuberculosis that make it a good invader?
Mycolic acid coating gives it structural rigidity and makes it hard for antibiotics to penetrate. Non-motile and obligate aerobe so colonises upper lobes normally. Transmitted via respiratory droplets but not very infectious so need chronic exposure.
68
What is the pathogenesis of tuberculosis?
Initially phagocytosed by alveolar macrophages but not destroyed due to mycolic acid coat. So drains to lymph nodes to form Ghon focus with local inflammation and local lymph node involvement.
69
What is latent TB?
The Ghon focus is contained and usually self heals but bacteria stay present in small numbers so can activate.
70
What are the risk factors for activation of latent TB?
Immunocompromised, diabetes, kidney disease, etc.
71
What is active TB?
Bacteria multiply and this manifests as symptoms of the disease.
Primary - direct progression from initial Ghon focus (5%)
Secondary (<5 years) and reactivation (>5 years) - re-emergence of bacteria despite initial containment of Ghon focus (95%).
72
How do INF gamma blood tests and sputum culture results differ in latent and active TB?
INF gamma blood - positive in latent and in active.
| Sputum cultue - negative in latent, positive in active.
73
What are the features of TB granulomas?
Immune granuloma made of lymphocytes, Langhan's giant cells, epitheloids. Central caseous necrosis.
74
What is the presentation of TB?
Risk factors from history: migrant to UK, low socio-economic status, HIV, close contact with relatives with TB.
Symptoms: fever and night sweats, anorexia and resultant cachexia, fatigue/malaise, productive cough, dyspnoea.
Signs: occasional pulmonary creackles, signs of cavitation/fibrosis (dull percussion), effusion signs (stony dulness in percussion).
75
What are the investigations of TB?
CXR where apices of lung have patchy consolidation with central cavitation.
Sputum analysis with ZN stain to look for acid fast bacteria.
Sputum cultures takes 1-3 weeks.
Check exposure to TB: Mantoux test intradermal infection that forms lump if encountered TB, interferon gamma releasing array detects antigen specific INF gamma.
76
How is TB treated?
RIPE:
Rifampicin for four-six months, interferes with TB RNA synthesis, but hepatotoxic and turns body secretions orange.
Isoniazid for four-six months, breaks down mycolic acid shell so rifampicin can access TB, but hepatotoxic and peripheral neuropathy.
Pyranzinamide for two months, inhibits trans-translation by binding ribosomes, but hepatotoxic.
Ethambutol for two months, obstructs cell wall formation, but visual disturbances.
77
What is atypical TB?
Not normal pulmonary TB that is susceptible to RIPE protocol, it's resistant (MDR to rifampicin and isoniazid, XDR to all fluoroquinolones and some of protocol), or miliary TB (diffuse through body from bacteraemia), extrapulmonary TB (from miliary TB or unique infection).
78
How is TB prevented?
Notifiable disease. BCG is 70-80% effective in preventing severe childhood TB, little evidence for preventing adult TB so only high risk. Barrier medicine - negative pressure isolation and limit number of different staff dealing with patient.
79
What are the risk factors of lung cancer?
Smoking, asbestos (mesothelioma), radon, genetics/familial factors, occupational carcinogens.
80
How is lung cancer staged?
```
TNM staging.
T1/2, N0, M0 = stage I.
T3/4, N0, M0 = stage II,
Any T, N1 or N2, M0 = stage III.
Any T, any N, M1 = stage IV.
```
81
What are the T stages of lung cancer?
```
T1a <2cm
T1b 2-3cm
T2a 3-5cm
T2b 5-7cm
T3 >7cm
T4 any
```
82
What are the N stages of lung cancer?
```
N1 = ipsilateral hilar lymph node
N2 = ipsilateral mediastinal lymph node
N3 = contralateral lymph node (hilar or mediastinal)
```
83
What are the symptoms of lung cancer?
Direct: none, cough/haemoptysis, dyspnoea, wheezing, chest pain, recurrent chest infections.
Local metastatic: bloated face, dyspnoea, dysphagia, hoarse voice, Horner's syndrome.
Systemic metastatic: pathological bone fracture, headaches, double vision, thirst and constipation, seizures.
84
What are the signs of lung cancer?
Elevated non-pulsatile JVP, clubbing, no signs (commonest).
| Paraneoplastic syndromes: Cushing's if small cell, SIADH.
85
What are the investigations of lung cancer?
Erect CXR, staging CT with or without contrast, PET scan, MRI, ultrasounds scan, biopsy to check malignancy, tumour screening for molecular markers - e.g. EGFR mutations.
86
How is the management strategy of lung cancer decided?
MDT to deal with it. Based on performance status grade: 0=fully active, 1=restricted by intensive work, 2=up and about >50% of time, 3=limited self care ambulatory <50% of time, 4=bed/chair bound, 5=dead. 0-2 have surgery, 3+ get palliative care.
87
What are the treatment options for lung cancer?
Surgery - for non-small cell, only 25% are operable.
Radiotherapy - radical is curative option, palliative for symptom control.
Chemotherapy - potentially curative in small cell, palliative in non-small cell.
Palliative - >2 WHO grade, analgesia, patient support, low dose radiotherapy/chemotherapy.
88
What are the features of addiction?
Continued used despite knowledge of negative consequences, craving during abstinence, failure to stop, denial.
89
What is the physiology of nicotine addiction?
NAChR stimulated to cause dopamine release so feel satisfied. Increased use leads to upregulation of receptors so more nicotine is needed for the same hit, so craving increases. Drop in nicotine leads to cravings and withdrawal.
90
How should nicotine addiction be managed?
Quitting:
- ask do you smoke, advice them to stop, act refer to NHS stop smoking services
- nicotine replacement therapy (twice as likely to quit)
- varenicline - partial NAChR agonist
Harm reduction:
- cutting down
- E-cigarettes
91
What is interstitial lung disease?
An umbrella term for the disease processes that affect the parenchyma between the alveoli.
92
What are the types of interstitial lung disease?
Idiopathic pulmonary fibrosis, asbestosis, drug induced, connective tissue disorders, extrinsic allergic alveolitits, sarcoidosis.
93
What are the features and treatment of idiopathic pulmonary fibrosis?
Cause unknown, in >80 year olds, treat with pirfenidine (bad side effects).
94
What are the features of asbestosis?
From asbestos exposure, formation of asbestos plaques and thickening of interstitium and can lead to mesothelioma, rounded atelectasis, and bronchogenic lung cancer.
95
What are the drugs that lead to drug induced interstitial lung disease?
Exposure for over 10 years to cause it: methotrexate, bleomycin, amiodarone, nitrofurantoin amongst others.
96
What are the connective tissue disorders that can cause interstitial lung disease?
Lupus, scleroderma, rheumatoid arthritis, polymyositis, Sjogren's syndrome.
97
What are the type of extrinsic allergic alveolitis?
Acute - farmer's lung, from thermophilic actinomyocytes in hay, inspiratory crackles.
Chronic - pigeon fancier's lung, from chronic immune response to antigens from pigeons so granulomas form with inspiratory crackles.
98
How is sarcoidosis treated?
High dose steroids to dampen immune system.
99
What are the patient features of interstitial lung disease?
Older, smokers, previous exposure to respiratory toxins, non-productive cough, dyspnoea, canosis, tachycardia, tachypnea, reduced SaO2, velcro crackles, clubbing, signs of cor pulmonale, ABG low O2 and low or high (late stage) pCO2, restrictive spirometry.
100
What is pleural effusion?
Collection of some types of fluid between the layers of the pleura.
101
What is the pathogenesis of pleural effusion?
Increased production - hydrostatic pressure increase (hypertension), permability increase (sepsis), oncotic pressure decrease (cirrhosis).
Decreased clearance - lymphatic blockage (tumour), increased venous pressure (right sided heart failure).
102
What is the difference between transudate and exudate in terms of causes of pleural effusion?
Exudate has high serum protein and high serum LDH and is caused by infection, malignancy, pancreatitis, sepsis etc.
Transudate has low serum protein, and low serum LDG and is caused by anything that affects Starling's forces - left sided heart failure, cirrhosis, kwashiorkor, atelectasis, hypertension.
103
What are the symptoms and signs of pleural effusion?
Breathlessness, pleuritic chest pain, stony dullness to percussion, coarse crackles, dry cough, paroxsymal nocturnal dyspnoea.
104
What are the less common types of pleural effusion?
Haemothorax - blood.
Empyema - acidosis from infection, systemically unwell.
Chylothorax - lymphatic fluid.
105
How is pleural effusion treated?
Thoracentesis to acquire fluid and test appearance to determine route cause.
Drain fluid, chemical pleurodesis to unite pleura together, surgery rarely.
106
What is a pneumothorax?
Air within the pleural space.
107
What are the types and causes of pneumothoraces?
Primary - in healthy patients, lanky and smokers.
Secondary - unferlying respiratory pathology.
Iatrogenic - central line etc.
108
What is the presentation of pneumothoraces?
Pleuritic chest pain and dyspnoea. Reduced air entry on one side and hyperresonance in affected area of lung.
109
How is a pneumothorax investigated?
Erect CXR - blackout where air is. If >2cm - large, if <2cm - small.
110
How are pneumothaces treated?
Small - leave it if no SOB.
Large or any size with SOB - simple needle aspiration, chest drain, chemical pleurodesis (last resort if surgery contraindicative), surgical pleurectomy.
111
What are the consequences of a pneumothorax?
Discharge whenever stable with a primary pneumothorax or after 24hrs of stable observations.
Can't fly until CXR shows complete resolution after 6+ weeks.
Diving avoided unless bilateral pleurectomy.
112
What is a tension pneumothorax?
Huge pneumothorax that is large enough to cause mediastinal deviation and compress great vessels, leading to circulatory compromise.
113
What are the signs of tension pneumothorax?
Almost absent chest movement, hyper resonance, tracheal deviation away from affected side, hypoxia signs, early signs of mechanical shock.
114
What is the treatment of tension pneumothoraces?
Emergency needle decompression, O2, chest drain, cardiothoracic surgical referral.
115
What is chest wall disease?
Any disease that distorts the shape of the thoracic cage and/or impact respiratory function.
116
What are the types of chest wall disease?
Congenital - pectus deformity, scoliosis, kyphosis, muscular dystrophy etc.
Acquired - trauma, iatrogenic, ankylosing spondylosis.
117
What is the presentation of chest wall disease?
Decreased ability to clear secretions through the coughing reflex so recurrent infections. Sleep discorded breathing - paroxysmal nocturnal dyspnoea. If severe, hypoventilation so type II respiratory failure.
