RESPIRATORY Flashcards
Most common cause of non-infectious lung granulomas
Sarcoidosis
Then GPA
Typical patient with sarcoidosis
Young to middle ages, F > M, pt of African descent
Sarcoidosis presentation
Bilateral hilar lymphadenopathy + skin (eh shin nodules) or eye lesions (uveitis). In half of cases, detected incidentally on CXR.
Histology difference between TB & Sarcoidosis
TB = caseating granulomas. Sarcoidosis = non-caseating gramulomas.
Lung lymphadenopathy / granulomas differential
Sarcoidosis, TB, Lupus, Lymphoma
Sarcoidosis cause
Auto-immune, may be triggered by infection
Granulomatous lung disease + vasculitis +ANCA
GPA
Granulomatous lung disease + vasculitis + no ANCA
RA, Lupus, systemic sclerosis
Antibiotic options for community acquired pneumonia + most likely pathogen
Amoxicillin. Strep pneumoniae.
Clarithromycin for penicillin allergy
Antibiotic options for hospital acquired pneumonia + most likely pathogen
Defined as acquired >48hr since admission.
Flucloxacillin for staph aureus. May need rifampicin or vancomysin if resistant.
1. Staph aureus
2.Gram neg enterobacteria
What factors affect the risk of developing a respiratory tract infection
- Commensal colonistation of upper airway - naso, oro & laryngopharynx - normally strep (virdidans) and staph epidermidis
- Swallowing - if can’t do this can aspirate into lungs (think neuro conditions, stroke, parkinsons, MND etc; also tumours and surgery)
- Normal lung physiology, eg. muco-ciliary escalator, airway dilatation and narrowing with sympathetic & parasympathetic innervation, cough reflex, alveolar wall space. Loads of conditions can affect these - cystic fibrosis, COPD, asthma, bronchiecstasis, interstitial lung diseases, emphysema.
4.Immune system.
Infiltration of B and T cell. Think of any immunocompromised individual.
List the signs of pneumonia
Dull to percussion
Bronchial breathing (high pitch inpspir & expirat, pause between breath)
Crackles +- wheeze
Hypoxia and signs of respiratory failure - nail beds - blue? under tongue - blue? - would see this in pathients with chronic lung disease + pneumonia
List the symptoms of pneumonia
Fever Chills/ rigor Chest pain - pleuritic SOB Cough - productive Arthralgia Myalgia
Investigations for pneumonia
CXR
Bloods - FBC (look at white cell count - bacterial or viral); U&E, LFT - check organ function, culture, CRP
Sputum - culture
Pulse oximetry
Describe the features of pneumonia on CXR
Bronchogram - airways that you can see within the consolidation - can now see them bc of consolidation in alveoli
Fluid-air levels - sign of an abscess
Diffuse = suggests viral or fungal - PCP
One area of consolidation = bacterial
Common pathogens for hospital acquired pneumonia - how would you know it was hospital acquired?
Staphylococcus aureus
Pseudomonas aeruginosa
Klebsiella pneumoniae
Would acquire it after 48 hours - new onset fever, cough etc (pneumonia signs).
The ones above are if it has been acquired after 5 days.
If under 5 days, same pathogens as community acquired but they have just got it in hospital
Common pathogens for community acquired pneumonia
Streptococcus pneumoniae Mycoplasma pneumoniae Chlamydophila pneimoniae Legionella pneumophila Haemophilus influenzae
What are the signs of pneumonia on a CXR
Air Bronchogram
Air fluid levels - indicates abscess
Multilobular, suggest strep pneumoniae, A aureus, Legionella
Diffuse - suggestions viral or fungal
Outline how to assess the severity of community acquired pneumonia
CURB65 score - 1 point for each C - confusion/ delerium U - urea >7mmol/L R - respiration >30 per minute B - BP , <90 systolic, or <60 diastolic >65 or over
0-1: manage in community - amoxicillin
2: admit to hospital - amoxicillin + clarithromycin - consider IV
3: admit to hospital, monitor closely - co-amoxiclav IV + clarithyromycin
4-5: critical care unit
If have hospital acquired, consider something like vancomycin for MRSA
What is the major complication of pneumonia and what groups are most at risk of this
Sepsis
Those with comorbidities
Those over 65
What pneumonia pathogen can you not use a macrolide (eg clarithromycin) on?
Klebsiella
Name two cephalosporins
Cefotaxime
Cefuroxime
What considerations should be made for atypical pathogens when looking for the cause of pneumonia
Basically just be aware there are some atypical bacteria that are hard to detect as they dont grow on agar - eg chlamydophila and Legionella - so need to do serology to look for antigens- these are the hospital acquired ones
Need to use macrolides for these
What antibiotics should be used for atypical pneumonia pathogens
Macrolides, fluroquinolones
NOT BETA LACTAMS
What extrapulmonary features are associated with mycoplasma pneumoniae
haemolytic anaemia (cold agglutinins),
Raynauds (cold agglutinins) erythema multiforme,
bullous myringitis (blisters on tympanic membrane),
encephalitis
Which atypical pneumonia pathogen is associated with epidemics
Mycoplasma pneumoniae - seen in younger adults, milder disease with more extra-pulmonary features
What atypical pneumonia pathogen causes diarrhoea
Legionella
*need a fluorquinolone prescribed for this
What microbiology tests should be done for pneumonia
Sputum - culture
Bloods - culture
Serology - atypicals, viruses
Urinary antigen - Legionella, s pneumoniae
PCR - for virus outbreaks and mycoplasma pneumoniae
NB - Always request acid fast bacilli if epidemiology or clinical features are suggestive
What is the differential diagnosis for pneumonia
TB - *history will tell you if this is a risk - travel
Pulmonary embolus - SOB & pleuritic chest pain
Cancer
Heart failure - SOB
Interstitial lung disease
What are the risk factors/ flags in a history for TB
Born outside of UK in TB endemic country
Travel to TB endemic country
What is the preferred method of testing for TB in a patient who has been vaccinated
Blood tests and IGRA testing. Interferon gamma release assays. The test measures how quickly CD4 cells release interferon gamma in response to TB antigen. If this is quick, suggests they have already been primed to do this and have had an active TB infection. Specific test - should not give false positive.
How could you test for TB in a patient who has never received a TB vaccine
Manoux skin test. Inject some TB antigen into the skin and see if there is an immune response. If there is = previous infection (or received vaccination).
Response - raised, hardened area around the site of injection. Redness should not be considered a positive reaction.
LIMITATION - Cant distinguish between TB & BCG.
What is the transmission route of TB
Aerosol droplets - only when patient coughs.
Pulmonary TB is the only communicable form.
What is latent TB
TB infection without disease, because of immune system containment.
Signs are granuloma on CXR, lymphadenopathy, +ve mantoux or blood test (depending on if vaccinated) but with no disease symptoms
Lifetime risk of reactivation is 5-10%
What causes re-activation in latent TB
Change in immune status of the patient
Cancer treatment
Immunosuppressant drugs - DMARs
HIV infection
What are the most common sites of TB infection
Lungs - pulmonary Lymphatics - extra thoracic (can see/ palpate) then intra-thoracic Pleural GI Spine Bone Miliary - disseminated - everywhere Meningitis GU TB is aerobic so it will prefer to be in apex of lungs or near a blood supply where it can get oxygen. It may go to deeper tissues but this is less common presentation.
What are the symptoms of pulmonary TB
Cough - dry then productive
Pleuritic chest pain (Pleurisy/ pleural effusion)
Haemoptysis (uncommon)
Systemic: Low grade fever Anorexia or weight loss Malaise Night sweats Clubbing
What is the treatment for TB
Rifampicin
Isoniazid
Pyrazinamide
Ethambutol
How would you differentiate between Pneumonia and TB
History - has the patient had contact with TB endemic groups? Travel? Deprivation?
TB - low-grade fever, night sweats, may cough blood
Pneumonia - fever and chills
CXR - can help to rule out
Blood tests - IGRA
SOB differential
- Think about patients with sickle cell - emergency if they have any chest signs - Acute Chest Syndrome
- Pt over 65 - higher risk for pneumonia related sepsis
“ILL”
Inflammation/ infection - pneumonia, TB, pleurisy
Lumps - cancer, PE (infective?), sickle crises
Liquids - Pleural effusion
Presentation of infective embolus
DVT signs & symptoms - swollen and painful leg, tender, discolouration and warm
+ Pneumonia signs - pleuritic chest pain, cough - productive, SOB etc
What are the main complications of pneumonia
- Sepsis - especially in older patients with comorbidities
- Parapneumonic effeusion - left over fluid in the pleural after infection - 3 types, uncomplicated, complicated and empyema - pus
- Empyema
What are the signs of parapneumonic effesion, what needs to be done to see if it is complicated or uncomplicated
Inflammatory markers dont settle
Pain on deep inspiration
Stony to dull percussion
Need to do thoracentesis - pleural tap - drain some of the fluid and culture/ test it
What are the signs of complicated parapneumonic effusion
Ph <7.4
Positive culture
Thick fluid - pus
Glucose <3.3 mmol/L
How many patients with community acquired pneumonia develop parapneumonic effusion.
How many of these are complicated effusions
Up to 50%
1%
What does parapneumonic effusion indicate
The infection hasn’t settled and is still there. Need to treat with antiobiotics. Cover aerobic and anerobic.
Co-amoxiclav, piperacillin-tazobactam or meropenam (need to include anaerobic coverage) x ≤3 wks
What is the difference between empyema and a lung abcess
Empyema is pus in the pleura
Lung abscess is pus in the lung
Empyema is pus that forms in a pre-existing cavity
Abscess is pus that forms where there is no cavity
Causes of lung abscess
1.Aspiration, alcoholics (think bc of liver infection?)
2.IVDU - DVT or Lemierres - in children/ younger person - sore throat and raised IJV pressure.
Need long term antibiotics, and possibly surgical drainage
Name two commonbeta lactams + beta lactamase inhibitor combiniations
Co-amoxiclav
Piperacillin-tazobactam
How would you treat hospital acquired pneumonia
If acquired <5 days - likely to be CAP pathogen - as in hospital treat with beta lactam + inhibitor. Co-amoxiclav or pipericillin-taxobactam
If acquired >5days - likely to be atypical hospital pathogen. DONT USE ANY BETA LACTAMS. May need vancomysin if MRSA, can use pipericillin-taxobactam for some. Cannot use macrolide on Klebsiella.
List the causes of pneumonia in immunocompromised individuals
Bacterial - all the usuals plus atypicals
Fungal - Pneumocystic jirovecci, aspergillus
Viral - cytomegalovirus, adenovirus, RSV
Commonest cause of bronchitis
Viral (spread from upper respiratory infection)
Rarely bacterial - if it is, it’s same ones as for CAP
Dont treat with antibiotics as usually viral
Cause of bronchiolitis in children
Respiratory syncitical virus - causes Inflammation of bronchioles and mucus production cause airway obstruction
What is the difference between acute and chronic bronchitis
Acute - 1-3 weeks
Chronic - x3 months of coughing, two years in a row - usually seen in COPD
What is the main difference in the treatment of pneumonia in community and hospital
In hospital you dont give beta lactams (amoxicillin), always give beta lactam + inhibitor (co-amoxiclav)
What two respiratory conditions cause systemic (fever, chills, arthralgia, myalgia etc) symptoms
Pneumonia
Influenza
Bronchitis dosen’t cause these
What antifungal treatment should be given for pneumocystis pneumonia
trimoxazole (ergosterol inhibitor), or pentamidine - IV for 2-3 weeks.
What are the common pathogens of upper respiratory tract infections
Viral
- Rhinovirus (50%)
- Influenza A (30%)
- Coronavirus
- Adenovirus
- Parainfluenza virus
What are the complications of upper respiratory tract infection
sinusitis
otitis media (middle ear infection)
bronchitis
rarely pneumonia
Describe the presentation of scarlet fever - what bacteria is this caused by
Pharyngitis or cellulitis
+ Rash - erythematous, finely papular, papillae - feels like sandpaper. Blanches on pressure.
Caused by strep pyogenes.
What is the complication of scarlet fever, what blood test should be done to assess the risk of complications
Rheumatic fever - antibodies against streptococcus attack joints
Should do Anti SLO test to assess risk - this is a blood test to measure the levels of anti streptolysis O antibody. If it is rising (>200 units adults; >400 units children), this is indicative of developing rheumatic fever. Also risk of glomerular nephritis.
What are GABHS associated diseases
Group A beta hemolytic streptococcus diseases
Scarlet fever
Rheumatic fever- carditis, arthritis, chorea, erythema marginatum, and subcutaneous nodules
What are the commonest causes of pharyngitis
Viral - EBV, Rhinovirus, Adenovirus (80%)
Bacterial - strep pyogenes (20%) - need to check for rash and ?scarlet fever in children and anyone immunocompromised
What is lemierre’s disease
Pharyngitis followed by a septic thrombophlebitis (blood clot) of the internal jugular vein and dissemination of the infection to multiple sites distant from the pharynx - look for enlarged internal jugular vein
Cause: Fusobacterium necrophorum
Bacterial causes of pharyngitis
GABHS Streptococcus pyogenes, Lancefield Group A b-haemolytic streptococci 10-30%
Other streptococci
Mycoplasma pneumoniae (3-14%) – like a nasty cold with associated headache / congestion, occurs in epidemics,
Neisseria gonorrhoea and other sexually transmitted infections
Fusobacterium necrophorum - “Lemierre’s Disease”
Corynebacterium diphtheria (travel e.g. Russia)
What is the treatment for strep throat
Amoxicillin
What is a differential feature of Diptheria
Grey/ thick membrane over tonsils
What is the presentation of Diptheria
Child with fever, sore throat, malaise, adherent membrane over tonsils, pharynx and/ or nasal cavity
What are the signs of Diptheria
Lymphadenopathy in neck, rapid breathing
Thick greyish membrane on tonsils
Travel to russia
What is the treatment of Diptheria
- Preformed antibodies to Diptheria toxin
2.Erythromycin (macrolide)
Antibiotic is used stop onwards carriage. Need antibodies to clear infection in the child.
What is the centor criteria
Criteria that give an indication about whether pharyngitis is due to bacteria
List the (centor) criteria and limits to be met for bacterial pharyngitis
- Tonsilar exudate
- Temperature >38
- Tender anterior cervical lymph nodes - the ones that run along sternocleidomastoid
- No cough
3/4 = PPV of bacterial cause, 40-60%
No 3/4 = NPP of 80%
How would you identify if an upper respiratory tract infection was viral or bacterial
Centor criteria
What is the presentation of sinusitis
Fever, facial pain, purulent (pus) nasal discharge, recent history of cold
What is the presentation of acute epiglottitis and what is the cause
fever, dysphagia, drooling and inspiratory stridor
Cause is haemophilus influenzae type b - but rare with vaccine
Treat with : Amoxicillin
20% Beta-lactamse producers so Doxycycline, Co-amoxiclav
Not susceptible to macrolides - erythromycin etc.
What is the presentation of whooping cough
Chronic cough - dry, may cause vomit, afebrile, or low grade fever, lungs are clear, runny nose, conjunctivitis
Incubation 1 - 3 weeks (runny nose/ fever)
Paroxysmal phase - cough, vomiting, leucocytosis - secondary complications happen at this point. Use erythromycin.
What is the microbiology of bordatella pertussis
Gram negative bacillus
Treat with macrolide - clarithromycin; erythromycin
How do you diagnose whooping cough
Have to do culture and serology and look for antibodies against BP toxin
Dx by culture, PCR, ELISA for IgG against PT
What are the clinical features of whooping cough
Clinical features
Incubation 7-10 (5-21d)
Catarrhal phase 1-2 weeks; rhinorrhoea, conjunctivitis, low-grade fever and at end of phase lymphocytosis
Paroxysmal phase 1-6 weeks coughing spasms ,inspiratory ‘whoop’ post-ptussive vomitting, cough>14d
Convalescent phase
Adults chronic cough, paroxysms of coughing and 50% post ptussive vomitting but fairly specific for pertussis
Complications; pneumonia, encephalopathy, subconjunctival haemorrhage
What is the presentation of croup (swelling of the larynx, trachea and bronchi)
Barking cough, febrile, cyanosed, intercostal recession, inspiratory stridor (a high pitched wheezing noise due to turbulent airflow in upper airway)
What is croup
Acute laryngo-treacheobronchitis
What is included in the dTaP vaccine
diphtheria, tetanus and acellular Pertussis
at 2,3, 4 mo. and 3-4 yo
What are the two serious infections that you want to rule out in a child that presents with sore throat (pharyngitis)
Strep pyogenes scarlet fever
Diptheria
What percentage of brain tumours are malignant
95%
List some cancers that can spread to the lung
breast colorectal prostate kidney melanoma thyroid lymphoma
List the different types of malignant tumours you can get in the pleura and benign tumours
Malignant: Mesothelioma - most common? Primary lymphoma Pleural Thyoma Pleural Sarcoma
Benign:
Fibrous
What is the different pathology of pleural cancers
- Mesothelial cells - epithelial cells that secrete serous fluid
- Lymphatics that drain the pleura
- Thymus cells
- Connective tissue between/ supporting epithelial cells of pleura
What are the different lung reactions to asbestos
Fibrous plaques - localised thicking of the pleura - exposure + a bit of local inflammation that has left some scar tissue. Not at risk of cancer. Benign - having these does not increase risk of mesothelioma over the normal population. Sign of asbestos exposure.
Asbestos effusion - fluid collection in pleura - sign of chronic inflammation.
Asbestosis (fibrosis) - lung fibrosis (base) + /- plaques 0 indicative of heavy asbestos exposure
Mesothelioma
Bronchial carcinoma
What are the two commonest cancers associated with asbestos exposure - explain why
Mesothelioma (more common - pleura more sensitive to asbestos)
Carcinoma - bronchials (squamous, adenocarcinoma)
What is the interval between asbestos exposure and development of mesothelioma
About 30 years (can be up to 50 years) - so need to ask patients about occupational/ social history throughout their whole life
- Have they worked in construction/ manufacturing industry? If so, what were they exposed to on a daily basis?
- Where did they grow up? Did any members of the family work in construction? Did they wash their clothes etc?
What are the different types if pathology of mesothelioma
Epithelioid
Sarcomatoid
Desmoplastic
Mixed / biphasic
Is there effective treatment for mesothelioma
No - treatment is palliative focused. Survival time is approximately 11 months.
When was asbestos most heavily mined and used?
1940 - early 2000. From 1980, decline.
Anyone who worked in a construction/ building/ manufacturing job during this period - you should ask more questions in the history about what they were exposed to, and try to get an idea about asbestos.
Anyone who was a builder, joiner etc in the 60/70’s are very likely to have had high asbestos exposure.
What are the clinical features of mesothelioma
chest pain breathlessness weight loss SVCO sweating abdominal pain
What investigations would you do for mesothelioma, what is the main differential
CXR CT scan Pleural aspiration - biopsy Blind or CT guided pleural biopsy VATS pleural biopsy
Main differential is a bronchial lung cancer - carcinomas
What is the treatment for mesothelioma
Symptom control
Palliative chemotherapy
Radical surgery/debulking surgery
Palliative radiotherapy
Name some of the benign tumours of the lung
hamartoma carcinoid lipoma chondroma leiomyoma nerve sheath tumours fibroma
Is lung cancer usually primary or secondary
Both are common but secondary - metastatic is more common
Metastatic carcinoma is more common than primary carcinoma - think about history of cancers
Is lung cancer more common in males or females
Males 2:1
List some of the paraneoplastic changes associated with lung cancer
•Secretion of PTH
•SIADH
•Secretion of ACTH and other hormones (sweating?)
•Hypertrophic pulmonary osteo-arthropathy (HPOA)
•Myasthenic syndrome (Eaton Lambert)
Finger Clubbing
NB: Haem/ cardio
Migratory thrombophlebitis
Non-infective endocarditis (Libman Sacks)
Disseminated intravascular coagulation (DIC)
List some of the non carcinoma cancers of the lung
- Bronchial gland neoplasm
- Pleural neoplasia
- Soft tissue sarcoma/benign tumour
- Lymphomas
- Hamartomas
What are the common lung carcinomas
25% squamous cell carcinoma 35% adenocarcinoma 10% large /non small cell undifferentiated carcinoma 20% small cell lung carcinoma 5% carcinoid tumours (etc NE tumours) 5% etc
What gene mutations are involved in lung cancer
p53 - cell cycle protein regulator
EGFR - epidermal growth factor receptor - mutation
What is the difference in grade between NSCLC and SCLC
SCLC is high grade, usually spread by presentation - surgery not an option. Limited (one hemithorax + ipslateral supreclavicular lymph nodes) or Extensive.
Chemo main treatment (maybe some palliative RTX).
NSCLC - variable grade. Surgery can be an option, new drugs being developed for this. Treatment depends on staging - 3&4 (metastatic = palliatives chemo only).
What do M0, M1a, M1b, MX mean in regards to lung cancer staging
[M0] absent [M1a] contralateral lung pleural or pericardial effusion/nodule [M1b] Distant spread outside chest [MX] not known
When is lung cancer considered to be metastatic
When it is in the contralateral lung, the pleura, pericardium, or N2-3 lymph nodes.
N2 = ipsilateral mediastinal nodes, subcarinal nodes
N3 = contralateral hilar, mediastinal or ipsilaterial surpclavicular. N2 or N3 = stage 3/ 4.
Explain node staging in lung cancer
*think about mediastinum and subcarina here
N0 = no nodes involved N1 = Some nodes involved, same side, not in mediastinum, above clavicle or near carina (some nearby, but not outside of lung or above carina). N2 = Nodes in mediastinum on same side as tumour, subcarina nodes. Outside of lung and above carina, but same side. N3 = nodes on other side (anywhere) or supraclavicular same side
List the most common causal agents for occupational asthma
Isocyanates Flour (bakers) Cleaning products Wood dusts (joiners) Enzymes, Amylase
Why is early identification of occupational asthma important . How can be this be done in the workplace?
SECONDARY PREVENTION
Exposure reduction improves asthma (FEV1) - get reversibility of disease
Can treat or even cure disease in some cases
Health surveillance programmes
What question is useful for identifying if asthma is occupational
Does it improve over the weekend? When they go on holiday? Are away from work?
What is the timescale for onset of occupational asthma
minutes (acute) to months to years
less common for it to be decades
Explain the different types of hypersensitivity reactions
Type 1 - IgE - allergy, anaphylaxis
Type 2 - IgG - cytotoxic - IgG against a cell goodpastures
Type 3 - IgG - immune-complex deposited in tissues
Type 4 - Delayed - T cell mediated.
What are the common occupational lung allergies - what are the most common causes
Occupational asthma - isocyanates (painters); flour (bakers)
Extrinsic allergic alveolitis / hypersensitivity pneumonitis - allergic reaction to organic dust (type III) - sensitise, develop IgG antibody, get immune complex deposition & acute inflammation on re-exposure = acute breathless and cough a few hours after exposure.
-then get type IV hypersensitivity bc T cells infiltrate the interstitium and granulomas form (non-caseating)
If remove antigen/ exposure, does not progress, if continue to be exposed, develop pulmonary fibrosis
What is hypersensitivity pneumonitis
Type III hypersensitivity reaction to organic dusts that leads to interstitial lung disease, and in some pulmonary fibrosis.
Presents with acute dyspnea + cough, a few hours post exposure
Common causes are:
Mould in hay (farmer’s lung)
Bird feces (Bird fanciers lung)
Cotton fibres
The mechanism is sensitisation via type III hypersensitivity, followed by chronic inflammation, non caseating granulomas
Can be occupational or environmental
Classified by duration
Acute (may be self-limiting)
Subacute
Chronic (scarring)
Causes of occupational EAA
Microorganisms
Farmers, wood pulp workers, sewage workers, maple bark strippers, cheese washers, metalworking engineers, mushroom workers, suberosis, bagassosis
Animals
Birds, wheat weevil, fish meal, rodent handlers
Vegetation
Coffee, wood
Chemicals
Vineyard sprayers, insecticide, isocyanates, anhydrides, plastics
What occupational hazard can increase lung sensitivity to TB
Silica
What percentage of COPD is occupational
10-15%
What are the causes of occupational COPD
Coal
Silica
Grain
What should patients who have occupational COPD always be advised to do
Stop smoking - this will improve FEV1 even if have COPD
What are pleural plaques
Calcified collagen
Sign of asbestos exposure
Not pre-malignant
What is asbestosis
Pulmonary fibrosis Subpleural, basal = UIP (usual interstitial pneumonitis) pattern With/without plaques History of heavy exposure No effective treatment May progress (without further exposure)
What is asbestos effusion
Follows benign effusion - it is diffuse pleural thickening
Obliteration of costophrenic angle
Can cause restriction due to thickened pleura
SOB, respiratory failure
No effective treatment
May progress slowly (without further exposure)
What is the relationship between asbestos exposure, smoking and lung cancer
Never smoker + any asbestos exposure = increased risk of Lung cancer bc of asbestos only
Past smoker + asbestos exposure (of any level) = increased risk of lung cancer over those exposed who did not smoke
Current smoker + asbestos exposure (of any level) = increased risk of lung cancer over past and never smokers.
Basically, current smoking hugely increases risk (by about x20) over ex-smokers, so smokers should be encouraged to quit
What is the presentation of mesothelioma
Progressive breathlessness and chest pain
Weight loss
Life expectancy ~11 months
What is the best way of managing occupational lung diseases
Prevention
Focus on exposure prevention or minimisation
Elimination (eg asbestos)
Substitution (eg latex to nitrile gloves)
Engineering controls (eg exhaust ventilation)
Worker education
RPE (masks and respirators)
List the most common occupational lung diseases
Direct injury (eg acute irritant asthma, pulmonary oedema
Infection - silicotuberculosis
Allergy (Asthma, Extrinsic allergic alveolitis/ hypersensitivity pneumonitis)
Chronic inflammation (COPD, bronchiolitis)
Destruction of lung tissues (emphysema)
Lung or pleural fibrosis (asbestos related)
Carcinogenesis (eg lung cancer, mesothelioma)
*Consider the interaction of smoking with all of these
What causes occupational lung disease
VGFD
Allergens - organic or inorganic
Hypersensitivity reactions
What regions of the lungs are usually affected by idiopathic pulmonary fibrosis
Lower lobes - subpleural regions - patchy
Describe the lung pattern of idiopathic pulmonary fibrosis
usual interstitial pneumonitis
Lower lobes - patchy, sub pleural
Loss of lung architecture
Dilated air spaces within fibrotic areas - honeycombing
What is the survival rate of idiopathic pulmonary fibrosis
50% 5 year survival
Which interstitial lung disease may be asymptomatic
Pneumonconiosis - coal works lung
But may have coexisting bronchitis
Which interstital lung disease should not be treated with steroids
Idiopathic pulmonary fibrosis
What are interstital lung diseases
Conditions with damage to the lung parenchyma and remodelled interstitium
List the causes of interstitial lung diseases
1.Occupational - pneumoconiosis Coal workers lung (can be asymptomatic) Silicosis (TB risk) Asbestosis (lower lobe - similar to IPF) 2.Allergic - type 3 Extrinsic allergic alveolitis Hypersensitivity pneumonitis Bird fanciers lung Pigeon fanciers lung etc 3.Idiopathic M>F 4.Drugs Methotrexate 5.Systemic disease Rheumatoid Systemic sclerosis Vasculitis Sarcoidosis
What is the pathology of interstitial lung disease
Injury/ insult to parenchyma (eg allergen, or dust particle; immune complex) –> macrophage –> chronic inflammation –> fibrosis –> architecture remodelling
What investigations should be done on patients who you suspect might have interstitial lung disease
1.CXR - look are shadow distribution - lower lobes = asbestosis & IPF, middle - sarcoid, upper - TB etc
CT - can be more sensitive
2.Bloods - look at neutrophil vs WBC count; ESR; CRP; Immunoglobulins (look for autoantibodies & antibody against organic allergens)
ABG - look for hypoxaemia
3.Spirometry - restrictive pattern? Gas transfer?
4.May need biopsy to rule out other things
Bloods, imagining, spirometry
What would you include in an interstitial lung disease differential
Obstructive airways disease - asthma, COPD?
Sytemic connective tissue disease - RA, SS, Sarcoidosis, Vasculitis (GPA) etc
Infection - TB, pneumonia?
What is the management for interstitial lung diseases
Remove/ reduce exposure - if there is allergen or dust as cause
Give steroids - if allergic cause
NEVER steroids on IPF
Treat other lung conditions - eg bronchitis
Supportive treatment - oxygen therapy, pain relief etc
List the different types of interstital lung diseases
Acute:
Adult Respiratory Distress Syndrome
Cryptogenic Organising Pneumonia
Chronic: Idiopathic pulmonary fibrosis Pneumoconiosis Coal workers lung Silicosis Asbestosis Hypersensitivity pneumonitis
What is caplan’s syndrome
Rheumatoid + coal workers lung
What does a CXR or fibrosis look like
Diffuse shadowing
What is the management of idiopathic pulmonary fibrosis
Supportive. Oxygen therapy, pain relief (opitates), palliative care. NEVER high dose steroids.
What is the management of industrial lung diseases
Avoid trigger. Treat other lung diseases. Supportive & symptomatic. Patients eligible for compensation.
Causes of bronchiecstasis
Post infection - Severe pneumonia, TB
CF
Bronchial obstruction
Pathology of bronchiecstasis
Enlarged bronchioles + lots of mucus secretion
Chronic inflammation of the bronchi and bronchioles leading to permanently dilated and thinning of airways
Tests for bronchiecstasis
Sputum - culture
CXR - cystic shadows, thickened bronchial walls - tramlines
Spirometry - obstructive
What is the management for bronchiecstasis
Airways clearance techniques
Mucolytics - chest physio
Antibiotics for infections
What is cystic fibrosis, what is the presentation
Mutation of CF transmembrane conductance regulator.
Cl- channel. Mutation leads to defective cl- secretion and increased Na+ absorption across the airway.
Symptoms - failure to thrive
Cough, wheeze, recurrent infections, bronchiecstasis, pneumothorax
Diagnosis - sweat test.
What are the causes of pleural effusion
Transudate - increased venous pressure - heart failure, constrictive pericarditis, hypoproteinaemia (cirrhosis etc)
Exudate - infection, inflammation, cancer
What are the symptoms of pleural effusion
Asymptomatic - maybe dyspnoea or pleuritic chest pain
What are the signs of pleural effusion
Decreased expansion
Stony dull percussion
Diminished breath sounds on the affected side
If large - may be tracheal deviations
What are the tests for pleural effusion
CXR - look at costophrenic angle
Ultrasound - useful for seeing fluid
Aspiration - culture, cytology, immunology
Biospy
What is the management of pleural effusion
Treat underlying cause
Drainage
Surgery
What are the causes of pneumothorax
Rupture of the pleura
Asthma,COPD, TB, pneumonia, sarcoidosis, trauma - anything that puts pressure on pleura and has capacity to rupture it
What are the signs and symptoms of pneumothorax
May be asymptomatic
Sudden onset dyspnoea or pleuritic chest pain
Hyper-resonance to percussion
Diminished breath sounds
CXR - if tension pneumothorax will push trachea to other side
What are the signs and symptoms of pulmonary embolism
Acute breathlessness, pleuritic chest pain, haemoptysis, dizziness *Ask about risk factors - recent surgery, leg fracture, prolonged bed rest, pregnancy, previous PE, family history Temperature Cyanosis Tachycardia Hypotension raised JVP Pleural rub Pleural effusion
What are the investigations for PE
Bloods - D-dimer
ABG - may show reduced PaO2
Imaging - CXR - may be normal , look for dilated PA
ECG - right ventricular strain?
What is the management for PE
If haemodynamically unstable - thromboembolise - eg alteplase
If stable - heparin - 5 days, then DOAC or warfarin
What should you consider in a patient that has no risk factors for PE (unprovoked)
cancer
What are the risk factors for PE
Surgery, immobility, leg fracture
OC pill, HRT, Pregnancy
Long haul flights/ travel (rare)
Inherited thrombophilia (antiphospholipid syndrome)- genetic predisposition; 5% population, familial
What is the presentation of PE
Differential diagnosis of chest pain and sob
Consider also musculoskeletal, infection, malignancy, pneumothorax, cardiac, gastro causes
Symptoms: breathlessness, pleuritic chest pain, may have signs/ symptoms of DVT, may have risk factors, no other diagnosis more likely
Signs: tachycardia, tachypnoea, pleural rub, those of precipitating cause, none of alternative diagnosis
What are the investigations for PE
CXR usually normal
ECG sinus tachy, (QI,SI,TIII)
Blood gases: type 1 resp failure, decreased O2 and CO2
Mainly done to exclude alternative causes
D-dimer: normal excludes diagnosis
Ventilation/ Perfusion scan: mismatch defects
CTPA spiral CT with contrast, visualise major segmental thrombi
What is the hilar point on a chest X ray
It is the angle between the pulmonary veins (coming from upper lobe) and pulmonary artery (going into lower lobe).
Its important to locate because there is are a number of conditions with pathology around the hilum - particularly lymph nodes (eg sarcoidosis)
What are the signs of heart failure on a CXR
Alveolar oedema
B Kerley B line (thickened interlobular septa)
Cardiomegaly
Distension (upper lobe veins)
Effusion - pleural effusion (meniscus line)
What is the sail sign on a CXR - what does it show
Left lower lobe collapse - the heart shadow should be consistent opacity - if it is not, there is something behind it - when you see the sail sign this is collapsed lower lobe - loose diaphragm line medially
Outline CXR method of review
Diaphragm
Heart borders
Hilar point ( where upper lobe veins cross pulmonary arteries)
Pleural edges
Review areas: Below diaphragm - bowel perforation? Hilar angle - adenopathy, moved? can show volume loss or mass effect Lung apices - cancer? Peripheral film - any bone breaks?
What are the signs of pneumonia on CXR
Consolidation - air bronchograms - these are lines of air that are more pronounced bc of consolidation in alveoli
What is a tension pneumothorax - how would you identify it on CXR
When air gets into pleura and increases so much that it is pushing on other structures.
If the space fills with air can impair venous return - risk of sudden cardiac arrest
Should be able to pick up pneumothorax by absent breath sounds, and if its tension - displacement of trachea
What is the sign of pleural effusion on CXR
Bilateral consolidation - Meniscus line
Describe how you would interpret a CXR based on if it was dense or lucent
- Dense or lucent?
- Mass effect or volume loss?
Mass effect - structures are being pushed - fluid, plural effusion? malignancy? Tension pneumothorax?
No change - lungs look normal - hilar correct place - consolidation - pneumonia (infection), malignancy, vascular event?
Volume loss - lung collapse? pneumothorax?
How can you identify which lobe of a lung is collapsed on a CXR
RML - RHB
RLL - Right hemi diaphragm
LUL - LHB
LLL - Left hemi diaphragm
RUL collapse - Horizontal fissure - has this moved?
What are the causes of pleural effusions
Think of this as similar to ascites
Transudates (low protein) to do with fluid overload - HF, liver disease
Exudates - infection, inflammation, malignancy - the problem is leaky membranes - so in the lungs could be a bronchial malignancy
What is the wells score and when is it used
Its used to assess a suspected Pulmonary embolus.
<4 = D dimer
>4 = Immediate CTPA or treat empirically with LMWH if cant do CT
What is D dimer, what does a positive result show
D-dimer is a produce of fibrin degradation - if it is positive it suggests that there has been a fibrin thrombus in the blood
What is included in Wells score
Clinical signs of DVT - sore leg, swelling Heart rate - >100 bpm Bed rideen or major surgery Previous DVT or PE Haemoptysis Cancer treatment - within last 6 months Alternative diagnosis less likely
Causes of type 1 respiratory failure
Think diseases that cause V/Q mismatch
Hypoxaemia on ABG = <8kPa
Pulmonary embolism Interstitial lung diseases (unless severe and cause type 2) Pneumonia Emphysema Pulmonary Fibrosis Asthma
Signs: peripheral cyanosis - peripheral common (low oxygen in blood)
Causes of type 2 respiratory failure
Think about hypoventilation problems
Hypoxaemia + hypercapnea on ABG
PaO2 = <8kPa
PaCO2 = >6kPa
COPD
End stage fibrosis
Sedative drugs, CNS tumour or trauma
Neuromuscular disease
What is the management for type 1 respiratory failure
Oxygen - 24-60% by facemask
Treat underlying cause - eg. thombolyse clot on lung
Assisted ventilation is PaO2 <8Kpa despite 60% oxygen
What is the management for type 2 respiratory failure
Treat underlying cause
Controlled oxygen therapy - start low (24%) and monitor - recheck ABG after 20 minutes, if PaCO2 lower or steady, can increase oxygen slightly
If this fails, consider ventilation & intubation.
What is the normal blood ph
7.35-7.45
<7.35 = acidosis
>7.45 = alkalosis
At what O2 partial pressure do RBCs start to significantly desaturate and respiratory rate increases
60mmHg - equivalent to 8kPa
What is a pink puffer and a blue bloater - what do they represent clinically
A pink puffer is a patient who is probably hypoxaemia (if they aren’t puffing) and is at risk of type 1 respiratory failure. Diseases - emphysema - airspaces are ventilated but oxygen cant diffuse because of obstruction - at the moment CO2 can be blown off
Blue bloater - hypoxemia + hypercapnea
Cant blow CO2 off = chemoreceptors desensitised = cynaotic. Hypoaemia now respiratory drive - 88-92% Type 2 respiratory failure
Patients can be anywhere in between these extremes
What is the differential diagnosis for COPD
Other causes of SOB Heart failure Pulmonary embolus Pneumonia Lung cancer Asthma Broncheictasis
What is the GOLD classification of airflow limitation
mild - FEV1 >80% predicated; FEV1/FVC = <70%
moderate - FEV1 between 50 - 80% predicted
severe - FEV1 between 30 - 50% predicted
very severe - FEV1 less than 30% predicted
What tool predicts outcomes in COPD
BODE index Bmi Obstrution (FEV1) Dyspnea Exercise capacity
Describe the pathology of COPD
Irritant gets into lung (cigarette smoke, or coal dust)
Gets into bronchiole epithelium and tissue/ alveolar macrophages. This sets off an inflammatory response, attracting neutrophils and CD8+ lymphocytes. Neutrophils secrete elastase and metalloproteinase’s. Macrophages also secrete MMPs - the combination breaks down alveolar elastin. CB8 cells release perforin and damage bronchiolar walls. Get fibrosis and thickening of walls. Also get goblet cells hyperplasia in response to ROS that are secreted by neutrophils. = thickening of the small airways by fibrosis and mucus production. Expansion of alveolar sacs by elastin degradation.
Airway collapse - bc lose the tension from alveolar elastin
Alveolar expansion - air trapping
Define COPD
COPD is characterised by airflow obstruction… usually progressive, not fully reversible and does not change markedly over several months. The disease is predominantly caused by smoking
Describe some of the pathological characteristics of COPD
Goblet cell hypertrophy
Thickened bronchioles due to inflammation and fibrosis
Bronchiole collapse
Alveolar expansion and elastic degradation
Ruptured alveolar walls
Loss of bronchiole splintering (holding open) by alveolar walls
CD8 infiltration
Neutrophil infiltration
Describe the vascular changes that take place with COPD
V/Q mismatch - bc bronchus not ventilated
= high pCO2 = vasoconstriction +
Progressive vascular fibrosis from inflammation = vascular thickening =
Pulmonary hypertension
Cor pulmonale
Blood vessels are narrowed or obliterated, impairing gas and exchange and with pulmonary vasoconstriction with hypoxia the pulmonary artery pressure rises. Usually this is to a sPAP of no more than 40 mmHg but occasionally it is higher, with poor prognosis.
Describe the clinical features of COPD
Old patients, smokers, male predominance Shortage of breath Cough, phlegm Wheeze Raised respiratory weight Hyperexpansion/barel shaped chest Cyanosis Weight loss ‘cor pulmonale’ = ‘heart failure’ raised JVP, SOA but CO maintained
What are the risk factors for COPD
Smoking
Occupational dusts/ smokes/ fumes
Environmental tobaccop smoke
Age
List 3 signs of COPD
Hyperinflated chest Use of accessory muscle to breathe Wheeze with no diurnal variation Cyanosis Fluid overload - cor pulmonale, odema, raised JVP Tachypnoea Reduced expansion Hyperresonant chest - bc of air trapping Quiet breath sounds over bullae
What are the complications of COPD
Infection Heart failure - cor pulmonale Polycythaemia Respiratory failure - type 2 Pneumothorax - ruptured bullae Lung carcinoma
What investigations should be done for COPD
FBC ABG - look for type 1 or 2 resp failure CXR CT Spirometry
What is the spirometry profile of someone with COPD
Obstructive
FEV1 <80%
FEV1/FVC <70%
Increased TLC - bc of airspaces
Increased RV - bc of airspaces and reduced FVC
Reduced DLCO (Diffusing capacity of the lungs for carbon monoxide) - transfer factor - bc of emphysema
How does COPD look on a flow-volume graph
The expiratory arm is scooped - this represents reduced air flow through smaller airways. The beginning bit represents flow through larger airways.
How do patients with COPD compensate for hypoventilation, what signs are there of this clinically
They hyperinflate the lungs and use accessory inspiratory muscles (sternocleidomastoid, pec major & minor, scalenus anterior) on inspiration
They do this to maintain a normal tidal volume
Decribe how a flow-volume graph would look for a patient with COPD when they are hyperinflating their lungs
The tidal circle in the middle would shift to the left, representing an increase in inspiratory volume
Describe the characteristics of COPD on CXR
Hyperinflation - barrel chest
Flat hemidiaphragms
Large pulmonary arteries
Air space enlargement
Describe the ECG of a patient with COPD
Right atrial and ventricle hypertrophy bc of cor pumonale
What would you include in a differential for a patient with suspected COPD
Asthma - is there any diurnal variation in SOB?
Heart Failure - left sided - cardiac history?
Pulmonary embolus - pleuritic pain or leg pain?
Pneumonia - productive cough?
Lung cancer - previous cancers?
Broncheictasis
What is the most common cause of COPD exacerbation
Upper respiratory tract infection
What is the treatment for COPD
Quit smoking!
Exercise therapy - aimed at preventing muscle wasting, disability and depression
Medicines - bronchial dilators to alleviate symptoms - SABA or LABA +Anti-muscurinic (to prevent flare up), steroids (sometimes BUT AT RISK OF PNEUMONIA, only considered if pt FEV1 <60%)
Oxygen therapy in pt that still have co2 drive and have hypoxemia
Non-invasive ventilation (in hospital pt) with acidosis
Preventing flare ups v important - DO NOT WANT LUNG INFECTION ON TOP OF ALL THIS INFLAMMATION - Flu vaccines, antibiotics & systemic corticosteroids if get infection.
How can you assess the severity of COPD
GOLD categorises into 4 stages, based on post broncho-dilator FEV1% predicted Mild Moderate Severe Very severe
When can O2 therapy be given in COPD patients
- If they are a stable non-smoker that is hypoxic despite other treatments
- In hypoxic patients who still have CO2 drive
- Hypoxia and pulmonary hypertension
What is the goal of drug therapy in COPD
Symptomatic relief of obstructed airways - dont treat disease
Bronchodilator medications are central to the symptomatic management of COPD.
Bronchodilators are prescribed on an as-needed or on a regular basis to prevent or reduce symptoms.
The principal bronchodilator treatments are beta2- agonists, anticholinergics, theophylline or combination therapy.
The choice of treatment depends on the availability of medications and each patient’s individual response in terms of symptom relief and side effects
What are the goals of COPD treatment
Relieve symptoms
Improve exercise tolerance
Improve health status
Prevent disease progression
Prevent and treat exacerbations
Reduce mortality
Describe how to manage a COPD exaccerbation
Short-acting inhaled beta2-agonists with or without short-acting anticholinergics are usually the preferred bronchodilators for treatment of an exacerbation.
Systemic corticosteroids and antibiotics can shorten recovery time, improve lung function (FEV1) and arterial hypoxemia (PaO2), and reduce the risk of early relapse, treatment failure, and length of hospital stay.
COPD exacerbations can often be prevented.
What is atopy
Atopy is the tendency to develop IgE mediated reactions to common aeroallergens
Summarise the pathology of eosinophilic atopic asthma
Eosinophilic ashma:
Allergen (fungal, aeroallergen, pets, occupation) -> airways - gets into bronchial epithelium & tissue macrophage -> CD4 cells (stimulate smooth muscle - bronchoconstriction; and eosinophils via IL-5) -> get a Th2 RESPONSE -> B cell (via IL-4) -> IgE -> IgE activates mast cells -> mast cells release granules that activate eosinophils, release histamine (vasodilation), leukotrienes, cytotoxic granules that cause bronchospasm
Basically massive pro-inflammatory response
Eosinophilic non atopic - same but no IgE pathway or B cells
Summarise the pathology of non eosinophilic asthma
Irritant - cigarette smoke - pathogens from infection (obesity)
Stimulates macrophage & epithelium -> CD4 cell migration -> Th1 RESPONSE -> smooth muscle contraction and bronchospasm, INF-gamma - keep supporting macrophages -> activate mast cells -> histamine release
In asthma, outcome is the same, mast cells are activated - but pathway different
What are common causes/ triggers for atopic asthma
Aeroallergens - pollen, fumes Pets Fungal Cold weather Exercise Night/ early morning Emotion
What is a typical presentation of asthma
Episodic wheeze
Nocturnal or early morning dyspnoea
Cough - may produce sectretions (sputum) but no pus (purulent)
Ask about allergens - history of hayfever, allergies?
Ask about symptoms at night/ early morning?
Ask about symptoms when its cols, during exercise?
Think about occupation - could it be linked, better at home/ holiday?
What are the signs of asthma on examination
Widespread expiratory wheeze on auscultation
May have hyperinflated chest
Hyperresonance
Tachypnoea
What investigations would you do for a patient suspected with asthma
If high probability (nocurnal dypnoea, episodic wheeze etc) - start on treatment and review response
If intermediate probability - do tests for airway obstruction reversibility and atopy.
Obstruction - PEFR monitoring, Reversibility testing
Atopy - bloods - eosinophilia; FeNO test, skin prick test
Low probability - consider other causes
What would you include in an asthma differential
If an adult:
Other respiratory disease - COPD? Bronchiecstasis, bronchiolitis, Pulmonary elbolus, Pulmonary oedema, Aspiration, Airway obstruction - cancer?
Other cardio disease - Pulmonary odema sec to HR? Cardiac history
If child:
CF - born in country where not screened? Airway obstruction?
What clinical features distinguish asthma from other differentials
Episodic wheeze - COPD is progressive Nocturnal dypnoea Symptoms worse in early morning Cough not purulent (may be with COPD) History of atopy Esinophilia Smoking history & occupational history
Outline the management of asthma
- Bronchodilators - mainly B2 agonists (not really antimuscurinics), LTRA leukotriene receptor antagonists, Theophylline
- Steroids
- Biolgics - atopic asthma only
Start on:
1.SABA - asymptomatic relief when required - Salbutamol
2.If using everyday or night symptoms step up to:
Regular (daily) low dose Inhaled corticosteroid (ICS) - beclometasone + SABA
3.If not controlled, step up to LABA + low dose ICS (combined)
if not controlled, medium dose ICS
4.If not controlled, can do add on dilator - LTRA
5.If not controlled, refer on, for higher dose steroids - oral prednisolone
What should you consider when giving Inhales corticosteroids to COPD patients - when is it acceptable to prescribe oral steroids to COPD patients
Consider pneumonia risk
Can give oral steroids with antibiotics to COPD pt with confirmed infection
What CD4 response is atopic asthma
Th2 - IgE producing
What CD4 response is non-eosinophilic astham
Th1 - non IgE producing
What do mast cells release
Cytotoxic granules Chemotaxins for eosinophils Leukotrienes Histamine - vasodilation Stimulate bronchospasm
Why is asthma reversible and COPD isnt
COPD inflammation involves CD8 & neutrophils cells that cause a lot of tissue damage by protinases - this causes fibrosis of the small airways that is not reversible
Asthma inflammation involves eosinophils, macrophages and CD4 cells - there is not fibrosis with this, like CD8, t/f when the inflammation is inhibited, the disease is reversed.
What peak flow is diagnostic of asthma
Decrease in >20% in PEFR from predicted 3/7 days a week
Improved PEFR after dilator or steroids - increase of 200 -400 ml
What spirometry is diagnostic of asthma
Obstructive pattern - reduced FEV1, FEV1/ FVC ratio
Increase of 12% in FEV1 after brochodilator indicator of asthma
What is brittle disease
Really bad unresponsive to treatment asthma
At risk of severe attacks
What PEFR would you see in an asthma attack
Severe - 35-50% predicted
Life threatening - <33%
Features of life threatening asthma attack
Arrhythmia/ Altered conscious level
Cyanosis, PaCO2 normal
Hypotension, Hypoxia (PaO2<8kPa, SpO2 <92%)
Exhaustion
Silent chest
Threatening PEF < 33% best or predicted (in those >5yrs old)
What is the management of an asthma attack
Oxygen Salbutamol - Steroid prednisolone Hydrocortisone IV T? Magnesium or aminophylline - IVE ABG Not responding - CXR - pneumothorax, consolidation?
Sign of severe asthma attack
Inability to complete sentences
What CXR signs would show bronchiecstasis
hyperinflation, tram tracks, increased linear markings, focal pneumonitis, ring shadows and atelectasis
What is the difference between bronchitis and bronchiectasis
Bronchitis is smoking related and to do with irritation and inflammation of the airways. This causes hyperplasia of submucosal glands and metaplasia of squamous cells in bronchioles to mucus cells = cough + obstruction. Over time - airway narrows from inflammation. Main symptoms is non-purulent productive cough for a few weeks (acute) or 3/12 in 2 consecutive yrs (chronic).
Bronchiectasis usually happens after infection, and the pathogen has secreted a load of proteases that have damaged elastin in airways and caused permanent dilatation. This is obstructive bc smaller airways are narrow from fibrosis or mucus plugging = obstruction. Main symptoms is purulent cough.
What are the commonest occupational lung diseases
Pleural disease, mesothelioma, COPD, asthma, EAA
What are the causes of occupational lung disease, give examples
Vapors - isocyanates (pains etc)
Gases -
Fumes - silica
Dust - wood (joiners), bakers and flour
Outline the different prevention strategies for occupational lung diseases
Primary: Eliminate (eg asbestos) Replace Control (eg ventilators) Monitor hazards Educate workers Masks
Secondary:
Health surveillance
Tertiary:
Eliminate exposure to reduce long term risk - move into role where their is not exposure
Outline some of the treatment options for occupational lung diseases
Remove the allergen/ hazard from the employees job
Re-locate role
Disability: what employers should do (reasonable adjustments)
•altering the person’s working hours
•allowing absences during working hours for medical treatment
•giving additional training
•getting special equipment or modifying existing equipment
•changing instructions or reference manuals
•changing an open plan working policy to accommodate someone with an anxiety condition or autism
•providing additional supervision or support
•making adjustments to premises
Mortality risk factors in flu
Chronic cardiac and pulmonary diseases
- Old age
- Chronic metabolic diseases
- Chronic renal disease
- Immunosuppressed
What is an outbreak
2 or more linked cases
What is an epidemic and whats a pandemic
More cases in a region/country
Epidemics that span international boundaries
When does influenza peak
December to march
What is a common cause for pandemic flu
Often created by the strain “jumping” from another species e.g. Flu virus found in ducks, chickens, horses, pigs, whales, seals…
What are the consequences of pandemic flu
High morbidity
• Excess mortality
• Social disruption
• Economic disruption
List some ways to prevent flu pandemic
- Cull affected birds/ animals
- Biosecurity and quarantine
- Disinfecting farms
- Control poultry movement
- Vaccinate workers – seasonal influenza vaccine
- Antivirals for poultry workers
- Personal Protective Equipment (PPE)
- Try to reduce chance of co-infection
What is Oseltamivir
Tamiflu - Tamiflu needs to be given with 24-48 hours of contact to have maximum effect
Evidence from seasonal flu is that it reduces hospitalisation by 50% and duration of disease by approximately 24hours (drug company studies…)
•Issues:
What happens if the virus develops resistance?
What about side effects?
Who do we give them to?
How do we distribute them?
Outline how a flu pandemic is managed
Containment - identify cases, contact tracing, treat, prophylaxis
Treatment - treat cases
When is it appropriate to wear face mask
If within 1 meter of someone with flu
Only if worn appropriately, changed frequently, removed properly, disposed properly
How long does it take to develop a flu vaccine
6-10 months
When is it acceptable to administer oxygen in COPD
Stable non-smoker
Hypoxic despite all avaiable treatment
Hypoxic + other complication, eg polycythemia, PH, peripheral oedema, noctural hypoxia
Must be maintained at 90% + (8kpa) sats, 15 hours a day
