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Phase 2 > RESPIRATORY > Flashcards

RESPIRATORY Flashcards

1
Q

Most common cause of non-infectious lung granulomas

A

Sarcoidosis

Then GPA

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2
Q

Typical patient with sarcoidosis

A

Young to middle ages, F > M, pt of African descent

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3
Q

Sarcoidosis presentation

A

Bilateral hilar lymphadenopathy + skin (eh shin nodules) or eye lesions (uveitis). In half of cases, detected incidentally on CXR.

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4
Q

Histology difference between TB & Sarcoidosis

A

TB = caseating granulomas. Sarcoidosis = non-caseating gramulomas.

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5
Q

Lung lymphadenopathy / granulomas differential

A

Sarcoidosis, TB, Lupus, Lymphoma

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6
Q

Sarcoidosis cause

A

Auto-immune, may be triggered by infection

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7
Q

Granulomatous lung disease + vasculitis +ANCA

A

GPA

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8
Q

Granulomatous lung disease + vasculitis + no ANCA

A

RA, Lupus, systemic sclerosis

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9
Q

Antibiotic options for community acquired pneumonia + most likely pathogen

A

Amoxicillin. Strep pneumoniae.

Clarithromycin for penicillin allergy

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10
Q

Antibiotic options for hospital acquired pneumonia + most likely pathogen

A

Defined as acquired >48hr since admission.
Flucloxacillin for staph aureus. May need rifampicin or vancomysin if resistant.
1. Staph aureus
2.Gram neg enterobacteria

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11
Q

What factors affect the risk of developing a respiratory tract infection

A
  1. Commensal colonistation of upper airway - naso, oro & laryngopharynx - normally strep (virdidans) and staph epidermidis
  2. Swallowing - if can’t do this can aspirate into lungs (think neuro conditions, stroke, parkinsons, MND etc; also tumours and surgery)
  3. 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.

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12
Q

List the signs of pneumonia

A

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

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13
Q

List the symptoms of pneumonia

A 
Fever
Chills/ rigor
Chest pain - pleuritic
SOB
Cough - productive
Arthralgia 
Myalgia
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14
Q

Investigations for pneumonia

A

CXR
Bloods - FBC (look at white cell count - bacterial or viral); U&E, LFT - check organ function, culture, CRP
Sputum - culture
Pulse oximetry

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15
Q

Describe the features of pneumonia on CXR

A

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

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16
Q

Common pathogens for hospital acquired pneumonia - how would you know it was hospital acquired?

A

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

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17
Q

Common pathogens for community acquired pneumonia

A 
Streptococcus pneumoniae
Mycoplasma pneumoniae
Chlamydophila pneimoniae
Legionella pneumophila 
Haemophilus influenzae
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18
Q

What are the signs of pneumonia on a CXR

A

Air Bronchogram
Air fluid levels - indicates abscess
Multilobular, suggest strep pneumoniae, A aureus, Legionella
Diffuse - suggestions viral or fungal

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19
Q

Outline how to assess the severity of community acquired pneumonia

A 
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

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20
Q

What is the major complication of pneumonia and what groups are most at risk of this

A

Sepsis
Those with comorbidities
Those over 65

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21
Q

What pneumonia pathogen can you not use a macrolide (eg clarithromycin) on?

A

Klebsiella

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22
Q

Name two cephalosporins

A

Cefotaxime

Cefuroxime

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23
Q

What considerations should be made for atypical pathogens when looking for the cause of pneumonia

A

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

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24
Q

What antibiotics should be used for atypical pneumonia pathogens

A

Macrolides, fluroquinolones

NOT BETA LACTAMS

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25
Q

What extrapulmonary features are associated with mycoplasma pneumoniae

A

haemolytic anaemia (cold agglutinins),
Raynauds (cold agglutinins) erythema multiforme,
bullous myringitis (blisters on tympanic membrane),
encephalitis

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26
Q

Which atypical pneumonia pathogen is associated with epidemics

A

Mycoplasma pneumoniae - seen in younger adults, milder disease with more extra-pulmonary features

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27
Q

What atypical pneumonia pathogen causes diarrhoea

A

Legionella

*need a fluorquinolone prescribed for this

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28
Q

What microbiology tests should be done for pneumonia

A

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

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29
Q

What is the differential diagnosis for pneumonia

A

TB - *history will tell you if this is a risk - travel
Pulmonary embolus - SOB & pleuritic chest pain
Cancer
Heart failure - SOB
Interstitial lung disease

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30
Q

What are the risk factors/ flags in a history for TB

A

Born outside of UK in TB endemic country

Travel to TB endemic country

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31
Q

What is the preferred method of testing for TB in a patient who has been vaccinated

A

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.

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32
Q

How could you test for TB in a patient who has never received a TB vaccine

A

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.

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33
Q

What is the transmission route of TB

A

Aerosol droplets - only when patient coughs.

Pulmonary TB is the only communicable form.

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34
Q

What is latent TB

A

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%

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35
Q

What causes re-activation in latent TB

A

Change in immune status of the patient
Cancer treatment
Immunosuppressant drugs - DMARs
HIV infection

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36
Q

What are the most common sites of TB infection

A 
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.
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37
Q

What are the symptoms of pulmonary TB

A

Cough - dry then productive
Pleuritic chest pain (Pleurisy/ pleural effusion)
Haemoptysis (uncommon)

Systemic:
Low grade fever
Anorexia or weight loss
Malaise
Night sweats
Clubbing
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38
Q

What is the treatment for TB

A

Rifampicin
Isoniazid
Pyrazinamide
Ethambutol

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39
Q

How would you differentiate between Pneumonia and TB

A

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

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40
Q

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
A

“ILL”
Inflammation/ infection - pneumonia, TB, pleurisy
Lumps - cancer, PE (infective?), sickle crises
Liquids - Pleural effusion

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41
Q

Presentation of infective embolus

A

DVT signs & symptoms - swollen and painful leg, tender, discolouration and warm
+ Pneumonia signs - pleuritic chest pain, cough - productive, SOB etc

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42
Q

What are the main complications of pneumonia

A
  1. Sepsis - especially in older patients with comorbidities
  2. Parapneumonic effeusion - left over fluid in the pleural after infection - 3 types, uncomplicated, complicated and empyema - pus
  3. Empyema
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43
Q

What are the signs of parapneumonic effesion, what needs to be done to see if it is complicated or uncomplicated

A

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

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44
Q

What are the signs of complicated parapneumonic effusion

A

Ph <7.4
Positive culture
Thick fluid - pus
Glucose <3.3 mmol/L

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45
Q

How many patients with community acquired pneumonia develop parapneumonic effusion.
How many of these are complicated effusions

A

Up to 50%

1%

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46
Q

What does parapneumonic effusion indicate

A

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

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47
Q

What is the difference between empyema and a lung abcess

A

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

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48
Q

Causes of lung abscess

A

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

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49
Q

Name two commonbeta lactams + beta lactamase inhibitor combiniations

A

Co-amoxiclav

Piperacillin-tazobactam

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50
Q

How would you treat hospital acquired pneumonia

A

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.

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51
Q

List the causes of pneumonia in immunocompromised individuals

A

Bacterial - all the usuals plus atypicals
Fungal - Pneumocystic jirovecci, aspergillus
Viral - cytomegalovirus, adenovirus, RSV

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52
Q

Commonest cause of bronchitis

A

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

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53
Q

Cause of bronchiolitis in children

A

Respiratory syncitical virus - causes Inflammation of bronchioles and mucus production cause airway obstruction

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54
Q

What is the difference between acute and chronic bronchitis

A

Acute - 1-3 weeks

Chronic - x3 months of coughing, two years in a row - usually seen in COPD

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55
Q

What is the main difference in the treatment of pneumonia in community and hospital

A

In hospital you dont give beta lactams (amoxicillin), always give beta lactam + inhibitor (co-amoxiclav)

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56
Q

What two respiratory conditions cause systemic (fever, chills, arthralgia, myalgia etc) symptoms

A

Pneumonia
Influenza

Bronchitis dosen’t cause these

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57
Q

What antifungal treatment should be given for pneumocystis pneumonia

A

trimoxazole (ergosterol inhibitor), or pentamidine - IV for 2-3 weeks.

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58
Q

What are the common pathogens of upper respiratory tract infections

A

Viral

  1. Rhinovirus (50%)
  2. Influenza A (30%)
  3. Coronavirus
  4. Adenovirus
  5. Parainfluenza virus
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59
Q

What are the complications of upper respiratory tract infection

A

sinusitis
otitis media (middle ear infection)
bronchitis
rarely pneumonia

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60
Q

Describe the presentation of scarlet fever - what bacteria is this caused by

A

Pharyngitis or cellulitis
+ Rash - erythematous, finely papular, papillae - feels like sandpaper. Blanches on pressure.
Caused by strep pyogenes.

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61
Q

What is the complication of scarlet fever, what blood test should be done to assess the risk of complications

A

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.

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62
Q

What are GABHS associated diseases

A

Group A beta hemolytic streptococcus diseases
Scarlet fever
Rheumatic fever- carditis, arthritis, chorea, erythema marginatum, and subcutaneous nodules

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63
Q

What are the commonest causes of pharyngitis

A

Viral - EBV, Rhinovirus, Adenovirus (80%)

Bacterial - strep pyogenes (20%) - need to check for rash and ?scarlet fever in children and anyone immunocompromised

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64
Q

What is lemierre’s disease

A

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

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65
Q

Bacterial causes of pharyngitis

A

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)

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66
Q

What is the treatment for strep throat

A

Amoxicillin

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67
Q

What is a differential feature of Diptheria

A

Grey/ thick membrane over tonsils

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68
Q

What is the presentation of Diptheria

A

Child with fever, sore throat, malaise, adherent membrane over tonsils, pharynx and/ or nasal cavity

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69
Q

What are the signs of Diptheria

A

Lymphadenopathy in neck, rapid breathing
Thick greyish membrane on tonsils
Travel to russia

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70
Q

What is the treatment of Diptheria

A
  1. Preformed antibodies to Diptheria toxin
    2.Erythromycin (macrolide)
    Antibiotic is used stop onwards carriage. Need antibodies to clear infection in the child.
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71
Q

What is the centor criteria

A

Criteria that give an indication about whether pharyngitis is due to bacteria

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72
Q

List the (centor) criteria and limits to be met for bacterial pharyngitis

A
  • 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%

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73
Q

How would you identify if an upper respiratory tract infection was viral or bacterial

A

Centor criteria

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74
Q

What is the presentation of sinusitis

A

Fever, facial pain, purulent (pus) nasal discharge, recent history of cold

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75
Q

What is the presentation of acute epiglottitis and what is the cause

A

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.

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76
Q

What is the presentation of whooping cough

A

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.

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77
Q

What is the microbiology of bordatella pertussis

A

Gram negative bacillus

Treat with macrolide - clarithromycin; erythromycin

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78
Q

How do you diagnose whooping cough

A

Have to do culture and serology and look for antibodies against BP toxin

Dx by culture, PCR, ELISA for IgG against PT

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79
Q

What are the clinical features of whooping cough

A

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

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80
Q

What is the presentation of croup (swelling of the larynx, trachea and bronchi)

A

Barking cough, febrile, cyanosed, intercostal recession, inspiratory stridor (a high pitched wheezing noise due to turbulent airflow in upper airway)

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81
Q

What is croup

A

Acute laryngo-treacheobronchitis

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82
Q

What is included in the dTaP vaccine

A

diphtheria, tetanus and acellular Pertussis

at 2,3, 4 mo. and 3-4 yo

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83
Q

What are the two serious infections that you want to rule out in a child that presents with sore throat (pharyngitis)

A

Strep pyogenes scarlet fever

Diptheria

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84
Q

What percentage of brain tumours are malignant

A

95%

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85
Q

List some cancers that can spread to the lung

A 
breast
colorectal
prostate
kidney
melanoma
thyroid
lymphoma
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86
Q

List the different types of malignant tumours you can get in the pleura and benign tumours

A 
Malignant:
Mesothelioma - most common?
Primary lymphoma
Pleural Thyoma 
Pleural Sarcoma

Benign:
Fibrous

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87
Q

What is the different pathology of pleural cancers

A
  1. Mesothelial cells - epithelial cells that secrete serous fluid
  2. Lymphatics that drain the pleura
  3. Thymus cells
  4. Connective tissue between/ supporting epithelial cells of pleura
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88
Q

What are the different lung reactions to asbestos

A

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

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89
Q

What are the two commonest cancers associated with asbestos exposure - explain why

A

Mesothelioma (more common - pleura more sensitive to asbestos)
Carcinoma - bronchials (squamous, adenocarcinoma)

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90
Q

What is the interval between asbestos exposure and development of mesothelioma

A

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?
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91
Q

What are the different types if pathology of mesothelioma

A

Epithelioid
Sarcomatoid
Desmoplastic
Mixed / biphasic

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92
Q

Is there effective treatment for mesothelioma

A

No - treatment is palliative focused. Survival time is approximately 11 months.

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93
Q

When was asbestos most heavily mined and used?

A

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.

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94
Q

What are the clinical features of mesothelioma

A 
chest pain
breathlessness
weight loss
SVCO
sweating
abdominal pain
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95
Q

What investigations would you do for mesothelioma, what is the main differential

A 
CXR
CT scan
Pleural aspiration - biopsy 
Blind or CT guided pleural biopsy
VATS pleural biopsy

Main differential is a bronchial lung cancer - carcinomas

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96
Q

What is the treatment for mesothelioma

A

Symptom control
Palliative chemotherapy
Radical surgery/debulking surgery
Palliative radiotherapy

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97
Q

Name some of the benign tumours of the lung

A 
hamartoma
carcinoid
lipoma
chondroma
leiomyoma
nerve sheath tumours
fibroma
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98
Q

Is lung cancer usually primary or secondary

A

Both are common but secondary - metastatic is more common

Metastatic carcinoma is more common than primary carcinoma - think about history of cancers

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99
Q

Is lung cancer more common in males or females

A

Males 2:1

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100
Q

List some of the paraneoplastic changes associated with lung cancer

A

•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)

101
Q

List some of the non carcinoma cancers of the lung

A
  • Bronchial gland neoplasm
  • Pleural neoplasia
  • Soft tissue sarcoma/benign tumour
  • Lymphomas
  • Hamartomas
102
Q

What are the common lung carcinomas

A 
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
103
Q

What gene mutations are involved in lung cancer

A

p53 - cell cycle protein regulator

EGFR - epidermal growth factor receptor - mutation

104
Q

What is the difference in grade between NSCLC and SCLC

A

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).

105
Q

What do M0, M1a, M1b, MX mean in regards to lung cancer staging

A 
[M0] absent
[M1a] contralateral lung
pleural or pericardial effusion/nodule
[M1b] Distant spread outside chest
[MX] not known
106
Q

When is lung cancer considered to be metastatic

A

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.

107
Q

Explain node staging in lung cancer

*think about mediastinum and subcarina here

A 
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
108
Q

List the most common causal agents for occupational asthma

A 
Isocyanates 
Flour (bakers)
Cleaning products
Wood dusts (joiners)
Enzymes, Amylase
109
Q

Why is early identification of occupational asthma important . How can be this be done in the workplace?
SECONDARY PREVENTION

A

Exposure reduction improves asthma (FEV1) - get reversibility of disease
Can treat or even cure disease in some cases
Health surveillance programmes

110
Q

What question is useful for identifying if asthma is occupational

A

Does it improve over the weekend? When they go on holiday? Are away from work?

111
Q

What is the timescale for onset of occupational asthma

A

minutes (acute) to months to years

less common for it to be decades

112
Q

Explain the different types of hypersensitivity reactions

A

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.

113
Q

What are the common occupational lung allergies - what are the most common causes

A

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

114
Q

What is hypersensitivity pneumonitis

A

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)

115
Q

Causes of occupational EAA

A

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

116
Q

What occupational hazard can increase lung sensitivity to TB

A

Silica

117
Q

What percentage of COPD is occupational

A

10-15%

118
Q

What are the causes of occupational COPD

A

Coal
Silica
Grain

119
Q

What should patients who have occupational COPD always be advised to do

A

Stop smoking - this will improve FEV1 even if have COPD

120
Q

What are pleural plaques

A

Calcified collagen
Sign of asbestos exposure
Not pre-malignant

121
Q

What is asbestosis

A 
Pulmonary fibrosis
Subpleural, basal = UIP (usual interstitial pneumonitis) pattern
With/without plaques
History of heavy exposure
No effective treatment
May progress (without further exposure)
122
Q

What is asbestos effusion

A

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)

123
Q

What is the relationship between asbestos exposure, smoking and lung cancer

A

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

124
Q

What is the presentation of mesothelioma

A

Progressive breathlessness and chest pain
Weight loss
Life expectancy ~11 months

125
Q

What is the best way of managing occupational lung diseases

A

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)

126
Q

List the most common occupational lung diseases

A

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

127
Q

What causes occupational lung disease

A

VGFD
Allergens - organic or inorganic
Hypersensitivity reactions

128
Q

What regions of the lungs are usually affected by idiopathic pulmonary fibrosis

A

Lower lobes - subpleural regions - patchy

129
Q

Describe the lung pattern of idiopathic pulmonary fibrosis

usual interstitial pneumonitis

A

Lower lobes - patchy, sub pleural
Loss of lung architecture
Dilated air spaces within fibrotic areas - honeycombing

130
Q

What is the survival rate of idiopathic pulmonary fibrosis

A

50% 5 year survival

131
Q

Which interstitial lung disease may be asymptomatic

A

Pneumonconiosis - coal works lung

But may have coexisting bronchitis

132
Q

Which interstital lung disease should not be treated with steroids

A

Idiopathic pulmonary fibrosis

133
Q

What are interstital lung diseases

A

Conditions with damage to the lung parenchyma and remodelled interstitium

134
Q

List the causes of interstitial lung diseases

A 
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
135
Q

What is the pathology of interstitial lung disease

A

Injury/ insult to parenchyma (eg allergen, or dust particle; immune complex) –> macrophage –> chronic inflammation –> fibrosis –> architecture remodelling

136
Q

What investigations should be done on patients who you suspect might have interstitial lung disease

A

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

137
Q

What would you include in an interstitial lung disease differential

A

Obstructive airways disease - asthma, COPD?
Sytemic connective tissue disease - RA, SS, Sarcoidosis, Vasculitis (GPA) etc
Infection - TB, pneumonia?

138
Q

What is the management for interstitial lung diseases

A

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

139
Q

List the different types of interstital lung diseases

A

Acute:
Adult Respiratory Distress Syndrome
Cryptogenic Organising Pneumonia

Chronic:
Idiopathic pulmonary fibrosis
Pneumoconiosis
Coal workers lung
Silicosis 
Asbestosis
Hypersensitivity pneumonitis
140
Q

What is caplan’s syndrome

A

Rheumatoid + coal workers lung

141
Q

What does a CXR or fibrosis look like

A

Diffuse shadowing

142
Q

What is the management of idiopathic pulmonary fibrosis

A

Supportive. Oxygen therapy, pain relief (opitates), palliative care. NEVER high dose steroids.

143
Q

What is the management of industrial lung diseases

A

Avoid trigger. Treat other lung diseases. Supportive & symptomatic. Patients eligible for compensation.

144
Q

Causes of bronchiecstasis

A

Post infection - Severe pneumonia, TB
CF
Bronchial obstruction

145
Q

Pathology of bronchiecstasis

A

Enlarged bronchioles + lots of mucus secretion

Chronic inflammation of the bronchi and bronchioles leading to permanently dilated and thinning of airways

146
Q

Tests for bronchiecstasis

A

Sputum - culture
CXR - cystic shadows, thickened bronchial walls - tramlines
Spirometry - obstructive

147
Q

What is the management for bronchiecstasis

A

Airways clearance techniques
Mucolytics - chest physio
Antibiotics for infections

148
Q

What is cystic fibrosis, what is the presentation

A

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.

149
Q

What are the causes of pleural effusion

A

Transudate - increased venous pressure - heart failure, constrictive pericarditis, hypoproteinaemia (cirrhosis etc)
Exudate - infection, inflammation, cancer

150
Q

What are the symptoms of pleural effusion

A

Asymptomatic - maybe dyspnoea or pleuritic chest pain

151
Q

What are the signs of pleural effusion

A

Decreased expansion
Stony dull percussion
Diminished breath sounds on the affected side
If large - may be tracheal deviations

152
Q

What are the tests for pleural effusion

A

CXR - look at costophrenic angle
Ultrasound - useful for seeing fluid
Aspiration - culture, cytology, immunology
Biospy

153
Q

What is the management of pleural effusion

A

Treat underlying cause
Drainage
Surgery

154
Q

What are the causes of pneumothorax

A

Rupture of the pleura

Asthma,COPD, TB, pneumonia, sarcoidosis, trauma - anything that puts pressure on pleura and has capacity to rupture it

155
Q

What are the signs and symptoms of pneumothorax

A

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

156
Q

What are the signs and symptoms of pulmonary embolism

A 
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
157
Q

What are the investigations for PE

A

Bloods - D-dimer
ABG - may show reduced PaO2
Imaging - CXR - may be normal , look for dilated PA
ECG - right ventricular strain?

158
Q

What is the management for PE

A

If haemodynamically unstable - thromboembolise - eg alteplase
If stable - heparin - 5 days, then DOAC or warfarin

159
Q

What should you consider in a patient that has no risk factors for PE (unprovoked)

A

cancer

160
Q

What are the risk factors for PE

A

Surgery, immobility, leg fracture
OC pill, HRT, Pregnancy
Long haul flights/ travel (rare)
Inherited thrombophilia (antiphospholipid syndrome)- genetic predisposition; 5% population, familial

161
Q

What is the presentation of PE

A

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

162
Q

What are the investigations for PE

A

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

163
Q

What is the hilar point on a chest X ray

A

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)

164
Q

What are the signs of heart failure on a CXR

A

Alveolar oedema
B Kerley B line (thickened interlobular septa)
Cardiomegaly
Distension (upper lobe veins)
Effusion - pleural effusion (meniscus line)

165
Q

What is the sail sign on a CXR - what does it show

A

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

166
Q

Outline CXR method of review

A

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?
167
Q

What are the signs of pneumonia on CXR

A

Consolidation - air bronchograms - these are lines of air that are more pronounced bc of consolidation in alveoli

168
Q

What is a tension pneumothorax - how would you identify it on CXR

A

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

169
Q

What is the sign of pleural effusion on CXR

A

Bilateral consolidation - Meniscus line

170
Q

Describe how you would interpret a CXR based on if it was dense or lucent

A
  1. Dense or lucent?
  2. 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?
171
Q

How can you identify which lobe of a lung is collapsed on a CXR

A

RML - RHB
RLL - Right hemi diaphragm
LUL - LHB
LLL - Left hemi diaphragm

RUL collapse - Horizontal fissure - has this moved?

172
Q

What are the causes of pleural effusions

A

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

173
Q

What is the wells score and when is it used

A

Its used to assess a suspected Pulmonary embolus.
<4 = D dimer
>4 = Immediate CTPA or treat empirically with LMWH if cant do CT

174
Q

What is D dimer, what does a positive result show

A

D-dimer is a produce of fibrin degradation - if it is positive it suggests that there has been a fibrin thrombus in the blood

175
Q

What is included in Wells score

A 
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
176
Q

Causes of type 1 respiratory failure

A

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)

177
Q

Causes of type 2 respiratory failure

A

Think about hypoventilation problems
Hypoxaemia + hypercapnea on ABG
PaO2 = <8kPa
PaCO2 = >6kPa

COPD
End stage fibrosis
Sedative drugs, CNS tumour or trauma
Neuromuscular disease

178
Q

What is the management for type 1 respiratory failure

A

Oxygen - 24-60% by facemask
Treat underlying cause - eg. thombolyse clot on lung
Assisted ventilation is PaO2 <8Kpa despite 60% oxygen

179
Q

What is the management for type 2 respiratory failure

A

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.

180
Q

What is the normal blood ph

A

7.35-7.45
<7.35 = acidosis
>7.45 = alkalosis

181
Q

At what O2 partial pressure do RBCs start to significantly desaturate and respiratory rate increases

A

60mmHg - equivalent to 8kPa

182
Q

What is a pink puffer and a blue bloater - what do they represent clinically

A

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

183
Q

What is the differential diagnosis for COPD

A 
Other causes of SOB
Heart failure
Pulmonary embolus
Pneumonia
Lung cancer
Asthma
Broncheictasis
184
Q

What is the GOLD classification of airflow limitation

A

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

185
Q

What tool predicts outcomes in COPD

A 
BODE index 
Bmi
Obstrution (FEV1)
Dyspnea 
Exercise capacity
186
Q

Describe the pathology of COPD

A

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

187
Q

Define COPD

A

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

188
Q

Describe some of the pathological characteristics of COPD

A

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

189
Q

Describe the vascular changes that take place with COPD

A

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.

190
Q

Describe the clinical features of COPD

A 
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
191
Q

What are the risk factors for COPD

A

Smoking
Occupational dusts/ smokes/ fumes
Environmental tobaccop smoke
Age

192
Q

List 3 signs of COPD

A 
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
193
Q

What are the complications of COPD

A 
Infection 
Heart failure - cor pulmonale 
Polycythaemia 
Respiratory failure - type 2
Pneumothorax - ruptured bullae
Lung carcinoma
194
Q

What investigations should be done for COPD

A 
FBC
ABG - look for type 1 or 2 resp failure 
CXR
CT
Spirometry
195
Q

What is the spirometry profile of someone with COPD

A

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

196
Q

How does COPD look on a flow-volume graph

A

The expiratory arm is scooped - this represents reduced air flow through smaller airways. The beginning bit represents flow through larger airways.

197
Q

How do patients with COPD compensate for hypoventilation, what signs are there of this clinically

A

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

198
Q

Decribe how a flow-volume graph would look for a patient with COPD when they are hyperinflating their lungs

A

The tidal circle in the middle would shift to the left, representing an increase in inspiratory volume

199
Q

Describe the characteristics of COPD on CXR

A

Hyperinflation - barrel chest
Flat hemidiaphragms
Large pulmonary arteries
Air space enlargement

200
Q

Describe the ECG of a patient with COPD

A

Right atrial and ventricle hypertrophy bc of cor pumonale

201
Q

What would you include in a differential for a patient with suspected COPD

A

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

202
Q

What is the most common cause of COPD exacerbation

A

Upper respiratory tract infection

203
Q

What is the treatment for COPD

A

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.

204
Q

How can you assess the severity of COPD

A 
GOLD categorises into 4 stages, based on post broncho-dilator FEV1% predicted 
Mild 
Moderate
Severe
Very severe
205
Q

When can O2 therapy be given in COPD patients

A
  • 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
206
Q

What is the goal of drug therapy in COPD

A

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

207
Q

What are the goals of COPD treatment

A

Relieve symptoms
Improve exercise tolerance
Improve health status

Prevent disease progression
Prevent and treat exacerbations
Reduce mortality

208
Q

Describe how to manage a COPD exaccerbation

A

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.

209
Q

What is atopy

A

Atopy is the tendency to develop IgE mediated reactions to common aeroallergens

210
Q

Summarise the pathology of eosinophilic atopic asthma

A

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

211
Q

Summarise the pathology of non eosinophilic asthma

A

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

212
Q

What are common causes/ triggers for atopic asthma

A 
Aeroallergens - pollen, fumes
Pets
Fungal
Cold weather 
Exercise 
Night/ early morning 
Emotion
213
Q

What is a typical presentation of asthma

A

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?

214
Q

What are the signs of asthma on examination

A

Widespread expiratory wheeze on auscultation
May have hyperinflated chest
Hyperresonance
Tachypnoea

215
Q

What investigations would you do for a patient suspected with asthma

A

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

216
Q

What would you include in an asthma differential

A

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?

217
Q

What clinical features distinguish asthma from other differentials

A 
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 &amp; occupational history
218
Q

Outline the management of asthma

A
  1. Bronchodilators - mainly B2 agonists (not really antimuscurinics), LTRA leukotriene receptor antagonists, Theophylline
  2. Steroids
  3. 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

219
Q

What should you consider when giving Inhales corticosteroids to COPD patients - when is it acceptable to prescribe oral steroids to COPD patients

A

Consider pneumonia risk

Can give oral steroids with antibiotics to COPD pt with confirmed infection

220
Q

What CD4 response is atopic asthma

A

Th2 - IgE producing

221
Q

What CD4 response is non-eosinophilic astham

A

Th1 - non IgE producing

222
Q

What do mast cells release

A 
Cytotoxic granules
Chemotaxins for eosinophils 
Leukotrienes 
Histamine - vasodilation
Stimulate bronchospasm
223
Q

Why is asthma reversible and COPD isnt

A

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.

224
Q

What peak flow is diagnostic of asthma

A

Decrease in >20% in PEFR from predicted 3/7 days a week

Improved PEFR after dilator or steroids - increase of 200 -400 ml

225
Q

What spirometry is diagnostic of asthma

A

Obstructive pattern - reduced FEV1, FEV1/ FVC ratio

Increase of 12% in FEV1 after brochodilator indicator of asthma

226
Q

What is brittle disease

A

Really bad unresponsive to treatment asthma

At risk of severe attacks

227
Q

What PEFR would you see in an asthma attack

A

Severe - 35-50% predicted

Life threatening - <33%

228
Q

Features of life threatening asthma attack

A

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)

229
Q

What is the management of an asthma attack

A 
Oxygen
Salbutamol - Steroid prednisolone 
Hydrocortisone
IV
T?
Magnesium or aminophylline - IVE
ABG
Not responding - CXR - pneumothorax, consolidation?
230
Q

Sign of severe asthma attack

A

Inability to complete sentences

231
Q

What CXR signs would show bronchiecstasis

A

hyperinflation, tram tracks, increased linear markings, focal pneumonitis, ring shadows and atelectasis

232
Q

What is the difference between bronchitis and bronchiectasis

A

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.

233
Q

What are the commonest occupational lung diseases

A

Pleural disease, mesothelioma, COPD, asthma, EAA

234
Q

What are the causes of occupational lung disease, give examples

A

Vapors - isocyanates (pains etc)
Gases -
Fumes - silica
Dust - wood (joiners), bakers and flour

235
Q

Outline the different prevention strategies for occupational lung diseases

A 
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

236
Q

Outline some of the treatment options for occupational lung diseases

A

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

237
Q

Mortality risk factors in flu

A

Chronic cardiac and pulmonary diseases

  • Old age
  • Chronic metabolic diseases
  • Chronic renal disease
  • Immunosuppressed
238
Q

What is an outbreak

A

2 or more linked cases

239
Q

What is an epidemic and whats a pandemic

A

More cases in a region/country

Epidemics that span international boundaries

240
Q

When does influenza peak

A

December to march

241
Q

What is a common cause for pandemic flu

A

Often created by the strain “jumping” from another species e.g. Flu virus found in ducks, chickens, horses, pigs, whales, seals…

242
Q

What are the consequences of pandemic flu

A

High morbidity
• Excess mortality
• Social disruption
• Economic disruption

243
Q

List some ways to prevent flu pandemic

A
  • 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
244
Q

What is Oseltamivir

A

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?

245
Q

Outline how a flu pandemic is managed

A

Containment - identify cases, contact tracing, treat, prophylaxis
Treatment - treat cases

246
Q

When is it appropriate to wear face mask

A

If within 1 meter of someone with flu

Only if worn appropriately, changed frequently, removed properly, disposed properly

247
Q

How long does it take to develop a flu vaccine

A

6-10 months

248
Q

When is it acceptable to administer oxygen in COPD

A

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

Phase 2 (12 decks)

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