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Year 3 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What are the paraneoplastic syndromes associated with lung cancer?

A

SIADH
Cushings
Hypercalcemia

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2
Q

Which lung cancer causes Cushings?

A

ACTH is released from small cell lung cancer

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3
Q

Which lung cancer causes SIADH?

A

ADH is released from small cell lung cancer

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4
Q

Which lung cancer causes hypercalcemia?

A

Parathyroid related peptide (PTHrP) from squamous cell carcinoma –> increased Ca absorption from gut, reabsorption from kidneys + bone resorption

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5
Q

Small cell lung cancer

A

Very aggressive + poor prognosis
Poorly differentiated neuroendocrine tumour
Often present with more disease in lymph nodes than lungs
Surgery usually pointless due to amount of extrapulmonary tissue therefore chemo

Histologically –> small cells with large, dark, irregular nuclei

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6
Q

Squamous cell carcinoma

A
  • Thought to derive from squamous metaplasia of the airways (from smoking)
  • Better prognosis than adenocarcinoma but more associated with smoking
  • Central forming cancer

Histologically –> must show keratin formation + intercellular bridges

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7
Q

Which carcinoma is described as lepidic?

A

Adenocarcinoma - spreads along surface of alveolar walls

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8
Q

Adenocarcinoma

A
  • Thought to derive from atypical adenomatous hyperplasia
  • Peripherally forming
  • Commonest type of lung Ca
  • More likely to have no smoking hx than SCC
  • Can show lepidic pattern which shows a groundglass appearance on CXR like infection

Histologically –> gland formation or mucin production

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9
Q

Which is the commonest type of lung Ca?

A

Adenocarcinoma

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10
Q

Metastasis in the lung

A

Actually the commonest type of tumour in the lung!
Commonest site of metastasis because dense capillary network captures circulating tumour
Usually multiple peripheral nodes on imaging

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11
Q

What staging is used for lung cancer?

A

TNM

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12
Q

What is a carcinoid tumour?

A

Low grade neuroendocrine tumour (other end of spectrum to small cell)
Low grade malignancy as behaviour difficult to predict - some do metastasise
Usually very well defined on imaging - diagnosis suspected before tissue diagnosis

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13
Q

What mutations are tested for in order to determine treatment of NSCLC?

A

EGFR mutation
ALK translocation
ROS1 translocation
PD-L1 expression

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14
Q

Which is the most malignant type of pleural tumour?

A

Metastases from lung + breast

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15
Q

What is the lag period between asbestos exposure and mesothelioma developing?

A

20-30 years

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16
Q

Clinical features of mesothelioma

A

Tumour encases lung + burrows into chest wall
Lymph node + distant metastases unusual
Indistinguishable from lung Ca on history but more chest pain + no lymphadenopathy

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17
Q

Diagnosis of mesothelioma

A

CT is distinctive - tumour wraps around lung, infiltrating into fissures

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18
Q

Histology of mesothelioma

A

Atypical mesothelial cells infiltrating surrounding tissue

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19
Q

What is a primary spontaneous pneumothorax?

A

Occurs in young people without known respiratory illness

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20
Q

Pneumothorax

A

Accumulation of air in the pleural space

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21
Q

What is a secondary spontaneous pneumothorax?

A

Occurs in people with pre-existing pulmonary disease

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22
Q

Clinical signs/symptoms of pneumothorax

A

May be minimal/absent in PSP

  • Sudden onset of pain
  • SOB (depending on size)
  • Tachycardia (>135 suggests tension)
  • Pulsus paradoxicus (HR slows with inspiration)
  • Hypotension
  • Raised JVP
  • Hyper-resonance + reduced breath sounds over area
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23
Q

Type 1 respiratory failure

A

Hypoxic but normal normocapnia
- V/Q mismatch (amount of air in doesn’t match BF to lung)

Give oxygen + treat cause: pneumonia, PE, pneumothorax, acute asthma, ARDS, COPD, pulmonary oedema

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24
Q

Type 2 respiratory failure

A

Hypoxia + hypercapnia
Alveolar hyperventilation

Acute - respiratory acidosis but normal bicarb
Chronic - high bicarb to maintain acid-base balance

Causes: COPD, exhaustion in asthma, obstructive sleep apnoea, opiates, NM disorders

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25
Q

Oxygen mask concentrations

A 
Air: 21%
Nasal cannula: 24-40%
Simple mask: 40-60%
Non-rebreathe: 90%
Venturi: 24, 28, 35, 40, 60%
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26
Q

Treatment for primary spontaneous pneumothorax

A

If >2cm + SOB - aspirate and if this doesn’t work then use chest drain

If <2cm and no SOB - leave it and review

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27
Q

Treatment for secondary spontaneous pneumothorax

A

If >2cm or SOB - Aspirate - if successful (<1cm) then admit + observe. If fails then add chest drain

If <2cm and no SOB - if 1-2cm then aspirate, if <1 then admit + observe

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28
Q

Examples of lung fibrosis affecting the lower, mid and upper zones

A

Lower - idiopathic pulmonary fibrosis
Mid - sarcoidosis
Upper - hypersensitivity pneumonitis

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29
Q

Clinical features of fibrosing lung disease

A

SOBOE, dry cough, fine end inspiratory crackles, joint or skin disease, clubbing

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30
Q

Histological features of fibrosing lung diseases

A

Fibrosis + remodelling of IS
Chronic inflammation
Hyperplasia of type II epithelial cells or type II pneumocytes

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31
Q

Most common interstitial lung disease?

A

Idiopathic pulmonary fibrosis

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32
Q

Idiopathic pulmonary fibrosis

A

Commonest cause of ILD
M>F 70yrs
Poor prognosis
Often associated with autoimmune disease

Features: SOB, dry cough, malaise, WL, arthralgia, clubbing, cyanosis, bilateral end-inspiratory crackles basally

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33
Q

Which drug slows disease progression in IPF?

A

Pirfenidone + nintedanib

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34
Q

How does coal workers pneumoconiosis occur?

A

Inhalation of coal particles - taken up by macrophages - die - release enzymes - cause fibrosis

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35
Q

What is progressive massive fibrosis?

A

progression of coal workers pneumoconiosis causing SOB, fibrosis and eventually cor pulmonale.
On a CXR - bilateral upper mid zone fibrotic masses developing from periphery towards the hilum

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36
Q

What does silicosis show on a CXR?

A

Diffuse military or nodular pattern in upper + mid zones and egg shell calcification of hilar nodes

37
Q

What does asbestosis show on a CXR?

A

Pleural plaques

38
Q

What is extrinsic allergic alveolitis?

A

Hypersensitivity to inhaled particles
Granuloma formation + obliterative bronchiolitis
4-6h post exposure - fever, rigors, malaise, SOB, dry cough, bibasal crackles
Chronic - clubbing, SOB, SOBOE, WL, type 1 respiratory failure

Avoid trigger!! Steroids may help

39
Q

What is spirometry used for?

A

Differentiating between obstructive + restrictive disease

Can monitor disease progression

40
Q

Obstructive pattern in spirometry

A

FEV1 reduced
FVC reduced but not as much
–> Fev1/FVC ratio reduced

41
Q

Restrictive pattern in spirometry

A

Fev1 reduced
FVC reduced
–> Fev1/FVC normal

42
Q

Bronchiectasis

A

Permanent dilatation + thickening of the airways characterised by chronic cough, excessive sputum production, bacterial colonisation + recurrent acute infections

43
Q

Causes of bronchiectasis

A

50% idiopathic
CF
Post infection e.g. pneumonia, measles, pertussis
ABPA - allergic bronchopulmonary aspergillosis

44
Q

Signs + symptoms of bronchiectasis

A

Chronic cough, sputum, SOB, chest pain, WL

Clubbing, coarse inspiratory crackles, wheeze

45
Q

Cause of fine crackles

A

Fibrosis

46
Q

Cause of coarse crackles

A

COPD
Pneumonia
Bronchiectasis
TB

47
Q

Which 2 diseases make up COPD?

A

Chronic bronchitis

Emphysema

48
Q

Emphysema

A

Alveoli are destroyed causing a loss of elasticity so air becomes trapped in them

Histological dx of enlarged air spaces distal to terminal bronchioles with destruction of alveolar walls

49
Q

Chronic bronchitis

A

inflammation of the lining of bronchial tubes

Cough + sputum on most days for 3m of 2 successive years

50
Q

Which disease are pink puffers?

A

Emphysema

Thin, less hypoxic, SOB, hyperinflated, tachypnoeaic, pink, low PCO2

51
Q

Which disease are blue bloaters?

A

Hypoxic, cyanosis + swollen feet/ankles/legs (HF or cor pulmonale)

52
Q

Signs + symptoms of COPD

A

SOB, cough + sputum, WL, frequent winter bronchitis, barrel chested, wheeze, coarse crackles

53
Q

Investigations of COPD

A

Bedside: sputum sample, ECG
Bloods: ABG, FBC (anaemia + polycythaemia), could check AAT level
Imaging: CXR, echo
Special tests: spirometry + reversibility

54
Q

Management of COPD

A

Conservative:

  • Lifestyle (stop smoking, exercise)
  • Chest physio
  • Pulm rehab + MDT
  • Vaccinate
  • Assess impact (MRC scale)

Medical:

  • SABA or SAMA. If still breathless then next step determined by asthmatic features e.g. steroid responsiveness so LABA + LAMA +/- ICS
  • Then specialist e.g. theophylline, LTOT
  • Consider carbocysteine
55
Q

What is in a COPD rescue pack?

A

5 days supply of prednisolone, 5 day supply of amoxicillin/doxy (use if purulent sputum)

56
Q

CXR findings of COPD

A
  • Hyperinflation - >6 anterior ribs
  • Prominent pulmonary arteries
  • Peripheral oligaemia
  • Bullae
57
Q

Who gets LTOT?

A

Non-smokers with: PaO2 <7.3, PaO2 7.3 - 8 when stable + 2nd polycythemia, nocturnal hypoxaemia, peripheral oedema, pulmonary HTN

Required for 15h a day for benefit

58
Q

Severity of COPD

A

Mild - FEV1 >80% predicted
Mod - FEV1 50-79%
Severe - FEV1 30-49%
V. severe - FEV1 <30% (or <50% with resp failure)

59
Q

MRC dyspnoea scale

A
  1. Not troubled by breathlessness except on vigorous exertion
  2. SOB when hurrying or walking up inclines
  3. Walks slower than contemporaries because of breathlessness or has to stop for breath when walking at own pace
  4. Stops for breath after walking 100m or stops after a few minutes walking on level
  5. Too breathless to leave the house or breathless on dressing or undressing
60
Q

What is the most common organise of an infective exacerbation of COPD?

A

Haemophilus influenza

61
Q

Things to not forget in an asthma history

A 
C - compliance with medication 
R - reliever usage
O - occupation 
S - sleep interference 
S - smoking
E - eczema, atopy?
D - days missed from work
62
Q

Management of acute asthma

A 
O - oxygen 15L non rebreathe, sit pt up
S - nebulised salbutamol back to back 
H - hydrocortisone IV 
I  - nebulised ipatropium
T - IV theophylline 
Magnesium sulphate IV if no improvement

Normal/high CO2 is very worrying - ITU

63
Q

Inhaler technique

A 
Remove cap
Shake
If not used for wk/new then spray
Hold upright
Breathe out as much as possible
Start to breathe in slow + deep then press 
Hold breath for as long as possible
If need 2nd dose - wait 30secs
64
Q

% of oxygen for litres

A 
4l = 35%
6l = 50%
8l = 55%
10l = 60%
65
Q

HAP

A

Occurs 48h after admission or anytime from an institution

Always typical

66
Q

CAP

A

Can be typical or atypical

67
Q

Signs + symptoms of pneumonia

A

Fever, rigors, malaise, cough + sputum, haemoptysis, pleuritic chest pain

Increased RR, increased HR, cyanosis, confusion, consolidation - reduced air entry + expansion, dull to percuss, crackles, bronchial breathing, pleural rub

68
Q

Typical of CAP

A

Strep pneumonia, haemophilus influenza

69
Q

Atypical of CAP

A

chlamydophila, legionella, pneumocystis

70
Q

HAP organisms

A

Gram -ve enterobacteria

Staph aureus

71
Q

CURB 65 score

A

Confusion
Urea >7
RR >30
BP <90/60

Age 65

0-1 = outpatient
2 = hospital
3 or more = consider itu

72
Q

What is a pleural effusion

A

Fluid in the pleural space

73
Q

Name for blood in the pleural space

A

Haemothorax

74
Q

Pus in pleural space

A

Empyema

75
Q

Blood + air in pleural space

A

Haempneumothorax

76
Q

Chyle (lymph + fat) in pleural space

A

Chylothorax

77
Q

Causes of a transudative pleural effusion

A

Increased venous pressure (HF, constrictive pericarditis, fluid overload)
Hypoproteinaemia (LD, malabsorption)
Hypothyroidism

78
Q

Causes of an exudative pleural effusion

A

‘Leaky capillaries’

Infection, malignancy, TB, SLE, mesothelioma

79
Q

Signs + symptoms of pleural effusion

A

SOB, pleuritic chest pain

Stony dull percussion, decreased expansion, diminished breath sounds, may have bronchial breathing in rest of the lung above effusion, may be trachea deviation away from effusion if very large

80
Q

Pleural effusion on a CXR

A

Blunted costophrenic angles

81
Q

Level of protein in exudative v transudative

A

Transudative <25
Exudative >35

If 25-35 then use lights criteria to distinguish - if protein/serum >0.5 then exudative

82
Q

Primary TB infection

A

Non-immune host who is exposed may develop primary infection of the lungs - Ghon focus develops in lungs which can turn into Ghon complex (combination of ghon focus with hilar lymph node involvement)

83
Q

Secondary TB infection

A

When TB that may have been latent becomes reactivated in a person - usually when they have become immunocompromised. Can spread locally or distally - military TB

84
Q

What happens when TB is inhaled?

A

Ingested by macrophages - form giant cells with central necrosis

85
Q

What increases the probability of TB being transmitted?

A

Infectiousness of case i.e. number expelled into air
Enviro factors e.g. air flow
Duration, proximity and frequency of exposure
Susceptibility of exposed person

86
Q

Is extrapulmonary TB infectious?

A

Not usually

87
Q

Latent TB contact screening

A

Mantoux (tuberculin skin test)
IGRA (IFN g release assay) - blood test with blood with TB and see if WBCs produce IFNg - if yes then do they have TB? if no then do they need the BCG?

If signs of active TB DO NOT use these tests

88
Q

Symptoms of TB

A

Long hx as slow growing e.g. 3m of fever

Fever, WL, fatigue, night sweats (TNFa), cough, haemoptysis

89
Q

How to diagnose TB?

A
  • Acid fast bacilli test for initial screen (if +ve then highly infectious) if +ve do ziel nelson stain to confirm
  • CXR - infiltration of upper zones + hilar lymphadenopathy
  • Broncho-alveolar or gastric lavage
  • Grow the organism (takes 4wks!) then another 4 wks to see what abx!!
  • Whole genome sequencing effective tool for predicting drug susceptibility + resistance - get results in 5-7d (looks at SNPs)

Year 3 (14 decks)

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