Chest Medicine Flashcards

1
Q

What do the following sputum colours indicate?

Clear and colourless:

Yellow-green/brown:

Red

Black

Frothy white-pink

A

Clear and colourless: Chronic bronchitis

Yellow-green/brown: Pulmonary infection

Red: Haemoptysis

Black: smoke, coal dust

Frothy white-pink: pulmonary oedema

If indicated ask for zn stain and pcr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does peak expiratory flow tell you?

A

It is the maximum forced expiration. You do it 3 times and take the best one. It correlated with forced expiratory volume over 1 second (FEV1) -> good for asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pulse oximetry measures the peripheral O2 saturation. What is the normal level in normal patients and COPD?

What should you do if O2 sats are below 92%?

What causes bad readings?

A

Normal: 94-98%

COPD: 88 - 92%

Do ABG if below 92%

poor perfusion, movement, skin pigmentation, nail varnish, dyshaemoglobinaemias and CO poison.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where is the ABG taken from?

What does it measure?

A

Radial/femoral artery(heperanized blood).

Brachial artery is used less as it is an end artery and it is near the median nerve.

It measures: pH, PaCO2, HCO3, PaO2, lactate, na+, cl-, K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is spirometery?

A

It measures lung function.

Forced expiratory volume in 1s(FEV1) and forced vital capacity are measured from a full forces expiration into a spirometer. FEV1 is less effort dependent than PEF. FEV1/FEV gives a good estimate of the severity of airflow obstruction -> can show if it is restrictive or obstructive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are restrictive defects and what are obstructive defects?

A

Restritive: fibrosis, sarcoidosis, pneumoconiosis, interstial pneumonias, connective tissue disease, pleural effusion, obesity, kyphoscliosis, neuromuscular problems

Obstructive defect: asthma, bronchiectasis, COPD, cystic fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

When are Total lung capacity and residual volume are increased in what disease?

A

Obstructive airway disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Total lung capacity and residual volume are decreased in what disease

A

Restrictive lung disease and musculoskeletal abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Gas transfer coeffecient represents the carbon monoxide diffusion capacity corrected for alveolar volume. Calculates the CO uptake from a single inspiration in a standard time (usually 10s) and lung volume by helium dilution.

When is this low and when is it high?

A

Low
in emphysema and interstitial lung disease

high in alveolar haemorrhage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

When is ultrasound used in chest medicine?

A

Ultrasound: Used in diagnosing and guiding

drainage of pleural eff usions (particularly loculated eff usions) and empyema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ventilation/perfusion (V/Q, p738) scans are occasionally used to

diagnose what?

A
pulmonary embolism (PE), eg in pregnancy (unmatched perfusion defects
are seen).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Computed tomography: Used for what in chest medicine?

A

diagnosing and staging lung cancer, imaging the hila, mediastinum, and pleura, and guiding
biopsies. Thin (1–1.5mm) section high-resolution CT (HRCT) is used in the diagnosis of
interstitial lung disease, emphysema, and bronchiectasis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

(CTPA) is used in the diagnosis of what?

A

PE.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Fibreoptic bronchoscopy is performed under local anaesthetic via the nose or mouth.

When would it be used diagnostically?

A

Performed under local anaesthetic via the nose or mouth. Diagnostic indications: Suspected lung carcinoma, slowly resolving pneumonia, pneumonia in the immunosuppressed, interstitial lung disease. Bronchoalveolar lavage fluid may be sent to the lab for microscopy, culture, and cytology.

Mucosal abnormalities may be brushed (cytology) and biopsied (histopathology).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the therapeutic indications for fibreoptic bronchoscopy

A

Aspiration of mucus plugs causing lobar collapse, removal of foreign bodies, stenting or treating tumours, eg laser.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Bronchoalveolar lavage

(BAL) is performed at the time of bronchoscopy by in-
stilling and aspirating a known volume of warmed, buff ered 0.9% saline into the distal airway.

What are the diagnostic indication for it?

Therapeutic indications are?

A

Suspected malignancy, pneumonia, in the immunosuppressed (especially HIV), bronchiectasis, suspected TB (if sputum negative), interstitial lung diseases (eg sarcoidosis, extrinsic allergic alveolitis, histiocytosis X).

Therapeutic indications: Alveolar proteinosis -

Pulmonary alveolar proteinosis causes cough, dyspnoea, and restrictive spirometry. It is caused by ac-
cumulation of surfactant-derived acidophilic phospholipid/protein compounds which fi ll alveoli and distal bronchioles. Diagnosis may require lung biopsy. Cause: primary genetic or antibody problem, or secondary
to infl ammation caused by inhaling silica, aluminium, or titanium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Percutaneous needle biopsy is performed under radiological guidance and is useful for?

A

peripheral lung and pleural lesions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Transbronchial biopsy performed at bronchoscopy may help in diagnosing?

A

Interstitial lung diseases, eg sarcoidosis, idiopathic pulmonary fibrosis.

Alterna-
tives: If unsuccessful, consider open lung biopsy or video-assisted thoracoscopy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What surgical procedures are perfoemd under general anaesthetic which are used to get biopsies in the chest?

A

Rigid bronchoscopy provides a wide lumen, enables larger mucosal biopsies, control of bleeding, and removal of foreign bodies.

Mediastinoscopy and mediastinotomy enable examination and biopsy of the mediastinal lymph nodes/lesions.

Thoracoscopy allows examination and biopsy of pleural lesions, drainage of pleural effusions, and talc pleurodesis and pleurectomy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Pneumonia is an acute lower respiratory tract infection associated with fever, symptoms and signs in the chest, and abnormalities on the chest x-ray—fi g 16.2, p723. Incidence: 5–11/1000, if very young or old (30% are under 65yrs). Mortality: ~21% in hospital.

What are the common pathogen causes pneumonia?

A

May be primary or secondary to underlying disease.

Typical organisms:

Streptococcus pneumoniae (commonest),

Haemophilus infl uenzae,

Moraxella catarrhalis.

Atypicals: Mycoplasma pneumoniae,Staphylococcus aureus, Legionella species, and Chlamydia. Gram-negative bacilli,
Coxiella burnetii and anaerobes are rarer (?aspiration). Viruses account for up to 15%. Flu may be complicated by community-acquired MRSA pneumonia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Define hospital acquired pneumonia.

what are the common causes of HAP?

A

Defi ned as >48h after hospital admission.

Most commonly: Gram-negative enterobacteria or Staph. aureus.

Also Pseudomonas, Klebsiella,
Bacteroides, and Clostridia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why do people get aspiration pneumonia?

A

Those with stroke, myasthenia, bulbar palsies, consciousness (eg post-
ictal or intoxicated), oesophageal disease (achalasia, reflux), or poor dental hygiene risk aspirating oropharyngeal anaerobes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What sort of pathogens do immunocompromised patients get?

A

Strep. pneumoniae, H. infl uenzae, Staph. aureus, M. catarrhalis, M. pneumoniae, Gram Ωve bacilli and Pneumocystis jirovecii (for-
merly named P. carinii, pp400–1). Other fungi, viruses (CMV, HSV), and mycobacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the clinical features of pneumonia? Signs and symptoms

A

Symptoms:Fever, rigors, malaise, anorexia, dyspnoea, cough, purulent sputum, haemoptysis, and pleuritic pain.

Signs: Pyrexia, cyanosis, confusion (can be the only sign in the elderly—may also be hypothermic), tachypnoea, tachycardia, hypotension, signs of consolidation (reduced expansion, dull percussion, increased tactile vocal fremitus/vocal resonance, bronchial breathing), and a pleural rub.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What tests would you do for pneumonia patient?

A
  • *Assess oxygenation**: oxygen saturation, p162 (ABGs if SaO2 <92% or severe
    pneumonia) and BP. Blood tests: FBC, U&E, LFT, CRP (GPs should consider a point of care CRP to guide antibiotic prescribing where LRTI is suspected, NICE 2014).

CXR (fi g 16.2, p723): lobar or multilobar infiltrates, cavitation, or pleural effusion. Sputum for microscopy and culture.

Urine: check for Legionella/Pneumococcal urinary antigens.

Atypical organism/viral serology (PCR sputum/BAL, complement fixation tests acutely, paired serology).

Pleural fluid - aspirated for culture. Respiratory physicians -> bronchoscopy and bronchoalveolar lavage -> immunocompromised or on ITU.

28
Q

What is the severity scoring system in community acquired pneumonia?

A

CURB - 65

Confusion (abbreviated mental test ≤8) - 1
Urea >7mmol/L -1
Respiratory rate ≥30/min -1
BP <90 systolic and/or 60mmHg diastolic) -1
Age ≥65. - 1

0–1, PO antibiotic/home treatment;

2, hospital therapy;

≥3, severe pneumonia indicates
mortality 15–40%—consider ITU. It may ‘underscore’ the young—use clinical judgement.

Other features increasing the risk of death are: comorbidity; bilateral/multilobar; PaO2 <8kPa.

29
Q

What is the management of pneumonia?

A

Antibiotics—refer to your local hospital antibiotic policy. When
none exists, consult table 4.2. If pneumonia not severe and not vomiting (CURB-65 1–2)
give PO antibiotic; severe (CURB-65 >2) give IV. Oxygen: keep PaO2 >8.0 and/or saturation
≥94%. IV fl uids (anorexia, dehydration, shock) and VTE prophylaxis. Analgesia if
pleurisy. Consider ITU if shock, hypercapnia, or remains hypoxic.

Follow-up: at 6 weeks
CXR) - see if it has come back or cleared

30
Q
A
31
Q

Who should pneumococcal vaccines be given to?

A

At-risk groups:
• All adults ≥ 65yrs old.
• Chronic heart, liver, renal, or lung conditions.
• Diabetes mellitus not controlled by diet.
• Immunosuppression, eg decreased spleen function, AIDS, or on chemotherapy or prednisolone
>20mg/d, cochlear implant, occupation risk (eg welders), CSF fluid leaks.
Vaccinate every 5yrs.
CI: Pregnancy, lactation, increased T°, previous anaphylaxis to vaccine or one of its components.

32
Q

Pneumococcal pneumonia is the commonest bacterial pneumonia.

Who are usually more at risk of it?

What are the clinical features?

What are the treatment?

A

Affects all ages, but is commoner in the elderly, alcoholics, post-splenectomy, immunosuppressed, and patients with chronic heart failure or pre-existing lung disease.

Clinical features: Fever, pleurisy, herpes labialis. CXR shows lobar consolidation. If mod/severe check for urinary antigen.

Treatment: amoxicillin, benzylpenicillin, or cephalosporin.

33
Q

Staphylococcal pneumonia

Who are at risk?

What can it cause on the X ray?

Treatment?

What if it is MRSA?

A

Risk group: May complicate influenza infection or occur in the young, elderly, intravenous drug users, or patients with underlying disease, eg leukaemia, lymphoma, cystic fibrosis (CF).

It causes a bilateral cavitating bronchopneumonia.

Treatment: flucloxacillin ± rifampicin, MRSA: contact lab; consider vancomycin.

34
Q

Klebsiella pneumonia(Rare)

Who are at risk for this?

What does it look like on X-ray?

Treatment?

A

Risk: Occurs in elderly, diabetics, and alcoholics.

Xray: Causes a
cavitating pneumonia, particularly of the upper lobes, often drug resistant. Treatment: cefotaxime or imipenem.

35
Q

Pseudomonas

What conditions does this commonly occur in?

Is it more likely to cause CAP or HAP?

Wha is the treatment?

A

A common pathogen in bronchiectasis and CF.

It also causes
hospital-acquired infections, particularly on ITU or after surgery.

Treatment: antipseudomonal
penicillin, ceftazidime, meropenem, or ciprofl oxacin + aminoglycoside.
Consider dual therapy to minimize resistance.

36
Q

Mycoplasma pneumoniae

How does it present?

What does the CXR show?

How is it diagnosed?

What are the complications?

What are the treatment?

A

Occurs in epidemics about every 4yrs. It presents insidiously
with flu-like symptoms (headache, myalgia, arthralgia) followed by a dry
cough.

CXR: reticular-nodular shadowing or patchy consolidation often of one lower
lobe, and worse than signs suggest.

Diagnosis: PCR sputum or serology. Cold agglutinins
may cause an autoimmune haemolytic anaemia

Complications: Skin rash (erythema
multiforme, fi g 12.22, p563), Stevens–Johnson syndrome, meningo encephalitis or myelitis; Guillain–Barré syndrome.

Treatment: Clarithromycin (500mg/12h) or
doxycycline (200mg loading then 100mg OD) or a fl uroquinolone (eg ciprofl oxacin or norfloxacin).

37
Q

Legionella pneumophila

Where does this bacteria usually colonise?

What are the symptoms: Pulmonary and extra pulmonary?

What does the CXR show?

What does the blood rests show?

How is it diagnosed?

Treatment?

A

Colonizes water tanks kept at <60°C (eg hotel air-conditioning and hot water systems) causing outbreaks.

Flu-like symptoms (fever, malaise, myalgia) precede a dry cough and dyspnoea. Extra-pulmonary features include
anorexia, D&V, hepatitis, renal failure, confusion, and coma.

CXR shows bi-basal consolidation.

Blood tests may show lymphopenia, hyponatraemia, and deranged LFTS. Urinalysis may show haematuria.

Diagnosis: Urine antigen/culture.

Treatment: fluoroquinolone for 2–3wks or clarithromycin (p387). 10% mortality.

38
Q

Chlamydophila pneumoniae - commonest chlamydial infection

How is it spread?

What symptoms are seen?

How is it diagnosed?

What is the treatment?

A

Person-to-person spread, biphasic illness: pharyngitis, hoarseness, otitis, followed by pneumonia.

Diagnosis: Chlamydophila complement fixation test, PCR invasive samples

Treatment: Doxycycline or clarithromycin.

39
Q

Chlamydophila psittaci

What can cause this?

What are the symptoms and extra pulmonary features?

How is it diagnosed?

What is the treatment?

A

Causes psittacosis(parrot fever) and ornithosis acquired from infected birds (typically parrots).

Symptoms include
headache, fever, dry cough, lethargy, arthralgia, anorexia, and D&V. Extra-pulmonary features are legion but rare, eg meningo-encephalitis, infective endocarditis, hepatitis, nephritis, rash, splenomegaly. CXR shows patchy consolidation.

Diagnosis: Chlamydophila serology.

Treatment: doxycycline or clarithromycin.

40
Q

What is the commonest viral pneumonia and how is it prevented?

A

Infl uenza commonest (p396 and BOX), but ‘swine fl u’ (H1N1) is now
considered seasonal and covered by the annual ‘flu vaccine. Others: measles, CMV, varicella zoster.

41
Q

Pneumocystis pneumonia

Who usually gets it?

What are the symptoms?

What will the CXR show?

How is it diagnosed?

how is it treated?

A

Causes pneumonia in the immunosuppressed (eg HIV).
The organism responsible was previously called Pneumocystis carinii, and now
called Pneumocystis jirovecii.

Symptoms: It presents with a dry cough, exertional dyspnoea,
decreased PaO2, fever, bilateral crepitations

CXR: may be normal or show bilateral perihilar
interstitial shadowing

Diagnosis: Visualization of the organism in induced sputum,
bronchoalveolar lavage, or in a lung biopsy specimen

Drugs: High-dose co-trimoxazole
(pp400–1), or pentamidine by slow IVI for 2–3 weeks (p401). Steroids are beneficial if severe hypoxaemia. Prophyl axis is indicated if the CD4 count is <200≈106/L or after the 1st attack.

42
Q

Avian influenza

Who are most at risk?

How is it diagnosed?

How it is managed?

How are close contact of infected patients managed?

A

Most at risk: in contact with infected poultry

Diagnosis: Viral culture +- PCR -H5 N1 specific primer

Managements: Get help, control outbreat, ventilation support, O2 and antivirals - oseltamivir, peramivir, and zanamivir. Give nebulisers and high flow O2

Precaution: wear masks and aboid contact of utensils. start antiviral treatment

osetlamivier - <48 hrs. zanamivir - <36hr. Monitor for symoptoms such as SOB, feever, diarrhoea etc

43
Q

Coronaviruses: SARS and MERS.

What are the symptoms and how are they managed?

A

Severe acute respiratory syndrome (SARS) is caused by SARS-COV virus—a
corona virus. Major features are persistent fever (>38°C), chills, rigors, myalgia,
dry cough, headache, diarrhoea, and dyspnoea—with an abnormal CXR and WCC.
Respiratory failure is a complicating feature: ~20% progress to acute respiratory distress syndrome requiring invasive ventilation. 16 Mortality is 1–50%, depending on age, but no cases since 2004. Close contacts, or travel to an area with known cases should raise suspicion. The mechanism of transmission of SARS-CoV is human–human. Management: seek expert help. Largely supportive with good infection control measures.

Middle East respiratory syndrome (MERS) is a viral respiratory disease caused by novel coronavirus (MERS CoV) and was fi rst identifi ed in 2012 in Saudi Arabia.
Symptoms include fever, cough, shortness of breath, and gastrointestinal upset. Incubation period 14 days. Human-to-human transmission has been reported in most cases, but camels play a pivotal host role in animal-to-human transmission. Large outbreaks linked to healthcare facilities have been reported in the Middle East and South Korea. The World Health Organization has reported mortality as
high as 36% in known cases.

44
Q

What are the complications of pneumonia?

A

Respiratory Failure - type 1 - hypoxia. give high flow O2. ITU if not better. (PaCo2 rises etc). O2 in COPD - check abg frequently - consider elective ventilation if PaCO2 or acidosis worsens

Hypotension - dehydration or septic vasodilation. <90mmHg systolic. 250 ml fluid challenge 15 min. If not then use central line and give IV fluid to maintain systolic BP >90mmhg. If not better still then get ITU or use an ionotropic e.g digoxin.

Atrial fib - common in elderly. B blocker or digoxin can be given to slow ventricular response rate in short term.

Pleural effusion

Empyema - pus in pleural space - CXR(pleural effusion) - aspirated (yellow, turbid, ph<7.2, low glucose, high LDH) - drain it

Lung abscess - give antibiotics

Septicaemia - infection from lung to blood

Pericarditis + myocarditis - complicate pneumonia

Jaundice - sepsis or secondary to antibiotics eg flucox or comoxiclav

45
Q

Lung abscess

What are the causes?

Clinical features?

Tests ?

Treatment

A

Causes: •Inadequately treated pneumonia. •Aspiration (eg alcoholism, oesoph ageal obstruction, bulbar palsy). •Bronchial obstruction (tumour, foreign body). •Pulmonary infarction. •Septic emboli (septicaemia, right heart endocarditis, IV drug use). •Subphrenic or hepatic abscess.

  • *Clinical features:** Swinging fever; cough; purulent, foul-smelling sputum; pleuritic chest pain; haemoptysis; malaise; weight loss. Look for: fi nger clubbing; anaemia; crepitations. Empyema develops in 20–30%.
  • *Tests:** Blood: FBC (anaemia, neutrophilia), ESR, CRP, blood cultures. Sputum microscopy, culture, and cytology. CXR: walled cavity, often with a fluid level. Consider CT scan to exclude obstruction, and bronchoscopy to obtain diagnostic specimens.
  • *Treatment:** Antibiotics as indicated by sensitivities; continue until healed (4–6 wks). Postural drainage. Repeated aspiration, antibiotic instillation, or surgical excision may be required.
46
Q

Bronchiectasis.

Pathology

Common organisms

Causes of bronchiectasis?

Clinical features: Symptoms? Signgs? Complications?

What are the tests you can do?

How is it managed?

A

Pathology Chronic infl ammation of the bronchi and bronchioles leading to permanent dilatation and thinning of these airways.

Main organisms: H. infl uenzae; Strep. pneumoniae; Staph. aureus; Pseudomonas aeruginosa.
Causes Congenital: Cystic fi brosis (CF); Young’s syndrome; primary ciliary dyskinesia; Kartagener’s syndrome (OHCS p646). Post-infection: Measles; pertussis; bronchiolitis; pneumonia; TB; HIV. Other: Bronchial obstruction (tumour, foreign body); allergic bronchopulmonary aspergillosis (ABPA, p177); hypogammaglobulinaemia; rheumatoid arthritis; ulcerative colitis; idiopathic.

Clinical features

Symptoms: Persistent cough; copious purulent sputum; intermittent
haemoptysis.

Signs: Finger clubbing; coarse inspiratory crepitations; wheeze
(asthma, COPD, ABPA). Complications: Pneumonia, pleural effusion; pneumothorax; haemoptysis; cerebral abscess; amyloidosis.
Tests Sputum culture. CXR: Cystic shadows, thickened bronchial walls (tramline and ring shadows); see fi g 4.7. HRCT chest (p164) to assess extent and distribution of disease. Spirometry often shows an obstructive pattern; reversibility should be assessed. Bronchoscopy to locate site of haemoptysis, exclude obstruction and obtain samples for culture. Other tests: Serum immunoglobulins; CF sweat test; Aspergillus
precipitins or skin-prick test RAST(allergy) and total IgE.

Management •Airway clearance techniques and mucolytics. Chest physiotherapy and devices such as a fl utter valve may aid sputum expectoration and
mucus drainage.

•Antibiotics should be prescribed according to bacterial sensitivities.
Patients known to culture Pseudomonas will require either oral ciprofl oxacin
or suitable IV antibiotics. If ≥3 exacerbations a year consider long-term antibiotics
(may be nebulized).

•Bronchodilators (eg nebulized salbutamol) may be useful in
patients with asthma, COPD, CF, ABPA (p177). •Corticosteroids (eg prednisolone) and
itraconazole for ABPA.

•Surgery may be indicated in localized disease or to control
severe haemoptysis.

47
Q

Cystic fibrosis

Clinical features in neonates? Children and adults?

How is it diagnosed?

What tests would you do?

Management?

A
48
Q

What is the second most common cancer in the UK?

What are the risk factors for this cancer?

A

Lung cancer

13% of all new cancer cases and 27% of cancer deaths (40 000 cases/yr in UK).22
Incidence is increasing in women. Only 5% ‘cured’.

Risk factors: Cigarette smoking
(causes 90% of lung ca). Others: passive smoking, asbestos, chromium, arsenic, iron oxides, and radiation (radon gas).

49
Q

What are the histological difference between lung cancers and what are the common cancers of each?

A

NSCLC: Squamous (35%); adenocarcinoma (27%), large cell
(10%); adenocarcinoma in situ (rare, <1%).

**Small cell (oat cell) (20%)**: Arise from
endocrine cells (Kulchitsky cells), often secreting polypeptide hormones resulting in paraneoplastic syndromes (eg production of ACTH, Cushing’s syndrome).

Most (70%)
SCLC are disseminated at presentation.

50
Q

What are the symptoms and signs of lung tumours?

A

Symptoms: Cough (80%); haemoptysis (70%); dyspnoea (60%); chest pain (40%); recurrent or slowly resolving pneumonia; lethargy, anorexia; weight loss.

Signs: Cachexia; anaemia; clubbing; HPOA (hypertrophic pulmonary osteoarthropathy, causing wrist pain); supraclavicular or axillary nodes.

Chest signs: none, or consolidation;
collapse; pleural effusion. Metastases: bone tenderness; hepatomegaly;
confusion; fits; focal CNS signs; cerebellar syndrome; proximal myopathy; peripheral neuropathy.

51
Q

What are complications of lung cancers?

What are extra pulomonary manifestation of bronchial cancer?

A

Local: recurrent laryngeal nerve palsy; phrenic nerve palsy; SVC
obstruction; Horner’s syndrome (Pancoast’s tumour); rib erosion; pericarditis; AF.

Metastatic: brain; bone (bone pain, anaemia, Ca2+); liver; adrenals (Addison’s). Non-metastatic neurological: confusion; fits; cerebellar syndrome; proximal myopathy; neuropathy; polymyositis; Lambert–Eaton syndrome

52
Q

What tests can you conduct on lung tumours and what will you see in them?

A

CXR: peripheral nodule (fi g 4.8); hilar enlargement; consolidation; lung collapse;= pleural effusion; bony secondaries.

  • *Cytology:** sputum and pleural fl uid (send at least 20mL). Fine needle aspiration or biopsy (peripheral lesions/lymph nodes).
  • *CT** to stage the tumour (p176) and guide bronchoscopy.
  • *Bronchoscopy**: to give histology and assess operability, ± endobronchial ultrasound for assessment and biopsy.
  • *18F-deoxyglucose PET or PET/CT EBUS** scan to help in staging. Radionuclide bone scan: if suspected metastases.

Lung function tests: help assess suitability for lobectomy.

53
Q

Bronchial adenoma

Hamartoma

A

Bronchial adenoma: Rare, slow-growing. 90% are carcinoid
tumours; 10% cylindromas. Rx: surgery.

Hamartoma: Rare, benign; CT: lobulated mass
± fl ecks of calcifi cation; ?excise to exclude malignancy.

54
Q

Malignant mesothelioma

What is it normally associated with?

What are the clinical features

what are the tests?

How is it diagnosed?

What is management?

What is the prognosis?

A

A tumour of mesothelial cells that usually occurs in the pleura, and rarely in the peritoneum or other organs. It is associated with occupational exposure to asbestos but the relationship is complex. 23 90% report previous exposure to asbestos, but only 20% of patients have pulmonary asbestosis. The latent period between exposure and development of the tumour may be up to 45yrs. Compensation is often available.
Clinical features: Chest pain, dyspnoea, weight loss, fi nger clubbing, recurrent pleural effusions. Signs of metastases: lymphadenopathy, hepatomegaly, bone pain/tenderness, abdominal pain/obstr uction (peritoneal malignant mesothelioma).

Tests: CXR/CT: pleural thickening/effusion. Bloody pleural fluid.
Diagnosis: Made on histology, usually following a thoracoscopy. Often the diagnosis is only made post-mortem.
Management: Pemetrexed + cisplatin chemotherapy can improve survival. 24 Surgery is hard to evaluate (few randomized trials). Radiotherapy is controversial. Pleurodesis and indwelling intra-pleural drain may help.
Prognosis: Poor (especially without pemetrexed, eg <2yrs). >650 deaths/yr in UK.

55
Q

Differential diagnosis of nodule in the lung on a CXR

A
56
Q

PET-CT is offered before treatment for all patient for surgery. Some may be offerend endobronchial ultrasounded guided transbronchial needle aspiration for mediastinal masses.

What is done to stage to non-small cell lung cancer.

A
57
Q

How is NSCLC treated?

What is the prognosis

What is the prevention tips?

A

Lobectomy (open or thoracoscopic) is the treatment of choice
if medically fi t and aim is curative intent or parenchymal sparing operation for patients with borderline fi tness and smaller tumours ((T1a–b, N0, M0).

Radical radiotherapy for patient with stage I, II, III NSCLC.

Chemotherapy ± radiotherapy for more advanced disease. Regimens may be platinum based, eg with monoclonal antibodies targeting the epidermal growth factor receptor (cetuximab).

SCLC: consider surgery
with limited stage disease.

Chemotherapy ± radiotherapy if well enough.

Palliation: Radiotherapy is used for bronchial obstruction, SVC obstruction, haemoptysis, bone pain, and cerebral metastases. SVC stent + radio therapy and dexamethasone for SVC obstruction.

Endobronchial therapy: tracheal stenting, cryotherapy, laser, brachytherapy (radioactive source is placed close to the tumour).

Pleural drainage/pleurodesis for symptomatic pleural effusions.

Drugs: analgesia; steroids; antiemetics;
cough linctus; bronchodilators; antidepressants.

Prognosis Non-small cell: 50% 2yr survival without spread; 10% with spread. Small cell: median survival is 3 months if untreated; 1–1½yrs if treated.

Prevention Stop smoking (p93). Prevent occupational exposure to carcinogens

58
Q

What are the 5 ways aspergillus can affect the lungs?

A

Asthma - Type I hypersensitivity reaction to fungal spores

Allergic bronchopulmonary aspergillosis (ABPA) - Results from type I and III
hypersensitivity reactions to Aspergillus fumigatus.

Aspergilloma (mycetoma) - A fungus ball within a pre-existing cavity (often
caused by TB or sarcoidosis). It is usually asymptomatic but may cause cough,
haemoptysis (may be torrential), lethargy ± weight loss.

Invasive aspergillosis - Risk factors: immunocompromise, eg HIV, leukaemia,
burns, Wegener’s , and SLE, or after broad-spectrum antibiotic therapy.

Extrinsic allergic alveolitis(EAA)

59
Q

Allergic bronchopulmonary aspergillosis

What type of hypersentitivity reaction occurs after reaction to aspergillus fumigatus?

A

Affects 1–5% of asthmatics,
2–25% of CF patients.26 Initially bronchoconstriction, then permanent damage occurs causing bronchiectasis (fi g 4.9).

Symptoms: wheeze, cough, sputum (plugs of mucus containing fungal hyphae, see p408), dyspnoea, and ‘recurrent pneumonia’.

Investigations: CXR (transient segmental collapse or consolidation bronchiectasis); Aspergillus in sputum; positive Aspergillus skin test and/ or Aspergillus-specifi c IgE RAST (radioallergosorbent test); positive serum precipitins; eosinophilia; raised serum IgE.

Treatment: prednisolone 30–40mg/24h PO for acute attacks; maintenance dose 5–10mg/d. Itraconazole can be used in combination with corticosteroids. Bronchodilators for asthma. Sometimes bronchoscopic
aspiration of mucus plugs is needed.

60
Q

Aspergilloma (mycetoma):

What is it?

What are the symptoms?

Investigations?

treatment?

A

A fungus ball within a pre-existing cavity (often
caused by TB or sarcoidosis).

Symptoms: It is usually asymptomatic but may cause cough,
haemoptysis (may be torrential), lethargy ± weight loss.

Investigations: CXR
(round opacity within a cavity, usually apical); sputum culture; strongly positive
serum precipitins; Aspergillus skin test (30% +ve).

Treatment (only if symptomatic):
consider surgical excision for solitary symptomatic lesions or severe
haemoptysis. Oral itraconazole and other antifungals have been tried with limited success. Local instillation of amphotericin paste under CT guidance yields partial success in carefully selected patients, eg in massive haemoptysis

61
Q

Invasive Aspergillosis

Risk factors?

Diagnosis?

Treatment?

Prognosis?

A

Risk factors: immunocompromise, eg HIV, leukaemia,
burns, Wegener’s, and SLE, or after broad-spectrum antibiotic therapy. Investigations: sputum culture; BAL; biopsy; serum precipitins; CXR (consolidation, abscess). Early chest CT and serial serum measurements of galactomannan (an Aspergillus antigen) may be helpful.

Diagnosis may only be made at lung biopsy or autopsy.

Treatment: voriconazole is superior to IV amphotericin. Alternatives:
IV miconazole or ketoconazole (less effective).

Prognosis: 30% mortality.

62
Q

Asthma

What is it? What 3 factors contribute to airway narrowing?

Symptoms?

Percipitans?

Dirurnal variation?

Social problems?

Associated diseases?

Signs?

A

Definition: It is characterized by recurrent episodes of
dyspnoea, cough, and wheeze caused by reversible airways obstruction

3 factors: bronchial muscle contraction, triggered by a
variety of stimuli; mucosal swelling/inflammation, caused by mast cell and basophil degranulation resulting in the release of inflammatory mediators; and increased mucus production.

Symptoms: Intermittent dyspnoea, wheeze, cough (often nocturnal), and sputum

Percipitans: Cold air, exercise, emotion, allergens (house dust mite, pollen, fur), infection, smoking and passive smoking,29 pollution, NSAIDS, beta- blockers.

Diurnal variation: Symptoms or peak flow may vary over the day. Marked morning dipping of peak flow is common and can tip the balance into a serious attack, despite having normal peak flow (fi g 4.12) at other times.

Social problems: excercise intolerance, disturbed sleep, job(triggers there such as pain, animals etc), days off school or work, home(carpets, feathers, pets).

Associated disease: Acid reflux(40-60%)- treating can improve spirometry, atopic disease(eczema, hay fever, allergy, family history), polyarteritis nodosa, Churg-strauss syndrom, ABPA(Allergic bronchopulmonary aspergillosis)

Signs - Tachypnoea; audible wheeze; hyperinflated chest; hyper-resonant percussion note; less air entry; widespread, polyphonic wheeze. Severe attack: Inability to complete sentences; pulse >110bpm; respiratory rate >25/min; PEF 33–50% predicted. Life-threatening attack: Silent chest; confusion; exhaustion; cyanosis (PaO2 <8kPa but PaCO2 4.6–6.0, SpO2 <92%); bradycardia; PEF <33% predicted. Near fatal: increased PaCO2(muscle tiring)

63
Q

how do you test for asthma for

What symptoms or features increases liklihood of asthma?

What decreases probability of asthma

Diagnosis

A

Increase probability of asthma:

  • wheeze, SOB, chest tightness,
  • diurnal variation
  • worsen after excercise, allergen, beta blocker
  • symptoms after aspirin or beta blocker
  • history of atopy
  • family history of atopy/asthma
  • widespread wheeze heard on auscultation
  • Unexplained low FEV1 or PEF
  • Unexplained peripheral blood eosinophilia

Lower probability of asthma:

64
Q

What are the differential diagnosis you need to think about when you see someone with asthma?

A
Pulmonary oedema (‘cardiac asthma’); COPD (may co-exist);
large airway obstruction (eg foreign body, tumour); SVC obstruction (wheeze/dyspnoea not episodic); pneumothorax; PE; bronchiectasis; obliterative bronchiolitis (suspect in elderly).
65
Q

Difference between acute attack and chronic attack asthma management and diagnosis

A

Acute attack: PEF, sputum culture, FBC, U&E, CRP, blood cultures. ABG analysis usually shows a normal or slightly low PaO2 but low PaCO2 (hyperventilation). If PaO2 is normal but the patient is hyperventilating, watch carefully and repeat the ABG a little later.

If PaCO2 is normal or raised, transfer to high-dependency unit or ITU for ventilation, as this signifies failing respiratory effort. CXR (to exclude infection or pneumothorax).

Chronic asthma:

PEF monitoring:

a diurnal variation of >20% on ≥3d a wk for 2wks. Spirometry: obstructive defect (decreased FEV1/FVC, increased RV p162); usually ≥15% improvement in FEV1 following B2 agonists or steroid trial. CXR: hyperinflation. Skin-prick tests may help to identify allergens. Histamine or methacholine challenge. Aspergillus serology.

66
Q
A
67
Q
A