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Y3 Hard Qs > Buzz words: Respiratory > Flashcards

Buzz words: Respiratory Flashcards

1
Q 
SOB on exertion
“Winter bronchitis”
Wheeze
Chronic productive cough
Inv: post-bronchodilator Spirometry
A

COPD

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2
Q

Inv: post-bronchodilator Spirometry

A

COPD

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3
Q 
Fever
Chronic Cough
Weight loss
Asian
Lowenstein Jensen Medium
Red Ziehl-Nelson Stain
“Acid fast bacilli”
RIPE treatment
A

TB

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4
Q

Lowenstein Jensen Medium

A

TB

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5
Q

Red Ziehl-Nelson Stain

A

TB

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6
Q

“Acid fast bacilli”

A

TB

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7
Q

TB drug SE: orange tears

A

Rifampicin

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8
Q

TB drug SE: peripheral neuropathy

A

Isoniazid

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9
Q

Red-green colour blindness

A

Ethambutol

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10
Q 
Steatorrhoea, diabetes
Clubbing, Signet rings
Recurrent Infections
Bronchiectasis
Sodium >60mmol
A

Cystic Fibrosis

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11
Q

Shipyard/power station worker
End-inspiratory crackles
Non-productive cough
Pleural effusion

A

Mesothelioma

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12
Q

Mouldy hay

A

Farmer’s lung (EAA)

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13
Q

Parakeets/Pigeons

A

Bird fancier’s lung (EAA)

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14
Q

Lung Ca:
Horner’s syndrome
Arm pain

A

Pancoast’s tumour

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15
Q

Lung Ca:
Hypercalcaemia (constipation, polyuria)
Ectopic PTHrP
Epithelial cells

A

Squamous cells carcinoma

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16
Q 
Lung Ca:
Neuroendocrine symptoms
Paraneoplastic syndomes:
ACTH: cushing’s
ADH: SIADH
Anti-Ca ABs: Lambert Eaton
Mets early
A

Small cell carcinoma

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17
Q

Lung Ca:
Goblet cell origin
NON-smoker, woman

A

Adenocarcinoma

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18
Q

Lung Ca:
Goblet cell origin
NON-smoker, woman
Mets

A

Adenocarcinoma

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19
Q 
Fever, SOB, productive cough
Bronchial breath sounds
Coarse creps
Assess with CURB-65
CRP, urea, RR, BP, >65yo
IV clarithromycin, oral amoxicillin
A

Pneumonia

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20
Q

Pneumonia:

rusty sputum, younger pt

A

S. pneumoniae

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21
Q

Pneumonia:
small segmental
infiltrates, sinusitis, pharyngitis, laryngitis

A

Chlamydia pneumonia

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22
Q

Pneumonia:
adolescents,
erythema nodosum, pericarditis,
haemolytic anaemia

A

Mycoplasma pneumoniae

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23
Q

Pneumonia:

Abscesess

A

S. aureus

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24
Q

Pneumonia:

purulent dark sputum

A

Klebsiella - Gram negative anaerobic rod

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25
Q

Pneumonia:
AIDS, widespread
infiltrates, low O2 sats

A

Pneumocytitis jiroveci

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26
Q

Pneumonia:
legionnaire’s, low
Na, low albumin, air conditioning

A

legionnaire’s, low

Na, low albumin, air conditioning

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27
Q

Pneumonia:
birds,
hepatosplnomegaly, conjunctivitis,
arthralgia, lower lobe consolidation

A

Chlamydophila psittaci

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28
Q

Child coughing up blood

A

Inhaled foreign body

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29
Q 
Night cough
Intermittent wheeze
Eczema/hayfever (atopy)
Stepwise Treatment
Diurnal variation
A

Stable asthma

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30
Q

Nocturnal cough

Diurnal variation

A

Stable asthma

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31
Q

Nocturnal cough

Diurnal variation

A

Stable asthma

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32
Q

Silent chest, apparent improving O2,
fatigue, bradycardia
IV magnesium sulphate, intubate

A

Life-threatening exacerbation of asthma

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33
Q

60% O2 via facemask
Back-to-back nebs
Systemic steroids

A

severe exacerbation of asthma

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34
Q

60% O2 via facemask
Back-to-back nebs
Systemic steroids

A

severe exacerbation of asthma

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35
Q

What are the 3 stages of Churg Strauss Syndrome?

A

The initial phase is characterised by allergy with many patients having a history of asthma or allergic rhinitis. This inflammation of the nasal passages can lead to the development of nasal polyps.

The second phase is eosinophilia

The third stage is the vasculitis itself which affects small and medium-sized blood vessels and therefore resulting in damage to many organs.

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36
Q

What antibody is Churg Strauss syndrome associated with?

A

pANCA

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37
Q

What is the other name for Churg Strauss Syndrome?

A

Eosinophilic granulomatosis with polyangiitis

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38
Q

What is a cause of chronic respiratory acidosis?

A

COPD

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39
Q

What are the causes of upper zone fibrosis?

A 
C - Coal worker's pneumoconiosis
H - Histiocytosis/ hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation
T - Tuberculosis
S - Silicosis/sarcoidosis
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40
Q

What are the causes of lower zone fibrosis?

A

Idiopathic pulmonary fibrosis

Most connective tissue disorders (except ankylosing spondylitis) e.g. SLE

Drug-induced: amiodarone, bleomycin, methotrexate
asbestosis

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41
Q

What are the 5 respiratory causes of clubbing?

A

Lung cancer

Pyogenic conditions: cystic fibrosis, bronchiectasis, abscess, empyema

Tuberculosis

Asbestosis, mesothelioma

Fibrosing alveolitis

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42
Q

What are some cardiac causes of clubbing?

A

Cyanotic congenital heart disease (Fallot’s, TGA)

Bacterial endocarditis

Atrial myxoma

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43
Q

What are some other causes of clubbing?

A

Crohn’s, to a lesser extent UC

Cirrhosis, primary biliary cirrhosis

Graves’ disease (thyroid acropachy)

Rare: Whipple’s disease

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44
Q

What is transfer factor?

A

The transfer factor describes the rate at which a gas will diffuse from alveoli into blood. Carbon monoxide is used to test the rate of diffusion. Results may be given as the total gas transfer (TLCO) or that corrected for lung volume (transfer coefficient, KCO)

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45
Q

What are some causes of a raised TLCO?

A

Asthma

Pulmonary haemorrhage (Wegener’s, Goodpasture’s)

Left-to-right cardiac shunts

Polycythaemia

Hyperkinetic states

Male gender, exercise

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46
Q

What are some causes of a decreased TLCO?

A

pulmonary fibrosis

pneumonia

pulmonary emboli

pulmonary oedema

emphysema

anaemia

low cardiac output

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47
Q

How do you manage a primary pneumothorax?

A

If the rim of air is < 2cm and the patient is not short of breath then discharge should be considered
otherwise aspiration should be attempted

If this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted

Patients should be advised to avoid smoking to reduce the risk of further episodes

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48
Q

Some conditions may cause an increased KCO with a normal or reduced TLCO. Name these conditions?

A

Pneumonectomy/lobectomy

Scoliosis/kyphosis

Neuromuscular weakness

Ankylosis of costovertebral joints e.g. ankylosing spondylitis

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49
Q

How do you manage secondary pneumothorax?

A

If the patient is > 50 years old and the rim of air is > 2cm and/or the patient is short of breath then a chest drain should be inserted.

Otherwise aspiration should be attempted if the rim of air is between 1-2cm. If aspiration fails (i.e. pneumothorax is still greater then 1cm) a chest drain should be inserted. All patients should be admitted for at least 24 hours

If the pneumothorax is less the 1cm then the BTS guidelines suggest giving oxygen and admitting for 24 hours

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50
Q

How can you tell if a pleural effusion has a transudative cause of exudative cause?

A

Based on serum protein levels.

Transudative < 30g/L (first try treat the underlying cause before aspirations in transudative)
Exudative >30g/L

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51
Q

What are some causes of transudative pleural effusion?

A

Heart failure (most common transudate cause)

Hypoalbuminaemia (liver disease, nephrotic syndrome, malabsorption)

Hypothyroidism

Meigs’ syndrome

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52
Q

What are some causes of exudative pleural effusion?

A

Infection: pneumonia (most common exudate cause), TB, subphrenic abscess

Connective tissue disease: RA, SLE

Neoplasia: lung cancer, mesothelioma, metastases

Pancreatitis

Pulmonary embolism

Dressler’s syndrome

yellow nail syndrome

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53
Q

What is Meig’s Syndrome?

A

Its a transudative cause of Pleural effusion.

Cardinal signs of Meig’s syndrome: Benign ovarian tumour, ascites, and pleural effusion.

54
Q

What are some signs of Kartagener’s Syndrome?

A

Primary ciliary dyskinesia

Dextrocardia or complete situs inversus

Bronchiectasis

Recurrent sinusitis

Subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)

55
Q

What are some signs of Wegener’s Granulomatosis (Granulomatosis with polyangiitis)?

A

Upper respiratory tract: epistaxis, sinusitis, nasal crusting

Lower respiratory tract: dyspnoea, haemoptysis

Rapidly progressive glomerulonephritis (‘pauci-immune’, 80% of patients)

Saddle-shape nose deformity

Also: vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions

56
Q

What is ARDS?

A

Acute respiratory distress syndrome (ARDS) is caused by the increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli, i.e. non-cardiogenic pulmonary oedema. It is a serious condition that has a mortality of around 40% and is associated with significant morbidity in those who survive.

Pathologically, there is diffuse alveolar damage with hyaline membrane formation

57
Q

What are some causes of ARDS?

A 
Infection: sepsis, Pneumonia
Massive blood transfusion
Trauma
Smoke inhalation
Acute pancreatitis
Cardio-pulmonary bypass
58
Q

What are some clinical features of ARDS?

A

dyspnoea
Elevated respiratory rate
Bilateral lung crackles
Low oxygen saturations

59
Q

How do you manage ARDS?

A

Due to the severity of the condition patients are generally managed in ITU

Oxygenation/ventilation to treat the hypoxaemia

General organ support e.g. vasopressors as needed

Treatment of the underlying cause e.g. antibiotics for sepsis

60
Q

How do you differentiate ARDS from cardiogenic pulmonary oedema?

A

Pulmonary artery wedge pressure. If its raised then its a cardiac cause.

61
Q

What tests should you do before giving oral antibiotic prophylaxis for COPD?

A

Azithromycin

LFTs and an ECG to exclude QT prolongation should also be done as azithromycin can prolong the QT interval

62
Q

How do you classify the severity of COPD?

A 
As long as the ratio is <0.7
Mild: FEV1 >80%
Moderate: FEV1 = 50-79%
Severe: FEV1 = 30-49%
Very severe FEV1 = <30%
63
Q

What are 3 causes of trachea being pushed away from the white out?

A

Pleural effusion
Diaphragmatic hernia
Large thoracic mass

64
Q

What are 3 causes of central trachea when there is a white out?

A

Consolidation
Pulmonary oedema (usually bilateral)
Mesothelioma

65
Q

What are 3 causes of trachea being pulled toward the white out?

A

Pneumonectomy
Complete lung collapse e.g. endobronchial intubation
Pulmonary hypoplasia

66
Q

If you suspect asthma in a patient what should you do?

A

All patients should have spirometry with a bronchodilator reversibility (BDR) test

All patients should have a FeNO test

67
Q

What is the management plan for A1AT deficiency?

A

No smoking

Supportive: bronchodilators, physiotherapy

Intravenous alpha1-antitrypsin protein concentrates

Surgery: lung volume reduction surgery, lung transplantation

68
Q

What is atelectasis and when should you suspect it/ management?

A

Atelectasis is a common postoperative complication in which basal alveolar collapse can lead to respiratory difficulty. It is caused when airways become obstructed by bronchial secretions.

Features
it should be suspected in the presentation of dyspnoea and hypoxaemia around 72 hours postoperatively

Management
chest physiotherapy

69
Q

What are the signs of aspergilloma?

A

Often past history of tuberculosis.
Haemoptysis may be severe
Chest x-ray shows rounded opacity

70
Q

What are the 10 causes of haemoptysis?

A 
Lung Cancer
TB
Pulmonary Oedema
Pulmonary Embolism
Bronchiectasis
LRT infection
Mitral Stenosis
Aspergilloma
Granulomatosis with Polyangiitis
Goodpastures syndrome
71
Q

Dyspnoea

Bibasal crackles and S3 are the most reliable signs

A

Pulmonary Oedema

72
Q

Pleuritic chest pain
Tachycardia, tachypnoea
Possibly hypotension, cyanosis, and signs of right heart strain (such as a raised JVP, parasternal heave, and loud P2).

A

Pulmonary embolism

73
Q

Haemoptysis
Systemically unwell: fever, nausea
Glomerulonephritis

A

Goodpasture’s Syndrome

74
Q

Upper respiratory tract: epistaxis, sinusitis, nasal crusting
Lower respiratory tract: dyspnoea, haemoptysis
Glomerulonephritis
Saddle-shape nose deformity

A

Granulomatosis with Polyangiitis

75
Q

What acid base disturbance do opiate and salicyclate overdose cause?

A

Opiate overdose = Respiratory acidosis

Salicyclate overdose = respiratory alkalosis

76
Q

What is the most common organism isolated from someone with bronchiectasis?

A

Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae

77
Q

When would you do surgery in bronchiectasis?

A

When disease is localised (e.g to one lobe)

78
Q

How do you differentiate primary and secondary pneumothorax?

A

A pneumothorax is termed primary if there is no underlying lung disease and secondary if there is.

79
Q

How do you treat a secondary pneumothorax?

A

If the patient is > 50 years old and the rim of air is > 2cm and/or the patient is short of breath then a chest drain should be inserted.

Otherwise aspiration should be attempted if the rim of air is between 1-2cm. If aspiration fails (i.e. pneumothorax is still greater then 1cm) a chest drain should be inserted. All patients should be admitted for at least 24 hours

If the pneumothorax is less the 1cm then the BTS guidelines suggest giving oxygen and admitting for 24 hours

80
Q

How do you differentiate Lambert Eaton Syndrome and what’s it caused by?

A

Lambert-Eaton myasthenic syndrome is seen in association with small cell lung cancer, and to a lesser extent breast and ovarian cancer.

Repeated muscle contractions lead to increased muscle strength* (in contrast to myasthenia gravis).
Limb girdle weakness (affects lower limbs first)

81
Q

What type of lung cancer can lead to SIADH?

A

Small Cell Lung Cancer

82
Q

What is buproprion and what is its mechanism of action and contraindications?

A

A norepinephrine and dopamine reuptake inhibitor, and nicotinic antagonist used in smoking cessation.

Its contraindicated in pregnancy, epilepsy and breast feeding. Having an eating disorder is a relative contraindication.

83
Q

How does primary TB occur?

A

A non-immune host who is exposed to M. tuberculosis may develop primary infection of the lungs. A small lung lesion known as a Ghon focus develops. The Ghon focus is composed of tubercle-laden macrophages. The combination of a Ghon focus and hilar lymph nodes is known as a Ghon complex

In immunocompotent people the intially lesion usually heals by fibrosis. Those who are immunocompromised may develop disseminated disease (miliary tuberculosis).

84
Q

How does secondary TB occur?

A

If the host becomes immunocompromised the initial infection may become reactivated. Reactivation generally occurs in the apex of the lungs and may spread locally or to more distant sites. Possible causes of immunocomprise include:

Immunosuppressive drugs including steroids
HIV
Malnutrition

85
Q

What are the symptoms of sarcoidosis?

A

Acute: erythema nodosum, bilateral hilar lymphadenopathy, swinging fever, polyarthralgia

Insidious: dyspnoea, non-productive cough, malaise, weight loss

skin: lupus pernio ( chronic raised indurated (hardened) lesion of the skin, often purplish in color)

Hypercalcaemia: macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)

86
Q

What is the first line treatment for sarcoidosis?

A

Steroids

Patients with chest x-ray stage 2 or 3 disease who have moderate to severe or progressive symptoms. Patients with asymptomatic and stable stage 2 or 3 disease who have only mildly abnormal lung function do not require treatment
Hypercalcaemia
Eye, heart or neuro involvement

87
Q

What is the investigation of choice in idiopathic pulmonary fibrosis?

A

High resolution CT scanning

88
Q

What is the main investigations and treatment of extrinsic allergic alveolitis?

A

Chest x-ray: upper/mid-zone fibrosis
Bronchoalveolar lavage: lymphocytosis
Blood: NO eosinophilia

Avoid triggers

89
Q

What are some risk factors for aspiration pneumonia?

A 
Poor dental hygiene
Swallowing difficulties
Prolonged hospitalization or surgical procedures
Impaired consciousness
Impaired mucociliary clearance
90
Q

Management plan in SCLC?

A

However, most patients with limited disease receive a combination of chemotherapy and radiotherapy

Patients with more extensive disease are offered palliative chemotherapy

91
Q

What is a sign that the asthma attack is life threatening from the ABG?

A

Decreasing pH and a normal CO2 (indicates the patient is tiring - usually the CO2 should be dropping)

92
Q

What are the main DDx from bilateral hilar lymphadenopathy?

A 
Sarcoidosis
TB
Fungal infection (histoplasmosis and coccidioidomycosis)
93
Q

What weeks would you expect symptoms of pneumonia to resolve?

A

1 week Fever should have resolved

4 weeks Chest pain and sputum production should have substantially reduced

6 weeks Cough and breathlessness should have substantially reduced

3 months Most symptoms should have resolved but fatigue may still be present

6 months Most people will feel back to normal.

94
Q

What causes SVC syndrome and what are the symptoms?

A

Superior vena cava (SVC) obstruction is an oncological emergency caused by compression of the SVC. It is most commonly associated with lung cancer.

Dyspnoea is the most common symptom
Swelling of the face, neck and arms - conjunctival and periorbital oedema may be seen

Headache: often worse in the mornings
visual disturbance
Pulseless jugular venous distension

95
Q

What causes SVC syndrome and what are the symptoms?

A

Superior vena cava (SVC) obstruction is an oncological emergency caused by compression of the SVC. It is most commonly associated with lung cancer.

Dyspnoea is the most common symptom
Swelling of the face, neck and arms - conjunctival and periorbital oedema may be seen

Headache: often worse in the mornings
visual disturbance
Pulseless jugular venous distension

96
Q

What is Currant jelly sputum a hall mark/ name another condition with same cause?

A

Klebsiella

97
Q

In Acute COPD, what should your aim o2 sats be?

A

Prior to availability of blood gases, use a 28% Venturi mask at 4 l/min and aim for an oxygen saturation of 88-92% for patients with risk factors for hypercapnia but no prior history of respiratory acidosis

Adjust target range to 94-98% if the pCO2 is normal

98
Q

What is the purpose and MoA of Varenicline? What are the contraindications?

A

A nicotinic receptor partial agonist used in smoking cessation.
contraindicated in pregnancy and breast feeding

99
Q

What are the 5 x ray findings you would see in heart failure?

A 
ABCDE
Alveolar oedema (bat’s wings)
Kerley B lines (interstitial oedema)
Cardiomegaly
Dilated prominent upper lobe vessels
Effusion (pleural)
100
Q

A patient has gotten a spontaneous pneumothorax, secondary to marfans syndrome. What are they at risk of developing?

A

Acute aortic dissection

101
Q

Describe the percussion note in COPD?

A

Hyper resonant

102
Q

Coarse crepitations
Clubbing
Haemoptysis

A

Bronchiectasis

103
Q

What leads to consolidation?

A

Lung tissue fills with liquid as a result of an inflammatory response

104
Q

An initial chest x-ray demonstrates diffuse bilateral consolidation, and a sputum culture reveals gram positive cocci in clusters.

A

Staph Aureus

Management:
Treatment involves adding flucloxacillin, or vancomycin/ teicoplanin if you suspect methicillin resistant Staphylococcus aureus (MRSA). Treatment should be for 14-21 days

105
Q

When should you place a chest tube in suspected pleural infection?

A

pH <7.2

Turbid aspirate

106
Q

Whats the criteria to differentiate between transudate and exudate?

A

Light’s Criteria

Exudates have a protein level of >30 g/L, transudates have a protein level of <30 g/L

if the protein level is between 25-35 g/L, Light’s criteria should be applied. An exudate is likely if at least one of the following criteria are met:

  • pleural fluid protein divided by serum protein >0.5
  • pleural fluid LDH divided by serum LDH >0.6
  • pleural fluid LDH more than two-thirds the upper limits of normal serum LDH
107
Q

What are other characteristic pleural fluid findings?

A

low glucose: rheumatoid arthritis, tuberculosis

raised amylase: pancreatitis, oesophageal perforation

heavy blood staining: mesothelioma, pulmonary embolism, tuberculosis

108
Q

What are some paraneoplastic features of squamous cell carcinoma?

A

Parathyroid hormone-related protein (PTH-rp) secretion causing hypercalcaemia

clubbing

hypertrophic pulmonary osteoarthropathy (HPOA)

hyperthyroidism due to ectopic TSH

109
Q

What are some paraneoplastic features of adenocarcinoma?

A

gynaecomastia

hypertrophic pulmonary osteoarthropathy (HPOA)

110
Q

What are some paraneoplastic features of small cell carcinoma?

A

ADH

ACTH - not typical, hypertension, hyperglycaemia, hypokalaemia, alkalosis and muscle weakness are more common than buffalo hump etc

Lambert-Eaton syndrome

111
Q

What is the classic presentation of pneumonia from S. pneumoniae?

A

Accounts for 80% of cases
Particularly associated with high fever, rapid onset and herpes labialis (blisters on the lower lip)
A vaccine to pneumococcus is available

112
Q

What is the classic presentation of pneumonia from S. aureus?

A

Often occurs in patient following influenza infection

113
Q

What is the classic presentation of pneumonia from H. influenzae?

A

Common in COPD patients

114
Q

What is the classic presentation of pneumonia from Mycoplasma pneumoniae?

A

One of the atypical pneumonias, which often present a dry cough and atypical chest signs/x-ray findings
Autoimmune haemolytic anaemia (cold) and erythema multiforme (round lesions with a bullseye appearance) may be seen

115
Q

What is the classic presentation of pneumonia from L. pneumophilia?

A

Another one of the atypical pneumonias
Hyponatraemia and lymphopenia common
Classically seen secondary to infected air conditioning units

116
Q

What is the classic presentation of pneumonia from klebsiella pneumoniae?

A

Atypical

Alcoholics

117
Q

What is the classic presentation of pneumonia from pneumocystitis jiroveci?

A

Typically seen in patients with HIV

Presents with a dry cough, exercise-induced desaturations and the absence of chest signs

118
Q

If there is clear evidence that the cause of a pleural effusion is heart failure, what is the investigation of choice?

A

Transthoracic Echocardiogram

119
Q

What are the primary investigations in sarcoidosis?

A

CXR
Serum ACE
High Ca

Non Caseating granulomas

120
Q

How does V/Q ratio change in COPD?

A

Emphysema refers to damage to the alveolar walls, enlarging the alveolar air spaces and destroying the capillary beds. Thus blood flow is impaired but ventilation may be relatively maintained, causing a higher V/Q ratio.

Chronic bronchitis refers to chronic airway inflammation and mucus production. This leads to a lower V/Q ratio, as the narrow airways leads to a drop in ventilation. This as such will lead to less oxygen in the alveoli, so less oxygen can transfer to the blood causing hypoxia.

121
Q

How do you treat heart failure?

A

First-line treatment for all patients is both an ACE-inhibitor and a beta-blocker*. Generally, one drug should be started at a time

Second-line treatment is now either an aldosterone antagonist, angiotensin II receptor blocker or a hydralazine in combination with a nitrate

If symptoms persist cardiac resynchronisation therapy or digoxin** should be considered. An alternative supported by NICE in 2012 is ivabradine. The criteria for ivabradine include that the patient is already on suitable therapy (ACE-inhibitor, beta-blocker + aldosterone antagonist), has a heart rate > 75/min and a left ventricular fraction < 35%

Diuretics should be given for fluid overload
Offer annual influenza vaccine
Offer one-off*** pneumococcal vaccine

122
Q

Whats the most common cause of HAP and how is it treated?

A

Mechanical ventilators
P. aerigunosa

Ciprofloxacin (same bio-activity when given orally or IV)
Gentamicin
Ceftazidime
Pipercillin-tazobactam
Meropenem
123
Q

What tests should you do when you suspect SLE in context of pleural effusion?

A

Anti-nuclear antibody (ANA) is useful if systemic lupus erythematosus (SLE) is suspected.

Complement is typically low in pleural effusions caused by rheumatoid arthritis or SLE.

124
Q

What is the scoring system for a pulmonary embolism?

A

Wells scoring system

Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3

An alternative diagnosis is less likely than PE 3

Heart rate > 100 beats per minute 1.5

Immobilisation for more than 3 days or surgery in the previous 4 weeks 1.5

Previous DVT/PE 1.5

Haemoptysis 1

Malignancy (on treatment, treated in the last 6 months, or palliative) 1

If the score is more than 4 - PE likely
If less than or equal to 4 its unlikely

125
Q

How do you decide investigations based on Wells Score?

A

If a PE is ‘likely’ (more than 4 points) arrange an immediate computed tomography pulmonary angiogram (CTPA). If there is a delay in getting the CTPA then give low-molecular-weight heparin until the scan is performed.

If a PE is ‘unlikely’ (4 points or less) arranged a D-dimer test. If this is positive arrange an immediate computed tomography pulmonary angiogram (CTPA). If there is a delay in getting the CTPA then give low-molecular-weight heparin until the scan is performed.

126
Q

In obstructive lung disease, where in the respiratory system is there greatest resistance to outflow?

A

Medium sized bronchi

127
Q

What are symptoms of a carcinoid tumour and what are the investigations?

A

flushing (often earliest symptom)
diarrhoea
bronchospasm
hypotension

Urinary 5-HIAA

128
Q

What is the management for SVC obstruction syndrome?

A

general: dexamethasone, balloon venoplasty, stenting
small cell: chemotherapy + radiotherapy
non-small cell: radiotherapy

129
Q

How do you diagnose pneumocystitis pneumonia and treat it?

A

Diagnosis can be aided by chest X-ray that may demonstrate bilateral perihilar interstitial shadowing (ground-glass appearance or be normal). Definitive diagnosis is confirmed by histological identification of pneumocystis jiroveci in sputum, bronchoalveolar lavage or lung biopsy. Staining with silver stain, toluidine blue, periodic acid Schiff stain or immunofluorescence will show the cysts.

Treatment is with cotrimoxazole or pentamidine for 21 days. Steroids can be added to treatment regimens for patients with severe hypoxaemia.

130
Q

What is the first line treatment for NSCLC?

A

Lobectomy

131
Q

How do you find mortality from the CURB-65 score?

A 
0 – 0.7%
1 – 3.2%
2 - 13%
3 - 17%
4 - 41.5%
5 - 57%

Y3 Hard Qs (8 decks)

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