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Phase 2a > Resp > Flashcards

Resp Flashcards

1
Q

What is COPD?

A

A common progressive disorder characterised by airway obstruction with little or no reversibility

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2
Q

What is chronic bronchitis?

A

Cough and sputum production on most days for 3 months of 2 successive years, improves with smoking cessation

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3
Q

What is emphysema?

A

Enlarged air spaces distal to terminal bronchioles, with destruction of alveolar walls

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4
Q

Epidemiology of COPD

A

Male, >35yrs

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5
Q

Risk factors for COPD

A

Smoking, occupational dust and chemicals, environmental tobacco smoke (ETS), indoor and outdoor air pollution, genes, infection, socio-economic status

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6
Q

Pathophysiology of chronic bronchitis

A

o Blue bloaters
o Bronchial wall inflammation and mucosal oedema ->
airways narrow -> body increases perfusion (CO) ->
V/Q mismatch -> hypoxia (blue)
o Obstruction -> increasing residual lung volume ->
bloating

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7
Q

Pathophysiology of emphysema

A

o Pink puffers
o Destruction of lung tissue distal to terminal
bronchioles -> loss of elastic recoil -> air trapping
o Damage to capillary bed -> inability to oxygenate ->
hyperventilation (puffing)

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8
Q

Signs of COPD

A

o Raised respiratory rate
o Hyperexpansion/barrel chest
o Cyanosis
o ‘Cor pulmonae’ – HF, oedema

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9
Q

Symptoms of COPD

A

o SOB
o Cough, phlegm
o Wheeze
o Weight loss

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10
Q

Investigations for suspected COPD

A

• Lung function tests – reduced FEV1/FVC, reduced
PEFR, raised TLC, obstructive pattern
• FBC – PCV increased
• CXR – hyperinflation, flat hemidiaphragms, large
central pulmonary arteries
• ECG – RA and RV hypertrophy
• ABG – PaO2 decreased ± hypercapnia
• CT – emphysema

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11
Q

Differentials for COPD

A

Pneumonia, heart failure, pulmonary embolus, lung cancer, asthma

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12
Q

Lifestyle management of COPD

A

Smoking cessation, regular physical activity encouraged

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13
Q

1st line drug treament for COPD

A

SABA/SAMA

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14
Q

2nd line drug treatment for COPD

A

LABA/LAMA

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15
Q

3rd line drug treatment for COPD

A

LABA/LAMA + corticosteroid

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16
Q

4th line drug treatment for COPD

A

LABA + LAMA + corticosteroid

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17
Q

5th line drug treatment for COPD

A

Long term oxygen therapy -> sats of 88-92%

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18
Q

Surgical management of COPD

A

Lung transplant if drugs insufficient

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19
Q

What is asthma?

A

Reversible obstruction of the airways, bronchospasm and excessive airway secretions, usually a hypersensitivity type 1 reaction

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20
Q

What is extrinsic asthma?

A

Asthma triggered by an allergen (dust, foods, animals, pollens) type 1 hypersensitivity, IgE mediated

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21
Q

What type of hypersensitivity is occupational asthma?

A

Type 1

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22
Q

What is intrinsic asthma?

A

Not immune-mediated, non-allergic, triggered by; cold, infection, stress, exercise, SO2, pollutants etc.

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23
Q

What are the 3 factors that contribute to airways narrowing in asthma?

A

o Bronchial muscle contraction
o Mucosal swelling/inflammation
o Increased mucus production

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24
Q

What causes mucosal swelling/inflammation in asthma?

A

Mast cell and basophil degranulation -> release of leukotrienes and prostaglandins

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25
Q

What are the two main phenotypes of asthma?

A

Eosinophillic and non-eosinophillic

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26
Q

Features of asthma

A

• Episodic cough, breathlessness
• Diurnal variation – worse at night
• Provoking factors – allergens, infections, menstrual
cycle, exercise, cold air, laughter/emotion
• Other atopic disease – eczema, hayfever

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27
Q

Signs of asthma

A
  • Tachypnoea
  • Audible wheeze
  • Hyperinflated chest
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28
Q

Investigations for suspected asthma

A
  • Spirometry – FEV1/FVC <70% + reversibility testing
  • PEF- keep diary
  • Sputum and blood culture, ABG, CXR
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29
Q

Differentials for asthma

A

Pulmonary oedema, COPD, tumour

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30
Q

Step 1 drug treament for asthma

A

SABA (salbutamol) PRN – max once daily

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31
Q

Step 2 drug treament for asthma

A

+ inhaled corticosteroid (beclomethasone) once daily

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32
Q

Step 3 drug treatment for asthma

A

+ leukotriene receptor antagonist (LTRA)

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33
Q

Step 4 drug treatment for asthma

A

+ LABA (salmeterol inhaler 12 hourly) ± LTRA

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34
Q

Step 5 drug treatment for asthma

A

+ oral prednisolone

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35
Q

Epidemiology of lung cancer

A
  • M:F, 2:1

* 1/3 of all cancer deaths

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36
Q

Causes of lung cancer

A
  • Cigarettes
  • Occupational – asbestos etc.
  • Lung fibrosis
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37
Q

Signs and symptoms of lung cancer

A
  • Cough
  • Recurrent chest infections
  • Haemoptysis
  • Increasing SOB
  • Extra-pulmonary changes
  • Malaise
  • Weight loss
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38
Q

Investigations for suspected lung cancer

A

o Sputum sample
o BAL
o Biopsy
o Lobectomy, wedge, pneumonectomy

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39
Q

What is the most common type of lung cancer?

A

Non-small cell lung carcinoma

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40
Q

What is the main treatment for small cell lung carcinoma?

A

Chemotherapy

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41
Q

At what stage does lung cancer usually present?

A

Late stage, metastases

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42
Q

What are the main treatments used for non-small cell lung carcinoma?

A

Radiotherapy and surgery

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43
Q

Symptoms of pulmonary embolism

A

Breathlessness, pleuritic chest pain, DVT signs/symptoms, RF’s

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44
Q

Risk factors for pulmonary embolism

A
  • Surgery, immobility
  • OC pill, HRT, Pregnancy
  • Long haul flights/ travel (rare)
  • Inherited thrombophilia - genetic predisposition
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45
Q

Signs of pulmonary embolism

A

Tachycardia, tachypnoea, pleural rub, none of alternative diagnosis

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46
Q

Investigations for suspected pulmonary embolism

A 
o	CXR usually normal
o	ECG – sinus tachycardia
o	Blood gases – type 1 respiratory failure
o	D-dimer 
o	CTPA spiral CT with contrast
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47
Q

Management of PE

A
  • LMW Heparin for min 5 days

* Oral warfarin (INR 2-3) for 6 months

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48
Q

Prevention of PE

A

Compression stockings, hydration and early mobilisation

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49
Q

Causes of adult respiratory distress syndrome (ARDS)

A

Shock, trauma, infections, gas inhalation (NO2 etc.), narcotic abuse

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50
Q

Pathology of ARDS

A

Lung damage and release of inflammatory mediators -> increased capillary permeability -> non-cardiogenic pulmonary oedema, alveolar infiltrate + hyaline membranes -> multiorgan failure

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51
Q

Signs and symptoms of ARDS

A

Acute onset, SOB, tachypnoea, tachycardia, peripheral vasodilation, bilateral inspiratory crackles, hypoxaemia -> cyanosis

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52
Q

Investigations for suspected ARDS

A

o Bloods – FBC, U&E, LFT, CRP, cultures, ABG
o CXR – bilateral pulmonary infiltrates
o Pulmonary artery catheter – measure pulmonary capillary wedge pressure <19mmHg

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53
Q

Management of ARDS

A

Admit to ITU, supportive therapy, treat underlying cause

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54
Q

What is fibrosing alveolitis (Idiopathic Pulmonary Fibrosis)?

A

Fibrosis of lung interstitium causing restrictive respiratory defect, cause unknown

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55
Q

Symptoms of pulmonary fibrosis

A

Breathlessness, respiratory failure -> cor pulmonae

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56
Q

Signs of pulmonary fibrosis

A

Finger clubbing, inspiratory basal crackles

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57
Q

Investigations for suspected pulmonary fibrosis

A

o CXR – ground glass -> honeycomb lung
o HRCT – most sensitive
o ABG – hypoxia
o Spirometry – FEV1/FVC ratio normal, FVC low

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58
Q

Management of pulmonary fibrosis

A

o Prednisolone

o Lung transplant

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59
Q

What is sarcoidosis?

A

Autoimmune granulomatous disease, wide-spread but mainly affecting the lungs

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60
Q

Epidemiology of sarcodosis

A

young Afro-American women

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61
Q

Cause of sarcoidosis

A

Mostly unknown, genetic link, autoimmune

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62
Q

Signs and symptoms of sarcoidosis

A

o General – fever, weight loss, fatigue
o Pulmonary – dry cough, dyspnoea
o Other – lymphadenopathy, hepatosplenomegaly,
conjunctivitis, glaucoma, erythema nodosum etc.

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63
Q

Investigations for suspected sarcoidosis

A

o CXR – bilateral hilar lymphadenopathy
o Bloods – high ESR, high ACE, high calcium
o Lung function tests – normal or restrictive
o Tissue biopsy – diagnostic
o Kveim test

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64
Q

Management of sarcoidosis

A

o Minimal symptoms – resolve spontaneously within
few weeks, remission in few years
o Severe symptoms – prednisolone
o Lung transplantation

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65
Q

What is bronchiectasis?

A

Permanent dilatation of bronchi and bronchioles due to obstruction or severe inflammation

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66
Q

Pathophysiology of bronchiectasis

A
  • Chronic inflammation of airways -> irreversible damage -> bronchioles scarred + dilated, cilia lost
  • Permanent dilatation impairs muco-ciliary clearance -> mucus builds up
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67
Q

Causes of bronchiectasis

A
  • Post-infection – H. influenzae, Strep. Pneumoniae
  • Congenital – CF, primary ciliary dyskinesia
  • Bronchial obstruction
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68
Q

Symptoms of bronchiectasis

A
  • Persistent cough with foul-smelling sputum
  • Haemoptysis
  • Dyspnoea
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69
Q

Signs of bronchiectasis

A
  • Finger clubbing
  • Inspiratory crepitations
  • Wheeze
70
Q

Investigations for suspected bronchiectasis

A
  • Sputum culture
  • CXR/CT – cystic shadows, thickened bronchial walls
  • Spirometry – obstructive pattern
  • Bronchoscopy
71
Q

Management of bronchiectasis

A
  • Airway clearance techniques and mucolytics
  • Antibiotics
  • Bronchodilators if asthma, COPD, CF
  • Corticosteroids if ABPA
72
Q

Cause of cystic fibrosis

A

Autosomal recessive inheritance – mutations in the CFTR gene on chromosome 7

73
Q

Epidemiology of cystic fibrosis

A

More common in Causcasians

74
Q

Pathology of cystic fibrosis

A

Mutated CFTR gene -> misfolded protein can’t migrate from endoplasmic reticulum to cell membrane -> lack of CFTR protein on epithelial surface -> can’t pump chloride ions out -> water not drawn in -> thick secretions

75
Q

CF signs and symptoms in a newborn

A

Meconium ileus, failure to thrive

76
Q

Signs and symptoms of CF in children and young adults

A

o Pancreatic – blocked pancreatic ducts:
- protein and fat malabsorption -> failure to gain
weight and thrive
- frequent pancreatitis -> fibrosis
- DM
o Respiratory:
- thick mucus -> defective mucociliary action ->
infection -> CF exacerbation (cough and fever, CXR
changes)
- bronchiectasis
- repeated exacerbations -> respiratory failure
o Other:
- infertility in males – lack vas deferens
- digital clubbing
- nasal polyps

77
Q

Investigations for cystic fibrosis

A
  • Newborn screening – detects IRT, present in CF
  • Sweat test – high Cl- >60mmol/L
  • Genetic testing
78
Q

Management of cystic fibrosis

A 
•   Fat soluble vitamins (ADEK), replacement pancreatic enzymes 
•   Pulmonary treatment:
    o  Chest physiotherapy
    o	Inhalers (bronchodilators)
    o	Mucolytics – Dornase alfa
    o	Lung function tests + annual CXR
    o	Lung transplant
79
Q

What is a pneumothorax?

A

Air in the pleural space between the lungs and chest wall, causing collapse of the lung

80
Q

Causes of pneumothorax

A
  • Often spontaneous (young, thin men)
  • Chronic lung disease – asthma, COPD, CF
  • Infection – TB pneumonia
  • Trauma
  • Carcinoma
  • Connective tissue disorders – Ehlers-Danlos
81
Q

Symptoms of pneumothorax

A
  • May be asymptomatic

* Sudden onset dyspnoea ± pleuritic chest pain

82
Q

Signs of pneumothroax

A
  • Reduced expansion
  • Hyper-resonance to percussion
  • Diminished breath sounds
  • Tracheal deviation if tension pneumothorax
83
Q

Investigations for suspected pneumothorax

A
  • CXR – area devoid of lung markings

* ABG

84
Q

Management of pneumothorax

A 
•   Primary – SOB or >2cm on CXR -> aspiration -> 
    chest drain if unresolved 
•   Secondary:
    o	<1cm – observe 24hrs
    o	1-2cm – aspirate
    o	>2cm/SOB – chest drain
85
Q

What is a tension pneumothorax?

A

Tension pneumothorax – air drawn into pleural space with each inspiration has no route of escape during expiration

86
Q

What is a pleural effusion?

A

A collection of excess fluid in the pleural space, can restrict lung expansion

87
Q

Pathophysiology of transudative pleural effusion

A

Too much fluid leaves capillaries due to increased hydrostatic pressure or decreased oncotic pressure

88
Q

Causes of transudative pleural effusion

A

Heart failure (-> PAH), cirrhosis, nephrotic syndrome

89
Q

Pathophysiology of exudative plerual effusion

A

Inflammation of pulmonary capillaries -> leakier

90
Q

Causes of exudative pleural effusion

A

Trauma, malignacy, lupus, infection

91
Q

Symptoms of pleural effusion

A
  • Pleurisy – pain on inhaling

* Dysnoea

92
Q

Signs of pleural effusion

A
  • Decreased breath sounds
  • Dullness to percussion
  • Decreased tactile fremitus
93
Q

Investigations for suspected pleural effusion

A

• CXR – decreased aeration, tracheal deviation,
blurred costophrenic angle
• Chest examination
• Thoracentesis – remove fluid and find out cause y

94
Q

How is a thoracentesis analysed/interpreted?

A

Light criteria:
o Transudate – clear, <25g//L protein
o Exudate – cloudy, >35g/L
o Lymphatic/empyema – milky

95
Q

Management of pleural effusion

A
  • Drain if symptomatic
  • Pleurodesis with talc if recurrent
  • Surgery
96
Q

What is pulmonary hypertension?

A

Chronic high blood pressure in pulmonary circulation, mean pulmonary arterial pressure >25mmHg

97
Q

Causes of pulmonary hypertension

A

• Left heart disease – HF, valve dysfunction
• Chronic lung disease – emphysema
• PAH – congenital heart defects, connective tissue
disorders, infections

98
Q

How does left heart disease lead to pulmonary hypertension?

A

Left side of heart unable to pump efficiently -> backup of blood in pulmonary circulation -> increased pressure in pulmonary arteries

99
Q

How does chronic lung disease, such as emphysema, lead to pulmonary hypertension?

A

o Diseased area in lung -> unable to deliver oxygen to blood -> pulmonary arterioles constrict -> blood shuttled away from damaged areas
o If widespread -> overall increase in pulmonary vascular resistance -> right side of heart must generate increased pressure -> pulmonary hypertension

100
Q

Signs and symptoms of pulmonary hypertension

A

• SOB – can be worse when lying flat
• Pulmonary oedema
• Right ventricular hypertrophy -> right heart failure ->
ankle swelling, hepatomegaly

101
Q

Investigations for suspected pulmonary hypertension

A

• Echocardiogram – increased pressure in right-
ventricle and pulmonary arteries
• Spirometry – underlying lung disease

102
Q

Management of pulmonary hypertension

A
  • Supplemental oxygen

* Treat underlying cause

103
Q

What are the fours types of occupational lung disease? Give and example of each

A

o Inert: coal worker’s pneumoconiosis
o Fibrous: progressive massive fibrosis
o Allergic: extrinsic allergic alveolitis
o Neoplastic: mesothelioma, lung cancer

104
Q

What cells are damaged by coal dust?

A

Alveolar macrophages

105
Q

Presentation of coal workers pneumoconiosis

A

o Progressive massive fibrosis (PMF)
o Emphysema
o Honeycomb lung and/or cor pulmonale

106
Q

Features of silicosis

A
  • Tissue destruction and fibrosis
  • Nodules are formed after many years of exposure
  • Interstitial fibrosis
  • Raised incidence of TB
107
Q

What lung conditions can asbestos cause?

A

Diffuse pulmonary fibrosis (asbestosis), diffuse pleural fibrosis, persistent pleural effusion, plaque, lung cancer, mesothelioma

108
Q

Give 2 causes of extrinsic allergic alveolitis

A

Bird fancier’s lung (protein in bird droppings), Farmer’s lung (fungus from mouldy hay)

109
Q

Pathophysiology of extrinsic allergic alveolitis

A

Type 3 hypersensitivity -> bronchiolitis -> chronic inflammation and granulomas -> resolve or lead to fibrosis

110
Q

Signs and symptoms of extrinsic allergic alveolitis

A

Dry cough, dyspnoea, weight loss, finger clubbing, type 1 resp failure, cor pulmonale

111
Q

Investigations for suspected extrinsic allergic alveolitis

A

o Bloods – ABG, antibodies, FBC, high ESR
o CXR – upper mottling/consolidation -> honeycomb
o CT – fibrosis, nodules
o Lung function tests – restrictive

112
Q

Management of extrinsic allergic alveolitis

A

o Allergen avoidance, or face mask

o Prednisolone

113
Q

What is Goodpasture’s syndrome?

A

An autoimmune disease characterised by kidney and lung symptoms

114
Q

Risk factors for Goodpasture’s syndrome

A

HLA-DR15 genes, infections, smoking, oxidative stress, hydrocarbon-based solvents

115
Q

Pathophysiology of Goodpasture’s syndrome

A

Autoantibodies attack collagen (most abundant in kidneys and lungs) – type II hypersensitivity

116
Q

Signs and symptoms of Goodpasture’s syndrome

A

• Respiratory (first) – haemoptysis, cough, restrictive
lung disease
• Kidneys – haematuria, proteinuria, nephritic
syndrome

117
Q

Investigations for suspected Goodpasture’s syndrome

A
  • CXR – infiltrates due to pulmonary haemorrhage

* Kidney biopsy – crescentic glomerulonephritis

118
Q

Management of Goodpasture’s syndrome

A

Vigorous immunosuppressive treatment and plasmapheresis

119
Q

What is mesothelioma?

A

A tumour of mesothelial cells that usually occurs in the pleura, rarely in peritoneum

120
Q

What is the main cause of mesothelioma?

A

Asbestos exposure

121
Q

Signs and symptoms of mesothelioma

A
  • Chest pain
  • Dyspnoea
  • Weight loss
  • Digital clubbing
  • Recurrent pleural effusions
122
Q

Investigations for suspected mesothelioma

A
  • CXR/CT – pleural thickening/effusion
  • Pleural fluid – bloody
  • Thoroscopy – histology diagnostic (post-mortem)
123
Q

Management of mesothelioma

A
  • Chemotherapy
  • Surgery and radiotherapy controversial
  • Pleural drainage
  • Incurable
124
Q

Risk factors for TB

A

Born in high prevalence area, IVDU, homeless, alcoholic, prisons, HIV+

125
Q

How us TB usually spread?

A

Aerosol

126
Q

What culture plate is used to culture mycobacterium tuberculosis?

A

Lowenstein-Jensen culture pate

127
Q

What stain is used to detect acid-fast mycobacterium?

A

Ziehl-Neelson stain

128
Q

Pathology of TB

A

o >95% have no disease – immune system kills
majority of infecting bacilli
o 2-5% develop primary pulmonary disease:
- Bacilli taken into lymphatics to hilar lymph nodes ->
enlarge
- Bacilli + macrophages form granuloma -> grows into
cavity in apex of lung -> cavity full of TB bacilli,
expelled when patient coughs

129
Q

Why do granulomas usually form in the apex of the lung?

A

More air/less blood and immune cells

130
Q

Signs and symptoms of TB

A

o Systemic - Weight loss, low grade fever, anorexia,
night sweats, malaise
o Pulmonary TB - cough >3 weeks, chest pain,
breathlessness, haemoptysis

131
Q

Investigations for suspected TB

A

o CXR – fibronodular/linear opacities
o 3x sputum - gold standard
o Urine, CSF, pleural fluid, biopsy specimen

132
Q

What test can be used to detect latent TB?

A

Tuberculin skin test ‘Mantoux’, Interferon-gamma release assays (IGRAS)

133
Q

What are the four drugs used to treat TB?

A

Rifampicin
Isoniazid
Pyrazinamide
Ethambutol

134
Q

Give a side effect of rifampicin

A

Orange urine/tears/sweat

135
Q

Give 2 side effects of isoniazid

A

Neuropathy, hepatitis

136
Q

Give 2 side effects of pyrazinamide

A

Arthralgia, hepatitis

137
Q

Give a side effect of ethambutol

A

Eyes - optic neuritis

138
Q

What causes seasonal flu epidemics?

A

Antigenic drift, usually influenza A

139
Q

What causes a flu pandemic?

A

Antigenic shift

140
Q

How is influenza spread?

A

Aerosol (coughs and sneezes), hand-to-hand contact

141
Q

What is the incubation period for influenza?

A

1-3 days

142
Q

Symptoms of influenza

A

Upper and/or lower respiratory tract symptoms, fever, headache, myalgia and weakness

143
Q

Management of influenza

A

o Supportive care – oxygenation, hydration/nutrition,
prevent/treat secondary infections, paracetamol
o Tamiflu if high risk
o Prevention – annual vaccine in UK

144
Q

Give 4 common pathogens that cause pneumonia

A

Strep. Pneumoniae, Haemophilus Influenza, Staph Aureus, Klebsiella Pneumoniae

145
Q

Give 2 pathogens that cause hospital acquired pneumonia

A

Chlamydia, Legionella

146
Q

Pathology of pneumonia

A

Bacteria colonise in lungs -> inflammation

147
Q

Symptoms of pneumonia

A

o Fever, sweats, rigors
o Cough, SOB, sputum
o Pleuritic chest pain (pain worse on deep breathing)
o Weakness, malaise

148
Q

What does rusty coloured sputum suggest?

A

Strep. pneumoniae infection

149
Q

Signs of pneumonia

A

o Raised respiratory and heart rates, low BP, fever,
dehydration
o Dull to percussion (consolidation), bronchial breath
sounds, crackles ± wheeze

150
Q

Investigations for suspected pneumonia

A

o Chest X-ray – consolidation
o Bloods – FBC, WCC, U&E, LFTs, CRP
o Sputum, blood cultures
o Urinary antigen test (Legionella’s = ELISA)

151
Q

How is pneumonia severity assessed?

A 
CURB65 – 3+ hospitalise, 2 short stay and monitor closely:
     o   Confusion 
     o   Urea (>7)
     o   Respiratory rate (>30)
     o   Blood pressure (>90/60)
     o   >65
152
Q

What antibiotics would you give to treat a H. Influenzae infection?

A

Amoxicillin

153
Q

What antibiotics would you give to treat a Stap, Aureus infection?

A

Flucloxacillin

154
Q

What antibiotics would you give to treat a Klebsiella Pneumoniae infection?

A

CO-amoxiclav

155
Q

What antibiotics would you give to treat a Legionella infection?

A

Clarithromycin

156
Q

What is the criteria used to determine the likelihood of a sore throat having a bacterial cause?

A 
Centor Criteria:
    o	Tonsillar exudate 
    o	Tender anterior cervical adenopathy 
    o	Fever >38⁰C
    o	No cough
157
Q

Give 3 common causes of bronchitis

A

Viral - adenovirus, rhinovirus, parainfluenzae

158
Q

Clinical features of bronchitis

A

o Cough, productive or non-productive, > 5 days

o SOB +/- wheeze, no signs of focal consolidation

159
Q

Causes of pharyngitis

A

Viral - adenovirus, rhinovirus

Bacterial - Strep. pyogenes

160
Q

What antibiotics would you give for a Strep. Pyogenes infection?

A

Amoxicillin

161
Q

Causes of sinusitis

A

o Usually viral – rhinovirus

o Less bacterial – strep. pneumoniae, H influenzae

162
Q

Cause of epiglottitis

A

Haemophilus influenzae type B (HIB)

163
Q

Presentation of epiglottitis

A

• Children 2-4 years old with fever, dysphagia,
drooling and stridor
• Thumb sign on XR

164
Q

What organism causes whooping cough

A

Bordetella pertussis

165
Q

What antibiotics would you give for a Bordetella pertussis infection?

A

Clarithromycin

166
Q

What is the incubation period of Bordetella pertussis?

A

7-10 days

167
Q

What are the 4 clinical features of whooping cough?

A

o Coughing spasms
o Inspiratory ‘whoop’
o Post-ptussive vomiting
o Cough >14 days

168
Q

Cause of Croup

A

Parainfluenza virus

169
Q

What blood test would you do to test for Goodpastures?

A

Anti-GBM

170
Q

What is the most common type of non-small cell carcinoma?

A

Adenocarcinoma

171
Q

Give 2 features of pulmonary hypertension on x-ray

A

o Enlargemeed pulmonary arteries

o Enlarged right atrium,

Phase 2a (9 decks)

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