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Phase 2a > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is COPD?

A

Non-reversible, long-term deterioration in air flow through the lungs caused by damage to lung tissue.

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2
Q

Explain the pathophysiology of COPD.

A

Damage to lung tissue causes air flow obstruction, making it difficult to ventilate the airways and making them more prone to developing infections.

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3
Q

What are the types of COPD?

A

Chronic bronchitis and emphysema.
-Also A1AT deficiency.

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4
Q

Explain the dyspnoea scale.

A

1 - Breathless of strenuous exercise.
2 - Breathless walking up hill.
3 - Breathless on flat land.
4 - Stop to catch breath after walking 100m on flat land.
5 - Unable to leave house due to breathlessness.

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5
Q

What are two risk factors for COPD?

A

Smoking and air pollution.

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6
Q

Describe the pathophysiology of chronic bronchitis.

A

Hypertrophy and hyperplasia of mucous glands, chronic inflammation cells infiltrate bronchi.

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7
Q

Describe the pathophysiology of emphysema.

A

Destruction of elastin layers in ducts, alveoli and respiratory bronchioles.
-Air is trapped distal to blockage, causing bullae.

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8
Q

Describe the pathophysiology of A1AT deficiency.

A

Autosomal dominant inheritance - no smoking history.
-A1AT usually degrades NE which protects elastin, no A1AT means no NE is active and elastin is damaged.

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9
Q

How does COPD present?

A

Older patient with chronic productive cough (sputum) and SOB.
-Wheezing and recurrent respiratory infections.

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10
Q

Which investigations are used for COPD? What are the results?

A

Spirometry - Obstructive (FEV1/FVC < 0.7).
Test for reversibility with b2 agonists:
-Large response - Asthma.
-Small/no response - COPD.
CXR and TLCO.

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11
Q

What is the long term management of COPD? (3 lines).

A

Smoking cessation and flu/pneumonia vaccines.
1st line - SAB2A (salbutamol) or SAMA (ipratropium bromide).
2nd line - SAB2A, LAB2A and LAM3A.
3rd line - SAB2A, LAB2A, LAM3A, ICS.

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12
Q

How is severe COPD managed?

A

Long term oxygen therapy.

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13
Q

What usually causes exacerbation of COPD?

A

Viral or bacterial infections.

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14
Q

How is COPD exacerbation managed at home?

A

Prednisolone, inhalers/nebulisers and antibiotics if evidence of infection.

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15
Q

How is COPD exacerbation managed in hospital?

A

Nebulised bronchodilators, steroids, antibiotics and ventilation.

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16
Q

What is asthma?

A

Chronic inflammatory condition of the airways that causes episodic exacerbations of bronchoconstriction.

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17
Q

Explain the pathophysiology of asthma.

A

Reversible airway obstruction that typically responds to bronchodilators (salbutamol).
-Bronchoconstriction causes an obstruction of airflow in the lungs.

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18
Q

What is the atopic triad?

A

Atopic rhinitis, asthma and eczema.

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19
Q

What are four risk factors for asthma?

A

History of atopy, low birth weight, not breastfed and exposure to allergens.

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20
Q

What are the types of asthma?

A

Allergic and non-allergic.

-Allergic - IgE mediated T1 hypersensitivity due to environmental trigger.
-Non-allergic - Non IgE mediated, usually due to smoking.

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21
Q

What are eight triggers for asthma?

A

Infections, early night/late night, exercise, animals, cold, dust, strong emotions and drugs (beta-blockers).

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22
Q

How does asthma typically present?

A

Episodic symptoms of dry cough, wheeze (bilateral widespread polyphonic) and SOB that is usually worse at night.
-Young patient with history and family history of atopy.

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23
Q

What are the investigations for asthma?

A

FeNO - Increased conc, in breath means inflammation.
Spirometry with bronchodilator reversibility.
Reduced FEV1, normal FVC. FEV1/FVC < 0.7.

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24
Q

What is the acute management of asthma?

A

Oxygen. salbutamol, ipratropium bromide, IV hydrocortisone, IV MgSO4.

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25
Q

Describe the long term management of asthma. (5 lines).

A

1st line - SAB2A.
2nd line - SAB2A and ICS.
3rd line - SAB2A, ICS and LTRA.
4th line - SAB2A, ICS, LTRA and LAB2A.
5th line - Increase ICS dose.

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26
Q

Explain the drugs used in asthma.

A

-SAB2A - Short acting beta-2 agonists (salbutamol): Used as a reliever - cause bronchodilation.
-ICS - Inhaled corticosteroids (beclomethasone): Reduce inflammation in airways - preventer.
-LTRA - Leukotriene receptor antagonists (montelukast): Block leukotrienes which cause inflammation and bronchoconstriction.
-LAB2A - Long acting beta-2 agonists (salmeterol): Same as SAB2As but longer action.
-LAMA -long acting antimuscarinics (tiotropium): Block Ach receptors - bronchodilation.

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27
Q

What is pneumonia?

A

Infection of the lung tissue which causes inflammation and sputum which fill the airways and alveoli.

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28
Q

How does pneumonia appear on XRAY?

A

Consolidation.

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29
Q

How is pneumonia classified?

A

Community (CAP) - Outside of hospital.
Hospital (HAP) - 48h after hospital admission.
Aspiration - As a result of aspirating foreign material like food.

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30
Q

What are five risk factors for developing pneumonia?

A

Immunocompromised, IVDU, pre-existing respiratory disease, very young/old.

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31
Q

What is the cause of pneumonia?

A

Typically can bacterial but can also be viral and fungal.
-Flu virus.
-PCP - P, jirovecci (aids defining illness).

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32
Q

What are the organisms that cause CAP? What is the most common? Which are atypical?

A

S. pnuemoniae (mc), H. influenzae.
-Mycoplasma pnuemoniae and legionella - atypical pneumonia.

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33
Q

What are the organisms that cause HAP?

A

Pseudomonas, E.coli, klebsiella and MRSA.

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34
Q

What is atypical pnuemonia?

A

Pneumonia caused by an organism that cannot be cultured in the normal way or detected using a gram stain.
-Don’t respond to penicillin so treated with macrolides (e.g. clarithromycin), fluoroquinolones (e.g. levofloxacin) or tetracyclines (e.g. doxycycline).

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35
Q

How does pneumonia present?

A

Productive cough (sputum) with SOB and fever.
-Pleuritic chest pain and haemoptysis.
-Sepsis.

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36
Q

How does atypical pneumonia present?

A

Dry cough and low grade fever.

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37
Q

What are six signs of pneumonia?

A

Tachypnoea, tachycardia, hypoxia, hypotension, fever, confusion.

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38
Q

What is the first line investigation of pneumonia?

A

CXR with consolidation.

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39
Q

What are other investigations for pneumonia?

A

Bloods - FBC which shows raised WCC. Raised CRP.

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40
Q

What are investigations for severe pneumonia?

A

Sputum sample and blood culutres.

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41
Q

How is pneumonia severity assessed?

A

CURB65:

-Confusion.
-Urea > 7.
RR > 30.
BP <90/60 mmHg.
65+ years old.

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42
Q

Why is pneumonia severity assesssed?

A

Predictor of mortality and guides treatment - home, hospital or ICU.

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43
Q

What is the management for pneumonia?

A

Analgesia for pain.
Broad spectrum antibiotics - dependent on bacteria and severity.

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44
Q

How is CAP treated?

A

CURB 0-2 - Amoxicillin.
CURB 3-5 - Co-amoxiclav and clarythromycin.

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45
Q

How is HAP treated?

A

IV co-amoxiclav and gentamicin.

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46
Q

What are five complications of pneumonia?

A

Sepsis, pleural effusion, empyema, lung abscesses and death.

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47
Q

What is tuberculosis?

A

Infectious granulomatous creating disease caused by the mycobacterium tuberculosis bacteria.

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48
Q

How is TB spread?

A

Airborne.

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49
Q

Is TB common in the UK?

A

No, more prevalent in non-UK born patients who are immunocompromised.

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50
Q

Where is TB common in the world?

A

South Asia and Sub-Saharan Africa.

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51
Q

What are four risk factors for TB?

A

Country/travel, immunocompromised, homeless/crowded housing, IVDU.

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52
Q

What is the difference between active and latent TB?

A

Active - Active infection in various areas of the body.
Latent - Infection is confined to granulomas but is still alive.

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53
Q

What is secondary TB?

A

When latent TB reactivates into active infection.

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54
Q

How is TB stained?

A

Stained via Zeihl-Neelsen stain to bright red due to acid-fastness (resistant to acids in staining procedure).

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55
Q

What is the presentation of latent TB?

A

Asymptomatic.

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56
Q

What is miliary TB?

A

When the immune system is unable to control the disease.

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57
Q

What is extrapulmonary TB?

A

When the TB spreads to other areas.

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58
Q

How does TB usually present?

A

Fever and night sweats, lethargy, weight loss, cough, haemoptysis.

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59
Q

What are the investigations for TB?

A

3 sputum cultures with positive Zeihl-Neelsen stains.
-Mantoux test = looks for previous immune response to TB.
CXR.

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60
Q

Describe the Mantoux test.

A

Tests for previous immune response to TB.
-Tuberculin injected into skin, the bleb is measured and if it is bigger than 5mm it is positive.
-Then test for active disease.

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61
Q

What is the management of latent TB?

A

Isoniazid and rifampicin for 3 months. OR:
Isoniazid for 6 months.

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62
Q

What is the management of active TB?

A

RIPE:

-Rifampicin for 6 months.
-Isoniazid for 6 months.
-Pyrazinamide for 2 months.
-Ethambutol for 2 months.

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63
Q

What are the side effects of active TB treatment?

A

Rifampicin - Red/orange urine and tears.
Isoniazid - Peripheral neuropathy.
Pyrazinamide - Hepatitis and gout (hyperuricaemia).
Ethambutol - Colour blindness and reduce visual acuity.

-All cause hepatotoxicity.

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64
Q

What is cystic fibrosis?

A

An autosomal recessive condition affecting the mucous glands.

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65
Q

Describe the genetics of cystic fibrosis.

A

Mutation on chromosome 7 in the CFTR gene.
-Autosomal recessive inheritance.

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66
Q

Describe the epidemiology of cystic fibrosis.

A

1 in 25 are carriers, 1 in 2500 children have it.

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67
Q

What is the prognosis for cystic fibrosis?

A

Median life expectancy is 47y.
90% develop pancreatic insufficiency.
50% develop diabetes.
30% develop liver disease.

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68
Q

What are two risk factors for cystic fibrosis?

A

Family history and white.

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69
Q

Explain the pathophysiology of CF.

A

The CFTR gene normally secretes chloride and sodium ions into ductal secretions to make them thin and water.
-This gene is defective so secretions become thicker with increased chloride and sodium ion retention.

70
Q

How does CF first present in neonates?

A

Meconium ileus - earliest stool that is too thick and sticky to pass through the bowel - causing a bowel obstruction and N+V.

71
Q

What are four symptoms of CF?

A

Thick sputum with chronic cough, recurrent upper respiratory tract infections, steatorrhoea, salty sweat/saliva.

72
Q

What is a sign of CF in males?

A

Bilateral absence/atrophy of vas deferens and epididymis resulting in infertility.

73
Q

How is CF diagnosed in newborns?

A

Newborn heel prick test.

74
Q

What is the gold standard investigation for CF?

A

Sweat test - chloride concentration is measured. Above 60mmol/L is positive.

75
Q

How is CF investigated during pregnancy?

A

Amniocentesis or chorionic villous sampling - genetic testing for CFTR gene.

76
Q

Why is there recurrent respiratory infections in people with CF?

A

As patients struggle to clear secretions, there is a perfect environment for microbial colonisers.

77
Q

What are five common colonisers in people with CF?

A

S. aureus, pseudomonas, H. influenzae, E. coli, klebsiella.

78
Q

What is a leading cause of mortality in people with CF and why?

A

Pseudomonas infection - resistant to antibiotics.

79
Q

What are four conservative management options of CF?

A

Chest physiotherapy, exercise, high calorie diet and no smoking.

80
Q

Explain four medications used in CF.

A

-Replacing pancreatic enzymes.
-Prophylactic flucloxacillin to reduce risk of infection.
-Bronchodilators (salbutamol).
-Nebulised DNase - making secretions less thick and easier to clear.

81
Q

Explain the monitoring in CF.

A

Check ups every 6 months to check for bacteria such as pseudomonas.
-Screening for diabetes, osteoporosis, vitD deficiency and liver failure.

82
Q

What is bronchiectasis?

A

Permanent dilation of bronchi/bronchioles with excessive mucous in them.

83
Q

What are three risk factors for bronchiectasis?

A

Post infection (pneumonia, TB), CF, HIV.

84
Q

Explain the pathophysiology of bronchiectasis.

A

Irreversible dilation, loss of cilia and mucous secretions - increased risk of infection as decreased mucociliary clearance.

85
Q

How does bronchiectasis present?

A

SOB with a productive cough and haemoptysis.
-Recurrent chest infections.

86
Q

What are the investigations for bronchiectasis?

A

HRCT (GS) and XRAY - shows dilated, thickened bronchi.

87
Q

What is pleural effusion?

A

Excess fluid accumulation between visceral and parietal pleural layers.

88
Q

What are the types of fluid in pleural effusion?

A

Exudative or trasudative.

89
Q

Describe exudative fluid in pleural effusion. What causes it?

A

High protein count due to inflammation causing increased vascular permeability (cloudy fluid).
-Due to lung cancer, TB, pneumonia, RA.

90
Q

Describe transudative fluid in pleural effusion. What causes it?

A

Low protein count due to increased hydrostatic or decreased oncotic pressure (clear fluid).
-Due to CHF, hypoalbuminaemia, hypothyroidism.

91
Q

What is empyema?

A

Infected pleural effusion.

92
Q

How does pleural effusion present?

A

SOB with pleuritic chest pain, cough and decreased breathing sounds.
-Dull percussion.

93
Q

What is the GS and 1st line investigation for pleural effusion? What does it show?

A

CXR - shows blunting of costophrenic angles, excess fluid and tracheal deviation.

94
Q

What is another investigation for pleural effusion?

A

Thoracocentesis - sample of pleuritic fluid.
-Testing for protein count, WCC, pH, glucose, LDH and microbiology.

95
Q

What is the management of pleural effusion?

A

If small - conservative, treat underlying cause.
Larger - aspiration or chest drain.

96
Q

What is pneumothorax?

A

Punctured lung - occurs when air gets into pleural space, separating the lungs from the chest wall.

97
Q

What is the typical patient in pneumothorax?

A

Young, tall, thin young man with sudden breathlessness and pleuritic chest pain.

98
Q

What is the difference between simple and tension pneumothorax?

A

Simple - Air can flow in and out, doesn’t worsen with each breath.
Tension - Medical emergency, one way valve with air only into pleural space and not out. Worsens with each breath.

99
Q

What are the primary causes of penumothorax?

A

Sponteanous.

100
Q

What are three secondary causes of pneumothorax?

A

Trauma, iatrogenic, lung pathology.

101
Q

How does pneumothorax present?

A

SOB with one sided sharp pleuritic chest pain with decreased breathing sounds.

102
Q

What is the GS and 1st line investigation of pneumothorax?

A

CXR - shows area between lung and chest wall with no lung markings.

103
Q

What is the management of simple pneumothorax?

A

If small (and no SOB) it will self heal.
-Larger -Aspiration. If this fails twice - chest drain.

104
Q

Why is tension pneumothorax dangerous?

A

Creates large pressure in thorax which pushes the mediastinum across and can cause cardiorespiratory arrest.

105
Q

What are four signs of tension pneumothorax?

A

Tachycardia, hypotension, reduced air entry to affected side, tracheal deviation away from side of pneumothorax.

106
Q

What is the management of tension pneumothorax?

A

Insert a large bore cannula into the second intercostal space in the midclavicular line.

107
Q

Where is the triangle of safety? What is the significance?

A

This is where chest drains are inserted.
-Triangle is formed by:

5th intercostal space.
Mid axillary line.
Anterior axillary line.

108
Q

Where are needles inserted in relation to the rib?

A

Just above the rib to avoid the neurovascular bundle.

109
Q

What is a pulmonary embolism (PE)?

A

An embolus typically from a DVT that blocks pulmonary artery circulation.

110
Q

What are the risk factors for PE?

A

Virchow’s triad:

-Venous stasis - Immobility, post-surgery, varicose veins, AF.
-Hypercoagulability - Pregnancy, obesity, malignancy, inherited diseases.
-Endothelial injury - Smoking, hypertension, trauma, catheters.

111
Q

How does a PE present?

A

SOB with or without blood (haemoptysis) and pleuritic chest pain.
-Tachycardia, raised RR.
-Signs of DVT (unilateral swollen red calf).
-History of immobility.

112
Q

What are the first investigations for PE?

A

Perform a Well’s score:
-If >4 and likely a PE, send for a CTPA.
-If unlikely, perform D-dimer and if positive do a CTPA.

113
Q

What other investigations are there for PE?

A

DUSS of leg - DVT.
ECG - S1Q3T3:
-S waves in lead I, Q waves in lead III, T waves inverted in lead III.

114
Q

What is the prophylaxis for VTE?

A

If increased risk - LMWH and compression stocking (CI - PVD).

115
Q

What is the supportive management for PE?

A

Analgesia, oxygen and monitoring.

116
Q

How is PE treated if patient is haemodynamically stable?

A

Anticoagulation - DOAC, LMWH, warfarin.

117
Q

How is PE treated if patient is haemodynamically unstable?

A

Thrombolysis with alteplase.

118
Q

What are the options for long term anticoagulation for PE?

A

Warfarin or DOACs.
-LMWH if pregnant or cancer.

119
Q

What does low pO2 indicate?

A

Hypoxia and respiratory failure.

120
Q

What is the difference between type 1 and type 2 respiratory failure?

A

Type 1 - Low pO2 and normal pCO2.
Type 2 - Low pO2 and high pCO2.

121
Q

What is the difference between hypoxia and hypoxemia?

A

Hypoxia - Low oxygen levels in tissues.
Hypoxemia - Low oxygen levels in blood.

122
Q

What are interstitial lung diseases?

A

Umbrella term to describe conditions that affect the lung parenchyma causing inflammation and fibrosis.

123
Q

How are interstitial lung diseases diagnosed?

A

HRCT showing ground glass and lung biopsy for histology.

124
Q

What is pulmonary fibrosis?

A

Scarring of lung tissue - most common interstitial lung disease commonly seen in smoking older men.

125
Q

What are the risk factors for pulmonary fibrosis?

A

Smoking, occupational (dust, coal), drugs (methotrexate) and viruses (EBV, CMV).

126
Q

How does pulmonary fibrosis present?

A

Exertional dyspnoea and dry unproductive cough.

127
Q

What are the investigations for pulmonary fibrosis?

A

Spirometry shows restriction (FEV1:FVC > 0.7 but FVC < 0.8.
HRCT (GS) - Ground glass.
Inspiratory crackles and finger clubbing.

128
Q

What is the management of pulmonary fibrosis?

A

Smoking cessation and vaccines.
-Pirfenidone (antifibrotic and anti-inflammatory).
-Nintendanib (monoclonal antibody against TK).
LR - Lung transplant.

129
Q

What is sarcoidosis?

A

Idiopathic granulomatous disease.

130
Q

What is hypersensitivity pneumonitis?

A

T3 hypersensitivity - immune antigen-antibody complex deposition at lung tissues.

131
Q

What causes hypersensitivity pnuemonitis?

A

Mostly occupation:
-Farmer’s lung (mouldy hay) pigeon fancier’s lung (shite).

132
Q

How is hypersensitivity pneumonitis treated?

A

Remove allergen.

133
Q

What is asbestosis?

A

Inhalation of asbestos which is fibrogenic and oncogenic.
-Results in lung fibrosis and mesothelioma.

134
Q

What is Goodpasture’s syndrome?

A

T2 autoimmune hypersensitivity response where anti-GBM autoantibodies attack lungs and kidneys - pulmonary fibrosis and glomerulonephritis.

135
Q

Which four drugs cause interstitial lung disase?

A

Amiodarone, cyclophosphamide, methotrexate and nitrofurantoin.

136
Q

What is the third most common cancer in the UK?

A

Lung cancer.

137
Q

What is the biggest cause of lung cancer?

A

Smoking.

138
Q

Are primary or secondary lung tumours more common?

A

Secondary lung tumours much more common.

139
Q

Why is secondary lung cancer more common than primary?

A

As all blood travels to the lungs so it spreads easily there.

140
Q

What is cancer of the pleura?

A

Mesothelioma.

141
Q

What leads to mesothelioma?

A

Linked to asbestos with very large latent period (up to 45y).

142
Q

What are the main two types of lung parenchyma cancer? How common are they?

A

Non-small cell (85%), small cell (15%).

143
Q

Describe the types of non-small cell lung cancer.

A

Adenocarcinoma (40%), squamous (20%), large cell carcinoma (10%), other (10%).

144
Q

What are five risk factors for lung cancer?

A

Smoking, asbestos, coal, ionising radiation, underlying lung disease.

145
Q

How does lung cancer present?

A

SOB with chest pain, cough and haemoptysis and recurrent pneumonia.
-Cancer symptoms - weight loss, TATT, night fever/sweats, pain.

146
Q

What are the first line and diagnostic investigations for lung cancer?

A

1st line - CXR and CT.
Diagnostic - Bronchoscopy and biopsy. Confirms type.

147
Q

What is another investigation to investigate lung cancer?

A

MRI/PET scan for TNM staging.

148
Q

Describe small cell lung cancer.

A

15% of lung cancer - Contain neurosecretory granules that can release neuroendocrine hormones - paraneoplastic syndromes.

149
Q

What is the management of small cell lung cancer? What is the prognosis?

A

Chemotherapy and radiotherapy - prognosis is generally worse than NSCLC.

150
Q

What is the management of non-small cell lung cancer?

A

Surgery - lobectomy.
Radiotherapy can be curative.
Chemotherapy can improve quality of life and survival.

151
Q

Which three paraneoplastic syndromes can small cell lung cancer cause?

A

SIADH due to ectopic ADH.
Cushing’s disease due to ectopic ACTH.
Lambert Eaton syndrome.

152
Q

What can squamous cell carcinoma in the lung cause?

A

Hypercalcaemia caused by ectopic PTH.

153
Q

What are four extrapulmonary manifestations of lung cancer?

A

-Recurrent laryngeal nerve palsy causing hoarse voice.
-Phrenic nerve palsy - diaphragm weakness and SOB.
-SVC obstruction - facial swelling, SOB and distended veins.
-Horner’s syndrome - Triad of partial ptosis, anhidrosis and miosis. Tumour on pulmonary apex pressing on sympathetic ganglion (Pancoast’s tumour).

154
Q

What is pulmonary hypertension?

A

Increased resistance and pressure of the blood in the pulmonary arteries.

155
Q

Describe the pathophysiology of pulmonary hypertension.

A

This increases strain on the right side of the heart causing a back pressure of blood into the systemic venous system resulting in cor pulmonale.

156
Q

What are the five types of pulmonary hypertension?

A

Group 1 - Primary pulmonary htn.
Group 2 - Left heart side failure due to MI or systemic hypertension.
Group 3 - Chronic lung disease (COPD).
Group 4 - Pulmonary vascular disease (PE).
Group 5 - Miscellaneous disorders.

157
Q

How does pulmonary hypertension present?

A

SOB and fatigue.
-Syncope, tachycardia, raised JVP, hepatomegaly, peripheral oedema.

158
Q

What is the gold standard investigation for pulmonary hypertension?

A

Right heart catheter to measure pressure.

159
Q

Describe the ECG and CXR changes in pulmonary hypertension.

A

CXR - Dilated pulmonary arteries and RVH.
ECG - RBBB, right axis deviation, RBH.

160
Q

What is the prognosis of pulmonary hypertension?

A

Poor - 35% 5 year survival, 65% 5 year survival with treatment.

161
Q

What is pharyngitis?

A

Inflammation of pharynx with or without exudate.

162
Q

What are the causes of pharyngitis?

A

Viral (EBV, adenoviruses), bacterial (group A strep).

163
Q

How does pharyngitis present?

A

Sore throat and fever.
-Viral = Cough and congestion.
-Bacterial = Exudate.

164
Q

What is sinusitis?

A

Inflamed mucosa of nasal cavity and sinuses.

165
Q

What are the causes of sinusitis, how does it present and how is it treated?

A

Mostly viral, bacterial is S. pneumoniae and H. influenzae.
-Nasal discharge, fever, sore throat.
-Self-limiting.

166
Q

What is otitis media? How is it diagnosed?

A

Inflamed middle ear typically in children.
Otoscopy shows inflamed erythematous tympanic membrane.

167
Q

What is epiglossitis?

A

Inflammation of epiglottis which obstructs the airway.

168
Q

How does epiglossitis present?

A

Young child with sore throat, SOB and tripoding (leaning forward and mouth open, tongue out).

169
Q

How is epiglossitis diagnosed?

A

GS - Laryngoscopy.

170
Q

What is whooping cough? Who does it affect?

A

Chronic cough caused by Bordetella pertussis.
-Pertussis toxin inhibits alveolar macrophages.

Affects mostly children - characteristic whoop in cough.

171
Q

What is croup?

A

Occasional complication of URTI particularly parainfluenza and measles.

172
Q

How does croup present and how is it treated?

A

Hoarse voice with barking cough and stridor.
-Single dose dexamethasone.

Phase 2a (14 decks)

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