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Phase 2a > Respiratory Diseases > Flashcards

Respiratory Diseases Flashcards

1
Q

What is the aetiology of pulmonary hypertension?

A

Increase in pulmonary vascular resistance or increase in blood flow

  • Pulmonary vascular disorders= PE, Primary PH
  • Diseases of lung= COPD
  • MSK diseases= Kyphoscoliosis, poliomyelitis
  • Resp diseases= Obesity, sleep apnoea
  • Cardiac= LV failure, mitral stenosis, congenital heart disease
  • Other= appetite suppression drugs, lipid storage diseases, sickle cell disease, familial, rheumatic autoimmune disease
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2
Q

What is the clinical presentation of pulmonary hypertension?

A
  • Exertional dysponea, lethargy, fatigue
  • Ankle Oedema
  • Chest pain
  • Syncope
  • RV failure= Abdominal pain and oedema due to hepatic congestion
  • Loud pulmonary second sound
  • Right parasternal heave due to RV hypertrophy
  • Features of RH failure= Increased JVP, Hepatomegaly, ascites, pleural effusion
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3
Q

Briefly explain the pathophysiology of pulmonary hypertension

A
  • Hypoxic vasoconstriction, cell proliferation and inflammation resulting in narrower vessels and increase in RV pressure
  • Damage to pulmonary endothelium leading to vasoconstrictors release, and increase pulmonary vascular resistance causing RV hypertrophy
  • Increased platelet and leukocyte adhesion
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4
Q

What are the differentials of pulmonary hypertension?

A

Cor pulmonale, cardiomyopathies, primary RV heart failure, congestive heart failure, portal hypertension

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5
Q

How is pulmonary hypertension diagnosed?

A
  • CXR: Enlarged proximal pulmonary arteries which taper distally. Enlarged heart. May reveal cause of PH
  • ECG: RV hypertrophy and P pulmonale (Tall and peaked P wave)
  • Echo cardiogram: RV dilation and/or hypertrophy. Can reveal cause of PH
  • LFTs to detect portal hypertension
  • Autoimmune screening
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6
Q

How is pulmonary hypertension treated?

A
  • Treat underlying cause
  • Oxygen
  • Warfarin= due to intrapulmonary thrombosis
  • Diuretics for oedema
  • Oral calcium channel blockers= Pulmonary vasodilators
  • Oral endothelin receptor receptor antagonists
  • Phosphodiesterase-5 inhibitors
  • Heart-lung transplant in young
  • Prostanoid (mediators of vasoconstriction) analogues
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7
Q

How is wegener’s granulomatosis diagnosed?

A
  • Bloods: cANCA positive, elevated PR3 antibodies, raised ESR and CRP
  • CXR: Nodular masses/ pneumotic infiltrates with cavitation, clear migratory pattern
  • CT: Diffuse alveolar haemorrhage
  • Urinalysis: Proteinuria+ haematuria= if positive then renal biopsy
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8
Q

How is wegener’s granulomatosis treated?

A
  • Depends on extent of disease
  • Severe disease should be treated with corticosteroid e.g. prednisolone, and cyclophosphamide or rituximab
  • Azathioprine or methotrexate used as maintenance
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9
Q

What are the clinical features of wegener’s granulomatosis?

A
  • Severe rhinorrhea (nasal cavity congested with mucous), and nasal mucosal ulceration- characteristic saddle nose deformity
  • Pleuritic pain
  • Haemoptysis
  • Renal disease causes rapidly progressive glomerulonephritis with crescent formation, proteinuria or haematuria
  • May be skin purpura or nodules, peripheral neuropathy, arthritis
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10
Q

Briefly explain the pathophysiology of wegener’s granulomatosis

A
  • Inflammation of blood vessels with granulomas
  • Autoantibodies are made to neutrophil proteins, so neutrophils are recruited where there is no infection
  • This results in formation of reactive oxygen species and neutrophil degranulation
  • This causes microabscesses recruitment of wbc to make granulomas
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11
Q

What is wegener’s granulomatosis?

A

Multisystem disorder of unknown origin characterised by necrosing granulomatous inflammation and vasculitis of small and medium vessels

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12
Q

What is the epidemiology of Goodpasture’s syndrome?

A
  • Rare in children

- More common in men

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13
Q

What is Goodpasture’s syndrome?

A

The co-existance of acute glomerulonephritis and pulmonary alveolar haemorrhage and the presence of circulating antibodies directed against an intrinsic antigen to the basement membrane of kidney and lung

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14
Q

Briefly explain the pathophysiology of Goodpasture’s syndrome

A

Specific autoimmune disease caused by a type II antigen-antibody reaction leading to diffuse pulmonary haemorrhage, glomerulonephritis (and often AKI and CKD)

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15
Q

What are the clinical features of Goodpasture’s syndrome?

A
  • Typically starts with symptoms of upper resp tract infection e.g. sneeze, nasal discharge, nasal congestion, runny nose and fever
  • Cough
  • Intermittent haemoptysis
  • Anaemia- persistent intrapulmonary bleeding, fatigue
  • Acute glomerulonephritis
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16
Q

How is Goodpasture’s syndrome diagnosed?

A
  • Presence of anti-basement membrane antibodies in blood
  • CXR; Transient patchy shadows/ pulmonary infiltrates due to pulmonary haemorrhage often in lower zones
  • Kidney biopsy; crescentic glomerulonephritis
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17
Q

How is Goodpasture’s syndrome treated?

A
  • Some patients may spontaneously improve
  • Other proceed onto renal failure
  • Treat shock
  • Vigorous immunosuppressive treatment= corticoids e.g. prednisolone, plasmapheresis
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18
Q

What is the epidemiology of mesothelioma?

A
  • More common in men
  • Most often presents between 40-70yrs
  • Exposure to asbestos is well established cause
  • Long latent period between exposure and tumour
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19
Q

What are the clinical features of mesothelioma?

A
  • Chest pain
  • Dyspnoea
  • Weight loss
  • Finger clubbing
  • Recurrent pleural effusions
  • Signs of metastasis= Bone pain/tenderness, hepatomegaly, lymphadenopathy, abdominal pain
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20
Q

How is mesothelioma diagnosed?

A
  • CXR and CT: Unilateral pleural effusion, pleural thickening
  • Bloody/straw coloured pleural fluid
  • Pleural biopsy
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21
Q

How is mesothelioma treated?

A
  • Surgery for extremely localised mesothelioma
  • Generally resistant to surgery, chemo and radiotherapy
  • Average 8 months from diagnosis to death
  • Refer all mesothelioma deaths to coroner
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22
Q

What is bronchiectasis?

A

Permanent dilation and thickening of the airways

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23
Q

What are the clinical features of bronchiectasis?

A
  • Usually lower lobes affected
  • Variance= Intermittent episodes of expectoration and infection, persistent daily expectoration of purulent sputum
  • Chest pain, dyspnoea, haemoptysis
  • Signs; coarse crackles and wheeze
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24
Q

Briefly explain the pathophysiology of bronchiectasis

A

Failure of mucocillary clearance and impaired immune function contribute to continued insult to bronchial wall through the recruitment of inflammatory cells. Airways dilate due to inflammation and scarring, as fibrosis contracts.

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25
Q

What are the causes of bronchiectasis?

A
  • Chronic inflammation of airways; large number of causative agents such as asthma, post infection and immunodeficiency
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26
Q

What is the epidemiology of bronchiectasis?

A
  • Elderly
  • Female
  • May develop after lung infections
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27
Q

How is bronchiectasis diagnosed?

A
  • HRCT: Bronchial wall dilation.
  • CXR to exclude other causes
  • Sputum culture
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28
Q

What are the major pathogens associated with bronchiectasis?

A
  • Haemophilius influenzae
  • Strep pneumoniae
  • Staph Aureus
  • Pseudomonas aeruginosa
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29
Q

How is bronchiectasis treated?

A
  • Stop smoking
  • Airways clearance
  • Medication; Antibiotics, bronchodilators
  • Surgery; lung resection
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30
Q

What are the clinical features of idiopathic pulmonary fibrosis?

A
  • Breathless, non productive cough
  • Finger clubbing
  • Exertional dyspnoea
  • Malaise
  • Weight loss
  • Arthralgia
  • Cyanosis
  • Inspiratory basal crackles
  • Resp failure, pulmonary hypertension
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31
Q

What is the epidemiology of idiopathic pulmonary fibrosis?

A

Usually >60 and male

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32
Q

Briefly explain the pathophysiology of idiopathic pulmonary fibrosis

A
  • Repetitive injury to alveolar epithelium due to unidentified stimuli
  • Wound healing mechanisms become uncontrolled, leading to over production of fibroblasts and deposition of increased extracellular matrix in the interstitium with little inflammation
  • Loss of elasticity and reduced gas exchange
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33
Q

How is idiopathic pulmonary fibrosis diagnosed?

A
  • CXR= Honeycomb lung
  • CT= Honeycombing, subplural reticulation, basal distribution, traction bronchiectasis
  • ABG= Hypoxia, normal CO2
  • Spirometry= ANA and RF antibodies in 1/3
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34
Q

How is idiopathic pulmonary fibrosis treated?

A
  • Lung transplant
  • Oxygen and pulmonary rehabilitation
  • Pirfenidone
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35
Q

What is acute coryza?

A

Common cold

Dilation and thickening of the airways

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36
Q

What are the clinical features of acute coryza?

A
  • Incubation period of 12 hrs- 5days

- Then, malaise, pyrexia, sore throat and watery nasal discharge

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37
Q

What causes acute coryza?

A

Infection by rhinovirus (droplet spread)

Virus binds to ICAM-1 receptors which causes inflammatory mediators to be released

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38
Q

What is sarcoidosis?

A

Multisystem chronic inflammatory condition- formation of non-caseating epithelioid granulomata.

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39
Q

What are the clinical features of sarcoidosis?

A
  • 50% of the time, asymptomatic
  • Lung; dyspnoea, non productive cough, chest pain
  • Erythema nodusum with/without polyarthralgia
  • Granulomatous uveitis, conjunctivitis, glaucoma
  • Fever, weight loss, fatigue
  • Hepatosplenomegaly
  • Hypercalciuria, renal stones
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40
Q

Briefly explain the pathophysiology of sarcoidosis

A

Non caseating granulomata form at various sites, particularly in the thoracic cavity, skin and eyes

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41
Q

What is the epidemiology of sarcoidosis?

A
  • Commonly 20-40yrs old
  • More common in women
  • More serious in black individuals
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42
Q

How is sarcoidosis diagnosed?

A
  • CXR= Staging
  • Blood tests= Increased ESR, Increased LFTs, Increased calcium, Increased serum ACE, Increased immunoglobulins
  • Bronchioscopy
  • Tissue biopsy= diagnostic (Shows the non caesating granulomata)
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43
Q

How is sarcoidosis treated?

A
  • If no pulmonary infiltration, no treatment
  • Prednisolone
  • Bed rest
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44
Q

What is pneumonia?

A

Acute lower resp tract inflammation, with intense infiltration of neutrophils.

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45
Q

What is the epidemiology of pneumonia?

A

5-14 % Mortality

Common in infants/ elderly

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46
Q

What are the causative agents of community acquired pneumonia?

A
  • Strep pneumoniae
  • Haemophilius influenzae
  • Mycoplasma pneumoniae
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47
Q

What are the causative agents of hospital acquired pneumonia?

A
  • Pseudomonas aeruginosa
  • E Coli
  • Klebsiella pneumoniae
  • Staph aureus
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48
Q

What is aspiration pneumoniae?

A

Acute aspiration of gastric contents into the lungs can cause an extremely severe pneumonia

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49
Q

What are the clinical features of pneumonia?

A
  • Vary depending on causative agent
  • Pyrexia, cough, pleurisy, pleural rub, pleural effusion
  • Raised resp rate, raised heart rate and low BP
  • Rigors, malaise, anorexia
  • Breathlessness
  • Purulent sputum
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50
Q

How is pneumonia diagnosed?

A
  • CXR: look for ‘air bronchogram’
  • FBC and sputum culture: ESR and CRP usually elevated
  • Pulse oximetry and ABG analysis
  • CURB 65 for severity (confusion, urea raised, resp rate raised, BP low, over 65)
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51
Q

How is pneumonia treated?

A
  • Oxygen for hypoxia
  • Antibiotics= Amoxicillin
  • IV antibiotics if severe= Co amoxiclav / clarithromycin for 7-10 days
  • Analgesics
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52
Q

What is asbestosis?

A

A type of interstitial lung disease= lung fibrosis

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53
Q

What are the clinical features of asbestosis?

A
  • Breathlessness and progressive dyspnoea
  • Finger clubbing
  • Bilateral basal end-inspiratory crackles
  • Pleural plaques
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54
Q

How is asbestosis treated?

A

Symptomatically e.g. corticosteroids

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55
Q

What is Raynaud’s phenomenon?

A
  • Intermittent spasm in the arteries supplying the fingers and toes, usually precipitatied by cold and relieved by heat
56
Q

What are the clinical features of Raynaud’s phenomenon?

A
  • Vasoconstriction causes skin pallor followed by cyanosis due to sluggish blood flow, then redness due to hyperaemia (White, then blue, then red)
  • Numbness, burning sensation and severe pain
57
Q

What conditions may exhibit Raynaud’s phenomenon?

A
  • Connective tissue disorders; SLE, Systemic sclerosis, RA, Dermatomyositis.
  • Occupational; vibrational tools
  • Drugs; Beta blockers, smoking
58
Q

How is Raynaud’s phenomenon treated?

A
  • Avoid cold provocation by wearing gloves and warm clothes

- Stop smoking and beta blockers

59
Q

What are the clinical features of alpha-1-antitrypsin deficiency in the lung?

A

COPD like symptoms (emphysema)

60
Q

Briefly explain the pathophysiology of alpha-1-antitrypsin deficiency

A
  • A1AT inhibits the action of neutrophil-protease enzymes in the lung (produced in the presense of inflamation, infection or smoking)
  • This means that elastase can break down elastin without inhibition, so destroys alveolar walls
61
Q

How is alpha-1-antitrypsin deficiency diagnosed?

A

Serum levels of alpha-1-antitrypsin

62
Q

How is alpha-1-antitrypsin deficiency treated?

A
  • Cessate smoking and drinking
  • Corticosteroids
  • Bronchodilators
  • Treat infections
  • Possible liver transplant
63
Q

What are the main causes of pulmonary embolism?

A
  • Clots breaking off and passing into the right heart before getting lodged in pulmonary circulation
  • RV thrombus (Post MI)
  • Septic emboli
  • Fat embolism
  • Air embolism
  • Foreign material (IV drug use)
64
Q

What are the risk factors for pulmonary embolism?

A
  • Change in blood flow ; immobility, obesity, pregnancy
  • Change in vessel; smoking, hypertension
  • Change in blood constituents; Dehydration, malignancy, high pestrogen
  • Leg fracture
  • Recent surgery
65
Q

What are the clinical features of pulmonary embolism?

A
  • Small may be asymptomatic
  • Sudden onset dyspnoea
  • Pleuritic chest pain and haemoptysis if infarct has occurred
  • Dizziness
  • Pyrexia
  • Cyanosis and tachypnoea
  • Tachycardia and hypotension
  • Raised JVP
66
Q

How are pulmonary emboli diagnosed?

A
  • Plasma D dimer (+ve result isn’t diagnostic, but -ve rules it out)
  • CT pulmonary angiography is gold standard
67
Q

How are pulmonary emboli treated?

A
  • High flow oxygen
  • Anticoagulate with low molecular weight heparin e.g. enoxaparin
  • Thrombolysis for massive PE
  • Surgical embolectomy and vena cava filter
68
Q

What is pneumothorax?

A
  • Pocket of air in the pleural cavity= Partial/ complete collapse of the lung on the affected side
69
Q

What is tension pneumothorax?

A
  • Pleural tear acts as a one way valve
  • Allows air into the cavity but not out
  • Increases the unilateral pressure
  • Clinical emergency
70
Q

What are the risk factors for pneumothorax?

A
  • Male
  • Smoking
  • Mechanical ventilation
  • Age= Most likely between 20-40
71
Q

How are pneumothorax diagnosed?

A
  • CXR: Area devoid of lung markings

- ABG: In dyspnoeic patients check for hypoxia

72
Q

What are the causes of primary pneumothorax?

A
  • Congenital issue
  • Trauma
  • Smoking, COPD
73
Q

What are the causes of secondary pneumothorax?

A
  • Underlying lung disease
74
Q

What are the clinical features of pneumothorax?

A
  • Sudden onset of pain
  • Shortness of breath
  • Respiratory distress
  • Tension= Tachycardia, tachypnoea, low BP, low O2
75
Q

How is pneumothorax treated?

A
  • Chest drain
  • Needle aspiration to remove air
  • Oxygen for hypoxia
  • Smoking cessation
  • Surgery if persistent
76
Q

What are the clinical features of COPD?

A
  • Productive cough with white/ clear sputum
  • Wheeze and breathlessness
  • Abnormal posture, drowsiness/ mental confusion
  • Hyperinflated lungs
77
Q

What causes COPD?

A
  • Chronic inflammation of the airways usually due to smoking

- This causes mucous gland hypertrophy and increase in inflammation = breakdown of lung tissue

78
Q

How is COPD diagnosed?

A
  • Lung function test= Shows progressive airflow limitation
  • CXR
  • High resolution CT
79
Q

How is COPD treated?

A
  1. Stop smoking
  2. SABA or long acting antimuscarinic
    • LABA or long acting antimuscarinic
  4. Inhaled glucocorticoids
  5. Long acting antimuscarinic +LABA +Inhaled steroid
    • Long term oxygen therapy
80
Q

What is a Blue bloater?

A

A patient with chronic bronchitis

81
Q

What is a Pink puffer?

A

A patient with emphysema

82
Q

What percentage of lung cancers are small cell cancers?

A

15%

83
Q

What is small cell lung carcinoma?

A

A cancer of the kulchisky cells (endocrine cells in the lung)

84
Q

How is small cell lung carcinoma treated?

A
  • Limited disease= Chemo and radiotherapy
  • Extensive disease= Chemo
  • Analgesia
  • Symptomatic relief
85
Q

What type of lung cancer is most strongly associated with cigarette smoking?

A

Squamous cell carcinoma

86
Q

What is the most common type of lung cancer?

A

Adenocarcinoma

87
Q

List some types of non-small cell lung carcinoma

A
  • Squamous cell carcinoma
  • Adenocarcinoma
  • Carcinoid tumours
  • Lymphomas
88
Q

What is the most common malignant tumour worldwide?

A

Bronchial carcinoma

89
Q

What are the risk factors for bronchial carcinoma?

A
  • Cigarette smoking
  • Asbestos
  • Coal and products of coal combustion
  • Radon exposure, ionising radiation
  • Pre existing lung disease
  • HIV
90
Q

What are the clinical factors of bronchial carcinoma?

A
  • Cough
  • Breathlessness and wheeze
  • Haemoptysis
  • Chest pain
  • Recurrent infections
  • Clubbing
  • Paraneoplastic changes= excess PTH, ACTH, HPOA
91
Q

Where does bronchial carcinoma typically spread to?

A
  • Adrenals
  • Liver
  • Bone
  • Brain
92
Q

How is bronchial carcinoma diagnosed?

A
  • CXR= Round shadow with a fluffy “spiked” appearance at the edge, hilar enlargement, consolidation
  • CT for staging
  • Bronchoscopy to give histology and assess operability and biopsy
  • Cytology of sputum
93
Q

What is the epidemiology of tuberculosis?

A
  • 1/3 of world population is infected
  • 9 million cases per year
  • Majority of cases in Africa and Asia
94
Q

What pathogen causes tuberculosis?

A
  • m. Tuberculosis
  • m. Bovis
  • m. Africanum
  • m. Microti
95
Q

What are the risk factors for tuberculosis?

A
  • Origination from a high-incidence country
  • HIV
  • Immunosuppressant therapy
  • Diabetes mellitus
  • IVDU
  • Aging
  • Malnutrition
  • Prisons
  • Homelessness
  • Smoking and alcohol
96
Q

What is reactivation tuberculosis?

A

Reactivation of a latent infection- usually occurs when there’s a depression of host immune system e.g. when older or in severe infection

97
Q

What is milliary tuberculosis?

A

Initial TB is not successfully controlled leading to a systemic infection

98
Q

What are the systemic features of tuberculosis?

A
  • Weight loss
  • Low grade fever
  • Anorexia
  • Night sweats
  • Malaise
99
Q

What are the pulmonary features of tuberculosis?

A
  • Productive cough with occasional haemoptysis
  • Cough for over 3 weeks
  • Pleuritic pain
  • Breathlessness
  • Hoarse voice if laryngeal involvement
100
Q

What are the extrapulmonary features of tuberculosis?

A
  • Bone pain
  • Lymph node swelling
  • Ascites
  • GU involvement
  • CNS TB
101
Q

How is active tuberculosis diagnosed?

A
  • CXR: Patchy or nodular shadow, loss of volume, consolidation, milliary shadows
  • Sputum: Auramine-phenol fluorescent test or Ziehl-Neelsen
  • Histology: Non caseating granulomata
  • Culture
  • NAAT
  • Lumbar puncture if milliary TB
102
Q

What is latent TB?

A

When the immune system contains the infection and the patient develops cell-mediated immunity. Bacteria are held in calcified caveated areas.

103
Q

How can latent TB be diagnosed?

A
  • Tuberculin skin test ‘matnoux’= TB antigen is injected and can see if there is a type IV hypersensitivity reaction
  • Interferon gamma release assays= Antigens specific to M. Tuberculosis.
104
Q

How is tuberculosis treated?

A
  • Rifampicin for 6 months
  • Isoniazid for 6 months
  • Pyrazinamide for 2 months
  • Ethambutol for 2 months
105
Q

What are the side effects of rifampicin?

A

Red urine, hepatitis and drug interactions

106
Q

What are the side effects of isoniazid?

A

Hepatitis and neuropathy

107
Q

What are the side effects for pyrazinamide?

A

Hepatitis. arthralgia/ gout and rash

108
Q

What are the side effects of ethambutol?

A

Optic neuritis

109
Q

What is hypersensitivity pneumonitis?

A

Inhalation of allergens provokes a hypersensitivity reaction, with alveolar infiltrate and granuloma formation

110
Q

What are the causes of hypersensitivity pneumonitis?

A
  • Farmer’s ling
  • Bird fancier’s lung
  • Bagassosis lung
  • Humidifiers fever
  • Malt worker’s lung
  • Mushroom workers lung
  • Cheese washer’s lung
111
Q

What are the clinical features of hypersensitivity pneumonitis?

A
  • 4-6 hrs post exposure= Fever, rigors, myalgia, dry cough, dyspnoea, crackles
  • Chronic= Increasing dyspnoea, weight loss, type 1 resp failure, cor pulmonale
112
Q

How is acute hypersensitivity pneumonitis diagnosed?

A
  • Bloods= FBC (Neutrophilia), raised ESR, ABGs and +ve serum precipitins
  • CXR= Upper-zone mottling/consolidation
  • LFT= Reversible restrictive defects
113
Q

How is chronic hypersensitivity pneumonitis diagnosed?

A
  • Blood tests
  • CXR= Upper zone fibrosis; honeycomb lung
  • LFT= Persistent changes
  • Broncheoalveolar lavage fluid shows increased lymphocytes and mast cells
114
Q

How is acute hypersensitivity pneumonitis treated?

A
  • Remove allergen and give O2

- Oral prednisolone

115
Q

How is chronic hypersensitivity pneumonitis treated?

A
  • Avoid exposure- facemask or +Ve pressure helmet
  • Compensation
  • Long term steroids
116
Q

What is cystic fibrosis?

A

A mutated CFTR cl- transport protein leading to dysfunction of secretions and multiple organ dysfunction

117
Q

What are the clinical features of cystic fibrosis in infancy?

A
  • Recurrent resp infections
  • diarrhoea
  • failure to thrive
  • rectal prolapse,
  • nasal polyps
  • acute pancreatitis
  • variceal haemorrhage
  • steatorrhoea
118
Q

What are the clinical features of cystic fibrosis in adults?

A
  • Recurrent resp infections
  • Atypical asthma
  • Bronchiectasis
  • Male infertility
  • Heat exhaustion
  • Portal hypertension
  • Steatorrhoea
119
Q

What are some signs of cystic fibrosis?

A
  • Finger clubbing
  • Cough with purulent sputum
  • Crackles
  • Wheezes
  • Respiratory obstruction
120
Q

What is the epidemiology of cystic fibrosis?

A
  • Most common inherited condition
  • 1/2000 live births
  • Less common in Afro-Caribbean and Asian populations
121
Q

Briefly explain the pathophysiology of cystic fibrosis?

A

Mutation of the CFTR gene, resulting in defects in cl- secretion, and increased Na+ absorption, causing increased h2o absorption and thicker mucous. This causes dehydrated surfaces, mucous stasis, airway inflammation and recurrent infection.

122
Q

How is cystic fibrosis diagnosed?

A
  • Sweat test
  • Absent vas deferens and epididymis
  • Genetic testing and family history
  • Faecal elastase test (low or no elastase)
  • Sinus X ray
123
Q

How is cystic fibrosis treated?

A
  • Resp: regular physio, prophylactic antibiotics, B2 agonists, inhaled corticosteroids, symptomatic relief, mucolytics such as dornase alfa
  • Nasal polyps: Polyopectomy
  • Endocrine: Pancreatic enzyme replacement, amiloride
124
Q

What is asthma?

A

Reversible obstruction of the airways. Bronchospasm and excessive airway secretions

125
Q

What are the clinical features of asthma?

A
  • Wheeze, dyspnoea
  • Chest tightness
  • Cough
  • Sputum
  • Symptoms worse at night
  • Reduced chest expansion
  • Prolonged expiratory time
126
Q

What are the risk factors for asthma?

A

Personal history of atopy, family history of asthma or atopy, obesity, inner city environment, premature birth, socio-economic deprivation

127
Q

What is the epidemiology of asthma?

A

10-15% of population affected by 20. Common in aged 3-5 years

128
Q

What are the 2 types of asthma?

A
  • Atopy (70%); IgE antibodies produced against allergens

- Increased responsiveness to stimuli (30%); Histamine and methacholine release

129
Q

What are the 3 main characteristic of asthma?

A
  • Airflow limitation
  • Airway hyper-responsiveness
  • Bronchial inflammation with T lymphocytes, mast cells, eosinophils with associated plasma exudation, oedema, smooth muscle hypertrophy, mucous plugging and epithelial damage
130
Q

How is asthma diagnosed?

A
  • Lung function tests= peak expiratory flow rate, spirometry
  • Exercise tests
  • Trial of corticosteroids
  • Check for sputum eosinophilia
  • RCP3 questions
131
Q

How is asthma treated?

A
  1. SABA
  2. SABA +ICS
  3. SABA +LABA +ICS
  4. SABA+ LABA+ ICS+ 4th drug e.g. anti IgE monoclonal
132
Q

How is an acute asthma attack treated?

A
  • Oxygen therapy
  • Nebulised 5mg salbutamol (+ ipratropium if life threatening)
  • Prednisolone
133
Q

What is the most frequent serotype of influenza?

A

Serotype A

134
Q

How is influenza diagnosed?

A

Not usually needed. Serology shows a 4 fold increase in antibody titre over a 2 week period

135
Q

How is influenza treated?

A

Treat symptoms, paracetamol, bed rest, fluids

136
Q

What are the clinical features of influenza?

A
  • Incubation period of 1-3 days
  • Abrupt fever
  • Aching in limbs
  • Sore throat and dry cough

Phase 2a (31 decks)

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