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Respiratory > Diseases > Flashcards

Diseases Flashcards

1
Q

What is ACOS?

A

Asthma / COPD overlap syndrome

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2
Q

Define asthma

A

A chronic inflammatory disease of both large and small airways. Airway inflammation is the basic underlying process

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3
Q

What is the asthma triad?

A
  • reversible airflow obstruction
  • airway inflammation
  • airway hyperresponsiveness
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4
Q

What are the hallmarks of remodelling in asthma?

A
  • thickening of the basement membrane
  • collagen deposition in the submucosa
  • hypertrophy in the smooth muscle
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5
Q

Describe the inflammatory cascade in asthma

A
  • inherited or acquired factors; viral, allergen or chemical
  • eosinophilic inflammation
  • mediators - TH2 cytokines
  • twitch smooth muscle (hyper reactivity)
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6
Q

What would be prescribed for twitchy smooth muscle (hyper reactivity) ? (asthma)

A
  • bronchodilators
  • beta 2 agonists
  • muscarinic antagonists
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7
Q

What would be prescribed for mediators / TH2 cytokines? (asthma)

A
  • antileukotrienes or antihistamines
  • anti IgE
  • anti interleukin 5
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8
Q

What would be prescribed for eosinophilic inflammation? (asthma)

A
  • anti-inflammatory medication
  • corticosteroids
  • cromones
  • theophylline
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9
Q

Describe the triggers of asthma

A
  • allergens

- others such as exercise, viral infection, smoke, cold, chemicals, drugs (NSAIDs, beta blockers0

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10
Q

Describe the clinical signs of asthma

A
  • episodic symptoms and signs
  • diurinal variability - nocturnal/ early morning
  • non productive cough, wheeze
  • triggers
  • associated atopy, increased IgE (rhinitis, conjunctivitis, eczema)
  • blood eosinophilia >4%
  • responsive to steroid or beta-agonists
  • family history of asthma
  • wheezing due to turbulent airflow
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11
Q

Describe the diagnosis of asthma

A
  • history and examination
  • diruninal variation of peak flow rate
  • reduced forced expiratory ratio (FEV.FVC <75%)
  • reversibility to inhaled salbutamol
  • provocation testing = bronchospasm
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12
Q

Describe COPD

A
  • a multi-component disease process
  • mucociliary dysfunction
  • inflammation
  • tissue damage
  • leads to obstruction of airflow
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13
Q

Describe chronic bronchitis

A
  • chronic neutrophilic inflammation
  • mucus hypersecretion
  • mucociliary dysfunction
  • altered lung microbiome
  • smooth muscle spasm hypertrophy
  • partially reversible
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14
Q

Describe emphysema

A
  • alveolar destruction
  • impaired gas exchange
  • loss of bronchial support
  • irreversible
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15
Q

Describe the COPD clinical syndrome

A
  • chronic symptoms, not episodic
  • smoking
  • non atopic
  • daily productive cough
  • progressive breathlessness
  • frequent infective exacerbations
  • chronic bronchitis, wheezing
  • emphysema, reduced breath sounds
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16
Q

Describe the chronic cascade in COPD

A
  • progressive fixed airflow obstruction
  • impaired alveolar gas exchange
  • respiratory failure ; decrease PaO2 and increased PaCO2
  • pulmonary hypertension
  • right ventricular hypertrophy / failure
  • death
  • stopping smoking arrests further decline in lung volume
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17
Q

Describe ACOS

A
  • COPD with blood eosinophilia >4%
  • responds better to ICS with exacerbation reductions
  • more reversible to salbutamol
  • difficult from asthmatic smokers who have airway remodelling (reduced FVC)
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18
Q

The physiology of hypoventilation leads to what?

A

Hypoxaemia and then to hypercarbia

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19
Q

What guidelines are used in the treatment of asthma?

A

Sign guidelines

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20
Q

Describe the challenge test

A
  • use mannitol or histamine

- airways will narrow to a certain extent

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21
Q

Describe the benefit of flu vaccines

A
  • reduce flu rates
  • reduce admissions
  • reduce severity of flu
  • opportunistic vaccination
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22
Q

What are the challenges in primary care of asthma

A
  • non-attendance
  • SABA overuse
  • who to refer to secondary care
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23
Q

When would you refer for additional investigation and specialist advice for asthma?

A
  • diagnosis unclear
  • suspected occupational asthma (symptoms that improve when patient is not at-work, adult onset asthma and workers in high risk occupations)
  • poor response to asthma treatment
  • severe / life threatening asthma attack
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24
Q

Describe the ‘red flags’ and indicators of other diagnoses in reference to asthma

A
  • prominent systemic features (myalgia, fever, weight loss)
  • unexpected clinical findings (eg. crackles, clubbing, cyanosis, cardiac disease, monophonic wheeze or stridor)
  • present non-variable breathlessness
  • chronic sputum production
  • unexplained restrictive spirometry
  • chest x-ray shadowing
  • marked blood eosinophilia
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25
Q

Name some important mimics of asthma

A
  • COPD
  • hypersensitivity pneumonitis
  • inducible laryngeal obstruction
  • dysfunctional breathing
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26
Q

Describe inducible laryngeal obstruction

A
  • difficulty breathing in rather than out
  • feeling of something stuck in the throat
  • triggered by exercise, perfume, strong smells, flowers, change in temperature
  • not an allergic phenomenon
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27
Q

Describe the effects of smoking

A
  • reduces ciliary beat frequency
  • sputum retention
  • increased infection
  • steroids are much less effective in smokers
  • macrolide antibiotics are not effective in smokers
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28
Q

Describe allergic borncho-pulmonary aspergillosis

A
  • an allergic response to aspergillus
  • mucus plugging
  • proximal bronchiectasis
  • total IgE >1000, elevated aspergillus IgE
  • treatment = steroids and itraconazole
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29
Q

Describe allergic asthma

A
  • usually childhood onset
  • atopic triad; asthma, eczema, rhinitis
  • typically allergic to; HDM, grass, cats and dogs
  • dermatographism
  • treatment options; Montelukast, antihistamines, allergen avoidance, omalizumab (monoclonal antibody to IgE
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30
Q

Describe eosinophilic asthma

A
  • usually adult onset
  • female preponderance
  • usually more steroid resistant
  • often stuck on prednisolone
  • anti-allergen therapy not effective
  • anti IL5 therapy; mepolizumab, benralizumab
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31
Q

A combination of severe asthma is recognised by what criteria?

A
  • previous near fatal asthma eg. previous ventilation or respiratory acidosis
  • previous admission for asthma, especially in the last year
  • requiring three or more classes of asthma medication
  • heavy use of a beta 2 agonist
  • repeated attendances at ED for asthma care, especially in the last year

AND adverse behavioural or physiological features

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32
Q

Name the clinical signs of life-threatening asthma

A
  • altered conscious level
  • exhaustion
  • arrhythmia
  • hypotension
  • cyanosis
  • silent chest
  • poor respiratory effort
  • PEF <33% best or predicted
  • SpO2 <92%
  • PaO2 <8 kPa
  • normal PaCO2
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33
Q

What are the co-morbidities associated with COPD?

A
  • heart failure
  • ischaemic heart disease
  • obesity
  • interstitial lung disease
  • bronchiectasis
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34
Q

Describe the pharmacological management of COPD

A
  • bronchodilators
  • inhaled corticosteroids
  • combination therapies
  • oral therapies
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35
Q

Describe the use of bronchodilators in stable COPD

A
  • LABA and LAMA significantly improve lung function, dyspnoea, health status and reduce exacerbation rates
  • LAMA have a greater effect on exacerbation and decrease hospitalisations
  • LABA/LAMA combination increases FEV1 and reduces symptoms compared with monotherapy
  • theophylline exerts a small bronchodilator effect in COPD
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36
Q

Describe inhaled corticosteroids in COPD

A
  • an ICS combined with LABA is more effective than the individual components in improving lung function and health status
  • regular treatment with ICDS increases the risk of pneumonia, especially in those with severe disease
  • triple inhaled therapy improves lung function, symptoms and health status
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37
Q

When would you consider use of ICS treatment in COPD?

A
  • one moderate exacerbation of COPD per year

- blood eosinophils 100-300 cells / ul

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38
Q

What factors go against use of ICS in COPD

A
  • repeated pneumonia events
  • blood eosinophils <100 cells/ ul
  • history of mycobacterial infection
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39
Q

What are the key principles in treating COPD?

A
  • accurate diagnosis
  • treat co-morbidities
  • smoking cessation
  • vaccinations
  • pulmonary rehab
  • LABA/LAMA
  • trial of triple if high eos or frequent exacerbator
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40
Q

Who do you refer to secondary care in terms of COPD?

A
  • diagnosis uncertain
  • rapidly declining FEV1
  • for consideration of; LVRS, bronchoscopic values, lung transplant
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41
Q

Describe exacerbations in COPD

A
  • an exacerbation of COPD is defined as an acute worsening of respiratory symptoms that results in additional therapy
  • the symptoms are not specific to COPD - relevant differential diagnoses should be considered
  • exacerbation of COPD can be precipitated by several factors
  • the goal of treatment is to minimise the negative impact of the current exacerbation
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42
Q

Name the differential diagnoses of COPD exacerbation

A
  • pneumonia
  • pneumothorax
  • pleural effusion
  • pulmonary embolism
  • pulmonary oedema
  • cardiac arrhythmias
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43
Q

Describe exacerbation in COPD

A
  • increased short acting bronchodilators are recommended as initial management
  • systemic steroids can improve lung function, oxygenation and shorten recovery time. Duration of therapy should not be more than 5-7 days
  • antibiotics, when indicated, can shorten recovery time, reduce the risk of early relapse, treatment failure. Duration of therapy should be 5-7 days
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44
Q

Describe the approach in clinic in COPD

A
  • confirm the diagnosis of COPD
  • determine if there are additional diagnoses or exacerbating factors, particularly compliance
  • optimise therapy
  • consider surgical options
  • discuss anticipatory care and end of life management
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45
Q

Name the surgical options for COPD

A
  • bullectomy
  • lung volume reduction surgery
  • endobronchial valves and coils
  • lung transplant
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46
Q

Describe bullectomy

A
  • for bullae that occupy more than 50% of the thoracic cavity
  • not without challenge
  • need some other lung expand to take its place
  • giant bullae are often associated with cannabis use
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47
Q

Describe volume reduction surgery

A
  • effective for more heterogenous bullous emphysema
  • surgical removal of the upper lobe(s)
  • rarely done these days
  • must have been through PR
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48
Q

Describe endobronchial valves/coils

A
  • new technology
  • one way valves of self collapsing coils inserted via a bronchoscope
  • block ventilation to bullae, and areas of poor V/Q matching
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49
Q

Describe non-invasive ventilation

A
  • two levels of pressure
  • expiratory positive
  • expiratory positive airway pressure; lowers the work of breathing, overcomes intrinsic PEEP, reduces pCO2
  • inspiratory positive airways pressure; increases tidal volume and minute volume, reduces pCO2
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50
Q

What are the important considerations of non-invasive ventilation

A
  • will the patient tolerate the mask
  • does the patient have an ACP to avoid NIC
  • what will we do if NIV fails
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51
Q

Describe the clinical presentation of pulmonary neoplasia

A
  • local effects; obstruction of the airway, invasion of chest wall, ulceration
  • metastases; nodes, bones, liver, brain
  • systemic effects; weight loss, ectopic hormone production
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52
Q

Describe small cell cancer

A
  • rapidly progressive disease
  • early metastases
  • rarely suitable for surgery, most of the time at first presentation, it has spread beyond the primary site
  • good initial response to chemotherapy
  • the rapid growth of the tumour makes it more susceptible to cytotoxic chemotherapy, often backed up with radiotherapy
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53
Q

Describe non-small cell cancer

A
  • includes squamous and adenocarcinomas
  • curative options are surgery or radical radiotherapy
  • palliative chemotherapy and new targeted treatment
  • account for the majority of lung cancers
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54
Q

Describe cytotoxic chemotherapy

A
  • rarely curative but longer survival
  • better response in small cell cancer
  • major side effects
  • intravenous infusions every 3-4weeks
  • outpatient visits
  • more detailed imaging
  • whole body treatment
  • targets rapidly dividing cells
  • blood brain barrier; prophylactic cranial irradiation
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55
Q

Name some chemotherapy side effects

A
  • nausea and vomiting
  • tiredness
  • bone marrow suppression
  • opportunistic infection
  • anaemia
  • hair loss
  • pulmonary fibrosis
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56
Q

Describe radiotherapy

A
  • ionising radiation
  • usually xrays
  • external beam
  • radical; curative treatment
  • palliative; delaying tactic, useful for metastases
  • well tolerated
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57
Q

Name some cons of radiotherapy

A
  • maximum cumulative dose
  • collateral damage- spinal cord, oesophagus, adjacent lung tissue
  • only goes where you point the beam
  • not suitable for subclinical metastases
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58
Q

Describe stereotatic ablative radiotherapy (SABR)

A
  • many more beams
  • each beam is less powerful;
  • less collateral damage
  • total dose delivered to tumour is higher and more effective
  • 4D scanning required
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59
Q

Describe endobronchial therapy

A
  • stent insertion for stridor
  • photodynamic therapy
  • other laser therapy
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60
Q

Describe histological diagnosis of pulmonary neoplasia

A
  • bronchoscopy and biopsy of the tumour if seen
  • biopsy or needle aspiration metastases (especially mediastinal or supraclavicular lymph nodes)
  • endobronchial ultrasound guided specimens
  • we need a microscope diagnosis and also sufficient tissue for identification of molecular predictor or response to treatment
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61
Q

What is pleural effusion?

A
  • abnormal collection of fluid
  • common presentation of numerous diseases
  • does not always require drainage or sampling
  • large unilateral effusions should raise concern
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62
Q

Describe the workup for pleural effusion

A
  • history and examination
  • PA CXR
  • pleural aspirate
  • biochemistry (transudate or exudate)
  • cytology
  • culture
  • other tests; contrasted enhanced CT chest, repeat pleural tap, pleural biopsy (blind or thorascopy)
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63
Q

Describe the different appearances of pleural effusion and what they suggest

A
  • straw coloured = cardiac failure, hypalbuminaemia
  • bloody = trauma, malignancy, infection, infarction
  • turbid / milky = empyema, chylothorax, smells
  • foul smelling = anaerobic empyema
  • food particles = oesophageal rupture
  • bilateral = LVF (heart failure), PTE, drugs, systemic path
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64
Q

What does transudate mean?

A
  • failure of an organ
  • protein <30g/L
  • heart failure; liver cirrhoisis, hypoalbuminaemia, atelectasis, peritoneal dialysis
  • does not always have a benign aetiology
65
Q

What does exudate mean?

A
  • protein >30g/L
  • malignancy
  • infection including TB
  • pulmonary infarction
  • asbestos
  • always look for serious pathology
66
Q

When would glucose levels be low?

A
  • infection
  • TB
  • rheumatoid arthritis
  • malignancy
  • oesophageal rupture
67
Q

What do cytology and cell counts look for?

A
  • mostly looking for malignant cells
  • lymphocytes - think TB, malignancy, although any long standing effusion will eventually become lymphocytic
  • neutrophils suggest an acute process
68
Q

Why can a biopsy be negative?

A
  • technique is wrong, biopsy does not contain pleura
  • the involvement of pleural disease is discontinuous
  • the effusion is ancillary to malignancy but not malignant
69
Q

Describe mesothlioma

A
  • ASBESTOS
  • uncommon malignant tumour of the lining of the lung or very occasionally of the lining of the abdominal cavity
  • likelihood of developing mesothelioma increases with the degree and the length of time exposed to asbestos
  • often takes 30-40 years to develop
  • may cause breathlessness, chest pain, weight loss, fever, sweating and cough
70
Q

Name the asbestos fibre types

A
  • chrysotile (white asbestos, most common)
  • amosite (brown asbestos)
  • crocidolite (most dangerous)
71
Q

Name the investigations for mesothelioma

A
  • imaging; pleural nodularity, circumferential pleural thickening, local invasion, lung entrapment
  • pleural fluid aspiration; low cytological yield, avoid repeated aspiration
  • biopsy; thoracoscopy or CT/US guided
72
Q

Name the mesothelioma treatments

A
  • pleurodeses effusions
  • radiotherapy
  • surgery
  • chemotherapy
  • palliative care
  • report death to fiscal
73
Q

Describe the treatment of malignant pleural effusion

A
  • palliate symptoms
  • repeated pleural taps
  • drain and or pleurodesis (talc slurry or during thoracoscopy)
  • long term pleural catheters
  • surgical options (abrasion, pluerectomy)
74
Q

What are the complications of talc slurry?

A
  • minor pleuritic pain and fever
  • pneumonia
  • respiratory failure
  • talc pneumonitis/ ARDS
  • secondary empyema
  • local tumour implantation at port site in mesothelioma
75
Q

Describe long term pleural catheters

A
  • designed to allow patients to control their effusion and therefore their symptoms
  • inserted mostly in patients with malignant effusions
  • may need an overnight stay
  • drain is designed to remain in place for lifer though some people will stop producing pleural fluid
  • vacuum in drainage bottle that provides suction to drain pleural fluid
  • initially people will need to drain daily for a week or so
  • never drain more than 1 litre per day
76
Q

What are the complications of long term pleural catheters?

A
  • incorrect placement
  • bleeding
  • infection
  • flying can be tricky
  • bath or swim can be done but not recommended
  • 10 inserted each year
77
Q

Name investigations for pneumothorax investigations

A
  • chest xray; measured at hilar level not apex

- CT chest; useful to differentiate bullous lung disease or small pneumothoraxes

78
Q

What is the management of a pneumothorax?

A
  • oxygen even if no drain
  • no treatment if asymptomatic and small
  • aspiration 1st line in PSP; avoids chest drain, time consuming, may fail
  • chest drain
  • may need suction
  • surgical intervention
79
Q

What are the surgical intervention indicators for pneumothorax?

A
  • second ipsilateral ptx
  • first contralateral ptx
  • bilateral spontaneous ptx
  • persistent air leak
  • risk professions (pilots, drivers) after first ptx
80
Q

Describe the presentation of pneumothorax

A
  • PSP may be asymptomatic even if moderately sized
  • SSP usually symptomatic even if small
  • acute onset pleuritic chest pain
  • SOB, hypoxia
  • sings; tachycardia, hype-resonant percussion note, reduced expansion, quiet breath sounds on auscultation
81
Q

Describe tension pneumothorax

A
  • emergency, can lead to cardiac arrest
  • one way valve, progressively increasing pressure in pleural space
  • pushes other chest organs to opposite side of affected side
  • acute respiratory distress
  • signs; deviated trachea, hypotension, raised JVP, reduced air entry on affected side
82
Q

What is the treatment for tension pneumothorax?

A
  • needle decompression
  • usually a large bore venflon
  • second intercostal space anteriorly, mid-clavicular line
83
Q

Describe pleural infection

A
  • increasing incidence especially extremes of age
  • significant mortality (up to 20%)
  • does not necessarily follow pneumonia
  • can rapidly coagulate and organise to form fibrous peels even with antibiotics
  • do not let the sun set on a potentially infected pleural space
84
Q

Name some risks of pleural infections

A
  • diabetes mellitus
  • immuno-suppression including corticosteroids
  • gastro-oesophageal reflux
  • alcohol misuse
  • intravenous drug abuse
  • many patients have no apparent risk factors
85
Q

Name the types of pleural infections

A
  • simple parapneumonic effusion
  • complicated parapneumonic effusion
  • empyema
  • quickly sample pleural fluid to identify parapneumonic effusions that require urgent tube drainage
86
Q

Describe the management of pleural infection

A
  • antibiotics (often for several weeks)
  • drain effusion needed
  • early discussion with surgeons if persistent sepsis
  • nutrition
  • VTE prophylaxis
  • reassess patients who don’t improve
  • IV antibiotics for a week and then oral antibiotics for 6 weeks
87
Q

What shape of bacteria is m. TB?

A

rod shaped gram positive bacillus

88
Q

How is TB transmitted?

A

Through the aerosol route, bacillus is small enough to travel in the droplet

89
Q

Who gets TB?

A
  • immigrants
  • people who have had recent contact with someone who has TB
  • socially deprived
  • immunosuppressed
90
Q

Name the symptoms of TB

A
  • weight loss
  • night fevers / sweats
  • loss of appetite
  • coughing
  • haemoptysis
  • breathlessness
  • fatigue
  • chills
91
Q

What are the two types of TB?

A
  • primary

- reactivated

92
Q

What drugs are given for treatment of active TB?

A
  • 4 drugs for 2 months; rifampicin, isoniazid, pyrazinamide, ethambutol
  • 2 drugs for a further 4 months; rifampicin, isoniazid
93
Q

What drugs are given for treatment of latent TB?

A
  • 2 drugs for 3 months; rifampicin, isoniazid

- or 1 drug for 6 months; isoniazid

94
Q

What is the initial intracellular primary niche of MTB?

A

the macrophage

95
Q

At which anatomical location is the distinction between upper and lower respiratory tract infections?

A

Above the vocal cords is upper respiratory tract infections

Below the vocal cords is lower respiratory tract infections

96
Q

What do viral throat swab tests test for?

A
  • influenza A
  • influenza B
  • RSV
  • metapneumovirus
  • rhinovirus (particularly bad in asthmatic patients)
  • coronavirus
  • parainfluenza
  • adenovirus
  • enterovirus
  • parechovirus
97
Q

Describe strep throat

A
  • exudate (goo)
  • pus
  • sore throat
  • dysphagia
  • dysphonia
  • majority caused by virus
  • do not recommend bacterial swabs or antibiotics
98
Q

Describe tonsillitis

A
  • swollen tonsils
  • erythematous
  • dysphagia
  • recurrent = tonsillectomy
  • tonsils are lymphoid tissue
  • patients with bacterial infection will benefit from antibiotics
99
Q

What is the fever pain score?

A
  • used to help guide whether antibiotics are recommended or not
  • fever during previous 24 hours
  • purulence
  • attended rapidly
  • severely inflamed tonsils
  • no cough or coryza
100
Q

Describe quinsy

A
  • complication of tonsillitis
  • pre-tonsillar abscess
  • can be drained but must be aware of the internal carotid artery
  • airway obstruction - ludwigs angina
  • IV antibiotics and surgical drainage
  • retropharyngeal abscess
  • sepsis
  • can be described as ‘hot potato’
  • patients present being unable to swallow
101
Q

Describe epiglottitis

A
  • emergency situation
  • seen predominantly in infants
  • infection means it swells = airway obstruction
  • historically associated with influenza B
  • now most cases are usually strep pneumonia, pyrogenes or staph aureus
  • airway must be secured with and ET tube
  • urgent IV antibiotics - ceftriaxone, vancomycin or clindamycin
102
Q

Describe coryza (common cold)

A
  • acute viral infection of the nasal passages
  • often accompanied by sore throat
  • sometimes a mild fever
  • spread by droplets and fomites
  • complications can include sinusitis or acute bronchitis
103
Q

Describe sinusitis

A
  • frontal headache
  • retro-orbital pain
  • maxillary sinus pain
  • tooth ache
  • discharge
  • sinuses drain into the nose
104
Q

Describe acute sinusitis

A
  • preceded by a common cold
  • purulent nasal discharge
  • most viral aetiology
  • usually self limited
  • resolves in ten days
  • some need antibiotics
  • nasal decongestant; oxymetazoline
  • nasal steroids
  • pseudo-ephedrine
105
Q

Describe diphtheria

A
  • obstructs airway
  • life threatening due to toxin production
  • characteristic pseudo membrane
106
Q

Name some lower respiratory tract infections

A
  • acute bronchitis
  • acute exacerbation of COPD
  • pneumonia
  • influenza
  • fungal infection
107
Q

Describe acute bronchitis

A
  • the cold which ‘goes to the chest’
  • often preceded by common cold
  • clinical features; productive cough, fever, normal chest examination, normal chest x-ray, may have a transient wheeze
  • usually viral symptoms
  • cough really burns in the centre of the chest
  • treatment; usually self limiting and analgesia recommended. Can lead to significant morbidity in patients with chronic lung disease
108
Q

Describe an acute exacerbation of COPD

A
  • may be preceded by an URT infection
  • increased sputum production, increased sputum purulence, more wheezy, breathlessness
  • on examination; respiratory distress, wheeze, coarse crackles, may be cyanosed (in advanced disease- worsening ankle oedema)
  • management in primary care; antibiotics (doxycycline, amoxicillin), bronchodilator inhalers, short course of steroids in some cases
  • refer to hospital if; evidence of respiratory failure or not coping at home
109
Q

In which disease would red hepatisation of the lung occur?

A

In pneumonia

110
Q

Name the symptoms of pneumonia

A
  • malaise
  • anorexia
  • sweats
  • rigors (uncontrollable shaking)
  • myalgia
  • headache
  • arthralgia
  • confusion
  • cough
  • pleurisy
  • haemoptysis
  • dyspnoea
  • preceding URTI
  • abdominal pain
  • diarrhoea
111
Q

Name the signs of pneumonia

A
  • fevers
  • rigors
  • herpes labialis
  • tachypnoea
  • crackles
  • rub
  • cyanosis
  • hypotension
112
Q

When is a sputum sample sent?

A

If there is persistent or recurrent infection

113
Q

Name the investigations for pneumonia

A
  • blood culture
  • serology
  • arterial gases
  • full blood count
  • urea
  • liver function
  • chest x-ray
114
Q

What is CURB65?

A
  • severity score for community acquired pneumonia
  • c= new onset of confusion
  • u = urea >7
  • r = respiratory rate >30/min
  • b = blood pressure systolic <90 or diastolic <61
  • 65 years or older
115
Q

Name some other severity markers for pneumonia

A
  • temperature <35 or >40
  • cyanosis PaO2<8kPa
  • WBC <4 or >30
  • multi-lobar involvement
116
Q

Describe the management o community acquired pneumonia

A
  • antibiotics; doxycycline, amoxicillin
  • oxygen; maintain SaO2 94-98% or 89-92%
  • fluids
  • bed rest
  • no smoking
117
Q

What disease is associated with contact with birds?

A

Psittacosis

118
Q

Describe legionella

A
  • chest symptoms may be minimal
  • GI disturbance is common
  • confusion is common
  • levofloxacin
  • can catch from stagnant water
119
Q

When are IV antibiotics given?

A
  • when oral route isn’t available
  • sensitivities; drug resistant organisms (pseudomonas)
  • deep seated infection- abscesses, bone endocarditis, meningitis
  • first rapid- rapid increase in plasma concentrations
120
Q

Name the complications of pneumonia

A
  • respiratory failure
  • pleural effusion
  • empyema
  • death
121
Q

Describe the clinical presentation of influenza

A
  • fever; high, abrupt onset
  • malaise
  • myalgia
  • headache
  • cough; initially dry but becomes productive
  • prostration
  • generally feeling unwell
122
Q

Name the complications of flu

A
  • primary influenzal pneumonia; high mortality, seen in young adults, seen most during pandemic years
  • secondary bacterial pneumonia; more common in infants, elderly and debilitated, pre-existing disease and pregnant women, most common cause of death in fatal influenza
  • bronchitis
  • otitis media
  • influenza during pregnancy may also be associated with perinatal mortality, prematurity, smaller neonatal size and lower birth weight
123
Q

What disease should be thought of if there is shadowing in the upper zone cavities?

A

Tuberculosis

124
Q

Name some risk factors for developing chronic pulmonary infection

A
  • abnormal host response; immunodeficiency, immunosuppression
  • abnormal innate host defence; damages bronchial mucosa, abnormal cilia, abnormal secretions
  • repeated insult; aspiration, indwelling material
125
Q

Name some drugs or treatments which can be immunosuppressive

A
  • steroids
  • azathioprine
  • methotrexate
  • cyclophosphamide
  • monoclonal antibodies
  • chemotherapy
126
Q

Name some forms of chronic infection

A
  • intrapulmonary abscess
  • empyema
  • chronic bronchial sepsis
  • bronchiectasis
  • cystic fibrosis
127
Q

Describe the presentation of intrapulmonary abscesses

A
  • indolent presentation
  • weight loss common
  • lethargy; tiredness, weakness
  • cough +/- sputum
  • high mortality if not treated
  • usually a preceding illness of some sort; pneumonic infection, post viral, foreign body
128
Q

Describe the features of a simple parapneumonic effusion

A
  • clear fluid
  • ph >7.2
  • LDH <1000
  • glucose >2.2
129
Q

Describe complicated parapneumonic effusion

A
  • ph <7.2
  • LDH >1000
  • glucose < 2.2
  • requires chest tube drainage
130
Q

What is the D sign?

A

Empyemas are sticky and keep shape despite gravity (unlike effusion) so can appear as a d shape on scans

131
Q

Describe bronchiectasis

A
  • localised, irreversible dilation of the bronchial tree,
  • involved bronchi are dilate, inflamed and easily collapsible
  • airflow obstruction
  • impaired clearance of secretions
  • recurrent sputum production
132
Q

Describe the presentation of bronchiectasis

A
  • recurrent chest infections
  • recurrent antibiotic prescriptions
  • no response to antibiotics
  • short lived response to antibiotics
133
Q

What would CT scans show for bronchiectasis?

A
  • dilation of the airways, thickening of bronchial walls, lack of tapering airways
  • airways is larger in diameter than the accompanying pulmonary artery
134
Q

Name the causes of bronchiectasis

A
  • 50% idiopathic
  • bronchial obstruction
  • cystic fibrosis
  • youngs syndrome
  • kartanagers syndrome
  • ABPA
  • immunodeficiency
    rheumatoid arthritis
  • bronchopulmonary sequestrian
  • mounier-khun syndrome
  • yellow nail syndrome
  • traction bronchiectasis associated with pulmonary fibrosis
135
Q

What diseases feature failure of the mucociliary escalator?

A
  • cystic fibrosis
  • youngs syndrome
  • kartanagers syndrome
136
Q

Name the treatment options for bronchiectasis

A
  • stop smoking
  • flu vaccine
  • pneumococcal vaccine
  • reactive antibiotics; send sputum sample
  • when colonised with persistent bacteria; oral macrolide antibiotics, nebulised gentamicin, colomycin , pulsed IV abx. alternating oral antibiotics
137
Q

How would you treat acute exacerbations of bronchiectasis?

A
  • 2 weeks of antibiotics appropriate to the most recent positive sputum sample
  • send sputum every time
  • alter antibiotics if the sputum culture shows resistant organism
  • aggressively eradicate pseudomonas aeriginosa
138
Q

How many people carry the gene for cystic fibrosis?

A

1 in 25 people carry the gene

139
Q

What type of genetic disorder is CF?

A

Recessively inherited gene disorder

140
Q

Specifically, which molecule is affected by CF?

A

Cystic fibrosis trans-membrane conductance regulator

141
Q

What happens if there is no CFTR protein present or an abnormal CFTR protein?

A

This means there is no negative reinforcement of ENAC and Na+ can move into the cell freely. This causes water to flow out of the cell meaning secretions are much thicker as the is less water

142
Q

Name the consequences of CF

A
  • salty sweat
  • intestinal blockage
  • fibrotic pancreas
  • failure to thrive
  • recurrent bacterial lung infections
  • congenital bilateral absence of vas deferens
  • filled sinuses
  • gallbladder and liver disease
143
Q

Describe class 1 cf

A
  • no CFTR synthesis

- die in utero, not compatible with life

144
Q

Describe class 2 CF

A
  • delta f508
  • CFTR trafficking defect, cftr is made but not the correct shape
  • most common defect
  • die in 30s and 40s
145
Q

Describe class 3 CF

A
  • dysregulation of CFTR

- channel created but will not open

146
Q

Describe class 4 CF

A
  • defective chloride conductance or channel gating

- channel half open

147
Q

Describe class 5 CF

A
  • reduced CFTR transcription and synthesis
148
Q

In CF patients, if staph aureus was colonised, what treatment would be given?

A
  • oral flucloxacillin

- oral septrin

149
Q

In CF patients, if pseudomonas was colonised what treatment would be given?

A
  • oral azithromycin
  • nebulised colomycin
  • nebulised tobramycin
  • nebulised aztreoanam
  • inhaled tobramycin
150
Q

Describe endocrine failure

A
  • destruction of pancreatic islet cells, patty replacement of pancreatic tissues
  • annual OGTT,CGMS
  • usually need insulin as they have insulin production failure
151
Q

Describe exocrine failure

A
  • sludged up ducts, failure of secretion of lipases (amylases), digestive failure
  • give creon
  • patients hate taking it
152
Q

Describe DIOS

A
  • thick mucus blocks up the large and small intestine
  • symptoms similar to constipation
  • treatment; gastrograffin, laxido, fluids
  • prevention; laxido, hydration, keep moving
153
Q

What composes exacerbation management in CF patients?

A
  • antibiotics
  • physiotherapy; autogenic drainage, ACBT, with and without a physiotherapist
  • adequate hydration
  • increased dietary input; dietician, fridge in room
154
Q

Name the oral antibiotics used for CF patients

A
  • augmentin
  • flucloxacillin
  • minocycline
  • septrin
  • fusidin
  • ciprofloxacin
155
Q

Describe OHPAT

A
  • treatment at home for CF patients
  • start antibiotics as an inpatient, finish at home
  • 2 weeks antibiotics at home
  • well tolerated
  • safe
  • saves money
  • keeps patients at home
156
Q

Describe Ivacaftor

A
  • CFTR potentiator, opens the channel
  • improves chloride flow through the CFTR
  • tablet, twice a day
  • cant have grapefruit juice
157
Q

Describe symkevi

A
  • tezecaftor and ivacaftor
158
Q

Describe lung transplantation in CF patients

A
  • bilateral lung transplantation
  • consider once FEV1 <40%
  • patients with M abscesses no eligible
  • psychological assessment is key

Respiratory (7 decks)

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