Respiratory Presentations Flashcards

1
Q

What are the basics of adult life support?

A

-30:2 compression rate

-Chest compressions are continued while defibrillator charges

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2
Q

What are the types of rhythms in cardiac arrest (2 types)

A
  • shockable (VT/ pulseless VT)
  • non-shockable (asystole/ PEA)
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3
Q

what is meant by non-shockable rhythms?

A
  • organised cardiac electrical activity in the absence of any palpable pulses
  • caused by issues which don’t allow the heart to pump properly.
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4
Q

what are some causes of PEA

A
  • Tension pathologies
    (PE, Cardiac tamponade, tension pneumothorax)
  • ischaemia/ hypoxia
  • hypovalemia
  • acidosis
  • hyperthermia
    -hyperkalemia
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5
Q

Managment of Non- shockable rhythms?

A
  • 30:2 compression and breath rate.
  • continue compressions while the AED charges up.
  • 1mg of adrenaline which is given every 3-5 minutes

amiodarone 300 mg should be given to patients who are in VF/pulseless VT after 3 shocks have been administered.

amiodarone 300 mg should be given to patients who are in VF/pulseless VT after 3 shocks have been administered.

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6
Q

Managment of non- shockable rhythms?

A

30:2 compressions to resuce breaths.

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7
Q

Alteplase

A

Tissue plasminogen activator
thrombolytic agent

encourages thrombolysis

CPR should be continued for an extended period of 60-90 minutes

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8
Q

anitbodies associated with Churg Strauss Syndrome

A
  • MPO-ANCA
  • P-ANCA positive antibodies
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9
Q

Churg-Strauss syndrome

A

Eosinophilic granulomatosis with polyangiitis (EGPA), is a rare autoimmune condition characterized by inflammation of blood vessels (vasculitis)

various organs affected, but mostly affects small and medium- sized blood vessels

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10
Q

causes of Churg-strauss

A

Believed to involve an abnormal immune response, possibly triggered by an allergic reaction.

Eosinophils, a type of white blood cell, play a significant role in the inflammation process in this condition.

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11
Q

Symptoms assoicated with Churg-Strauss

A
  • asthma
  • sinusitis
  • allergic rhinitis
  • skin rashes
  • peripheral neuropathy
  • gastrointestinal problems,
  • symptoms related to kidney or heart involvement.
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12
Q

Myocardial infarction (description and patient likely to have)

A

Cardiac-sounding pain
heavy, central chest pain they may radiate to the neck and left arm
nausea, sweating
elderly patients and diabetics may experience no pain

Risk factors for cardiovascular diseas

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13
Q

Pneumothorax: when to suspect

A

History of asthma, Marfan’s etc
Sudden dyspnoea and pleuritic chest pain

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14
Q

Pulmonary embolism

A

Sudden dyspnoea and pleuritic chest pain
Calf pain/swelling
Current combined pill user, malignancy

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15
Q

Pericarditis

A

Sharp pain relieved by sitting forwards
May be pleuritic in nature

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16
Q

Dissecting aortic aneurysm

A

‘Tearing’ chest pain radiating through to the back
Unequal upper limb blood pressure

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17
Q

Gastro-oesophageal reflux disease

A

Burning retrosternal pain
Other possible symptoms include regurgitation and dysphagia

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18
Q

Musculoskeletal chest pain

A

One of the most common diagnoses made in the Emergency Department. The pain is often worse on movement or palpation.

May be precipitated by trauma or coughing

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19
Q

shingles

A

pain oftern preceeded by rash

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20
Q

what is aortic dissection ?

A

Flap or filling defect within the aortic intima.
Blood tracks into the medial layer and splits the tissues with the subsequent creation of a false lumen. ascending aorta or just distal to the left subclavian artery (less common).
Afro-carribean males aged 50-70 years.

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21
Q

Presentation of aortic dissection

A

Patients usually present with a tearing intrascapular pain, which may be similar to the pain of a myocardial infarct.
The dissection may spread either proximally or distally with subsequent disruption to the arterial branches that are encountered.

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22
Q

Type A and Type B aortic dissection

A
  • Stanford classification system
  • (Type A)-ascending aorta
  • (Type B)- descending aorta, typically beyond the left subclavian artery.
  • Type A lesions are usually treated surgically
  • Type B lesions are usually managed non operatively.
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23
Q

PE ECG findings

A

Diagnosis may be suggested by various ECG findings including
* S waves in lead I, Q waves in lead III
* inverted T waves in lead III.
—————————–
* Confirmation of the diagnosis is usually CTPA

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24
Q

treatment of PE

A

Treatment is with anticoagulation, in those patients who develop a cardiac arrest or severe compromise from their PE, consideration may be given to thrombolysis.

  • altepase
  • rivoraxiban
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25
Q

Diagnosis of MI

A

ECG changes (and cardiac enzyme changes). Inferior and anterior infarcts may be distinguished by the presence of specific ECG changes (usually II, III and aVF for inferior, leads V1-V5 for anterior).

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26
Q

treatment of MI

A

PCI in 120 mins of presentation

oral antiplatelet agents, primary coronary angioplasty and/ or thrombolysis.

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27
Q

perforated peptic ulcer presentation

A

Patients usually develop sudden onset of epigastric abdominal pain, it may be soon followed by generalised abdominal pain.

pain of gastric ulcer is typically worse immediately after eating.

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28
Q

Diagnosis of perforated peptic ulcer

A

erect chest x-ray which may show a small amount of free intra-abdominal air (very large amounts of air are more typically associated with colonic perforation).

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29
Q

Managment of perforated peptic ulcer

A

laparotomy, small defects may be excised and overlaid with an omental patch, larger defects are best managed with a partial gastrectomy.

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30
Q

Boerhaaves syndrome

A

Spontaneous rupture of the oesophagus that occurs as a result of repeated episodes of vomiting.

Rupture is usually distally sited and on the left side.

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31
Q

presentation of Bohaaves syndrome

A

Patients usually give a history of sudden onset of severe chest pain that may complicate severe vomiting.
Severe sepsis occurs secondary to mediastinitis.

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32
Q

Bohavees syndrome diagnosis

A

Diagnosis is CT contrast swallow.

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33
Q

Bohavees syndrome managment

A

thoracotomy and lavage, if less than 12 hours after onset then primary repair is usually feasible, surgery delayed beyond 12 hours is best managed by insertion of a T tube to create a controlled fistula between oesophagus and skin.
Delays beyond 24 hours are associated with a very high mortality rate.

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34
Q

Anteroseptal

A

V1-V4 Left anterior descending

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35
Q

Inferior

A

II, III, aVF Right coronary

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36
Q

anterior lateral region

A

V1-6, I, aVL Proximal left anterior descending

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37
Q
A
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38
Q

lateral region

A

I, aVL +/- V5-6 Left circumflex

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39
Q

posterior region

A

Changes in V1-3

Reciprocal changes of STEMI are typically seen:
horizontal ST depression
tall, broad R waves
upright T waves
dominant R wave in V2

Posterior infarction is confirmed by ST elevation and Q waves in posterior leads (V7-9) Usually left circumflex, also right coronary

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40
Q

features of lung cancer (9)

A

persistent cough
haemoptysis
dyspnoea
chest pain
weight loss and anorexia
hoarseness
seen with Pancoast tumours pressing on the recurrent laryngeal nerve
superior vena cava syndrome

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41
Q

3 exam findings of lung cancer

A
  • a fixed, monophonic wheeze may be noted
  • supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
  • clubbing
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42
Q

paraneoplastic features of SCLC

A

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

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43
Q

Paraneoplastic squamous cell cancer

A

parathyroid hormone-related protein (PTH-rp) secretion causing hypercalcaemia
clubbing
hypertrophic pulmonary osteoarthropathy (HPOA)
hyperthyroidism due to ectopic TSH

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44
Q

Paraneoplastic adenocarcinoma

A

gynaecomastia
hypertrophic pulmonary osteoarthropathy (HPOA)

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45
Q

presentation of acute brochitits

A

cough: may or may not be productive
sore throat
rhinorrhoea
wheeze

usually normal chest exaination, however some patients will also have

Low-grade fever
Wheeze

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46
Q

bronchitis vs pneumonia

A

History: Sputum, wheeze, breathlessness may be absent in acute bronchitis whereas at least one tends to be present in pneumonia.
Examination: No other focal chest signs (dullness to percussion, crepitations, bronchial breathing) in acute bronchitis other than wheeze. Moreover, systemic features (malaise, myalgia, and fever) may be absent in acute bronchitis, whereas they tend to be present in pneumonia.

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47
Q

Investigations of bronchitits

A

acute bronchitis is typically a clinical diagnosis
however, if CRP testing is available this may be used to guide whether antibiotic therapy is indicated

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48
Q

Managment of bronchitits

A

analgesia
good fluid intake
consider antibiotic therapy if patients:
are systemically very unwell
have pre-existing co-morbidities
have a CRP of 20-100mg/L (offer delayed prescription) or a CRP >100mg/L (offer antibiotics immediately)
NICE Clinical Knowledge Summaries/BNF currently recommend doxycycline first-line
doxycycline cannot be used in children or pregnant women
alternatives include amoxicillin

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49
Q

acute bronchitis

A

Result of inflammation of the trachea and major bronchi and is therefore associated with oedematous large airways and the production of sputum.

The disease course usually resolves before 3 weeks, however, 25% of patients will still have a cough beyond this time

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50
Q

viral URTI (aka cold/ coryzal symptoms)

A

Upper respiratory tract infections involve the mucosa of the nasal cavity, sinuses, nasopharynx, oropharynx and larynx.

Most commonly caused by rhinovirus

Other viruses include adenoviruses, influenza, parainfluenza, respiratory syncytial virus and enteroviruses.

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51
Q

epidemiology of URTI

A

Adults may be affected by URTIs 2-3 times per year on average, but children may average up to 5-6 infections

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52
Q

coryzal symptoms

A

The most common symptoms are nasal discharge, nasal obstruction, sore throat, headache, cough, tiredness and general malaise. Other symptoms include facial pain, earache, hoarseness and nausea.

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53
Q

signs of colds

A

Erythema or injection of the back of the throat
Nasal discharge
Tender cervical lymphadenopathy
Mild fever

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54
Q

assessment of coryzal symptoms

A

Examination of throat, ears and cervical lymph nodes
Respiratory examination to exclude pneumonia, significant wheeze etc
Assess hydration status, especially in young children and the elderly
Basic observations (heart rate, blood pressure, respiratory rate, temperature, oxygen saturations) - if significantly abnormal may need to consider other causes e.g. sepsis

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55
Q

useful features of assessments for coryzal symptoms (2 scales)

A

Children under 5 - NICE fever traffic light system

FeverPAIN score - used to assess likelihood of Strep infection in adult with sore throat and guide decision making re antibiotic usage

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56
Q

Investigations for coryzal symptoms

A

Generally not needed in healthy adults
May be required in less straightforward cases where more serious infections may present with similar symptoms e.g. baby/infant with fever, immunocompromised adult
Viral throat swabs may be needed in certain cases e.g. adult with suspected influenza being admitted to hospital for infection control purposes

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57
Q

Managment of coryzal symptoms

A

Supportive management only is usually sufficient
Admission for supportive care may be required in frail or elderly patients with low physiological reserve or multiple comorbidities
An uncomplicated cold in a healthy adult usually resolves in 7-10 days but may last up to 3 weeks
Provide reassurance that condition is self-limiting and recovery will not be aided by antibiotics
Advise paracetamol, fluids, rest and over the counter remedies if appropriate

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58
Q

Complications of coryzal symptoms

A

Sinusitis
Otitis media
Secondary bacterial infection e.g. pneumonia
Exacerbations of pre-existing respiratory conditions such as asthma, or COPD
Viral wheeze, bronchiolitis and croup in infants and young children

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59
Q

types of lung function tests

A
  • spirometry
  • peak expiratory flow (PEF)
    -PEC
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60
Q

obstructive lung function finding

A

FEV1 - significantly reduced
FVC - reduced or normal
FEV1% (FEV1/FVC) - reduced

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61
Q

examples of obstructive diseases

A

Asthma
COPD
Bronchiectasis
Bronchiolitis obliterans

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62
Q

restrictive lung function finding

A

FEV1 - reduced
FVC - significantly reduced
FEV1% (FEV1/FVC) - normal or increased

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63
Q

restriction lung disease examples

A

Pulmonary fibrosis
Asbestosis
Sarcoidosis
Acute respiratory distress syndrome
Infant respiratory distress syndrome
Kyphoscoliosis e.g. ankylosing spondylitis
Neuromuscular disorders
Severe obesity

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64
Q

pleural plaques

A

Pleural plaques are benign and do not undergo malignant change. They, therefore don’t require any follow-up. They are the most common form of asbestos-related lung disease and generally occur after a latent period of 20-40 years.

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65
Q

Pleural thickening

A

Asbestos exposure may cause diffuse pleural thickening in a similar pattern to that seen following an empyema or haemothorax. The underlying pathophysiology is not fully understood.

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66
Q

Asbestosis

A

The severity of asbestosis is related to the length of exposure.

This is in contrast to mesothelioma where even very limited exposure can cause disease.

The latent period is typically 15-30 years. Asbestosis typically causes lower lobe fibrosis.

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67
Q

Features of asbestosis

A

Features
dyspnoea and reduced exercise tolerance
clubbing
bilateral end-inspiratory crackles
lung function tests show a restrictive pattern with reduced gas transfer

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68
Q

Treatment of asbestosis

A
  • convervative mangament
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69
Q

Mesothelioma

A

Mesothelioma is a malignant disease of the pleura. Crocidolite (blue) asbestos is the most dangerous form.

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70
Q

Features of mesothelioma

A

progressive shortness-of-breath
chest pain
pleural effusion

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71
Q

Managment of mesothelioma

A

Patients are usually offered palliative chemotherapy and there is also a limited role for surgery and radiotherapy.
Unfortunately, the prognosis is very poor, with a median survival from diagnosis of 8-14 months.

Symptomatic
Industrial compensation
Chemotherapy, Surgery if operable
Prognosis poor, median survival 12 months

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72
Q

Investigations of mesothelioma

A

suspicion is normally raised by a chest x-ray showing either a pleural effusion or pleural thickening
the next step is normally a pleural CT
if a pleural effusion is present fluid should be sent for MC&S, biochemistry and cytology (but cytology is only helpful in 20-30% of cases)
local anaesthetic thoracoscopy is increasingly used to investigate cytology negative exudative effusions as it has a high diagnostic yield (around 95%)
if an area of pleural nodularity is seen on CT then an image-guided pleural biopsy may be used

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73
Q

Pathophys of mesothelioma

A

Malignancy of mesothelial cells of pleura
Metastases to contralateral lung and peritoneum
Right lung affected more often than left

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74
Q

features of mesothelioma

A

Dyspnoea, weight loss, chest wall pain
Clubbing
30% present as painless pleural effusion
Only 20% have pre-existing asbestosis
History of asbestos exposure in 85-90%, latent period of 30-40 years

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75
Q

features of pleural effusion

A
  • exudative causes
  • transudative causes
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76
Q

transudate causes of pleural effusion

A

(< 30g/L protein)
heart failure (most common transudate cause)
hypoalbuminaemia
liver disease
nephrotic syndrome
malabsorption
hypothyroidism
Meigs’ syndrome

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77
Q

exudative causes of pleural effusion

A

(> 30g/L protein)
infection
pneumonia (most common exudate cause),
tuberculosis
subphrenic abscess
connective tissue disease
rheumatoid arthritis
systemic lupus erythematosus
neoplasia
lung cancer
mesothelioma
metastases
pancreatitis
pulmonary embolism
Dressler’s syndrome
yellow nail syndrome

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78
Q

features of pleural effusion

A

dyspnoea, non-productive cough or chest pain are possible presenting symptoms
classic examination findings include dullness to percussion, reduced breath sounds and reduced chest expansion

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79
Q

imaging of pleural effusion

A

posterioranterior (PA) chest x-rays should be performed in all patients
ultrasound is recommended: it increases the likelihood of successful pleural aspiration and is sensitive for detecting pleural fluid septations
contrast CT is now increasingly performed to investigate the underlying cause, particularly for exudative effusions

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80
Q

pleural effusion aspiration approach

A

ultrasound is recommended to reduce the complication rate
a 21G needle and 50ml syringe should be used
fluid should be sent for pH, protein, lactate dehydrogenase (LDH), cytology and microbiology

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81
Q

Light’s criteria for pleural effusion

A

Exudates typically have higher protein concentration and LD activity and lower pH and glucose values than transudates

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82
Q

BTS criteria for borderline cases

A

exudates have a protein level of >30 g/L, transudates have a protein level of <30 g/L
if the protein level is between 25-35 g/L, Light’s criteria should be applied. An exudate is likely if at least one of the following criteria are met:
pleural fluid protein divided by serum protein >0.5
pleural fluid LDH divided by serum LDH >0.6
pleural fluid LDH more than two-thirds the upper limits of normal serum LDH

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83
Q

other characteristics for pleural effusion

A

low glucose: rheumatoid arthritis, tuberculosis
raised amylase: pancreatitis, oesophageal perforation
heavy blood staining: mesothelioma, pulmonary embolism, tuberculosis

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84
Q

Managment of pleural effusion

A

recurrent aspiration
pleurodesis
indwelling pleural catheter
drug management to alleviate symptoms e.g. opioids to relieve dyspnoea

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85
Q

Well’s criteria

A

Objectifies risk of pulmonary embolism.
- PE likely diagnosis
- clinical signs of DVT
-HR greater than 100
-Hemoptysis
-Immobilization at least 3 days OR surgery in the previous 4 weeks
Previous, objectively diagnosed PE or DVT
Malignancy w/ treatment within 6 months or palliative

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86
Q

Spontaneous pneumothorax

A

-primary spontaneous pneumothorax (PSP):

Occurs without underlying lung disease, often in tall, thin, young individuals. PSP is associated with the rupture of subpleural blebs or bullae.

-secondary spontaneous pneumothorax (SSP):

Occurs in patients with pre-existing lung disease, such as COPD, asthma, cystic fibrosis, lung cancer, Pneumocystis pneumonia. Certain connective tissue diseases such as Marfan’s syndrome are also a risk factor

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87
Q

traumatic pneumothorax

A

results from penetrating or blunt chest trauma, leading to lung injury and pleural air accumulation.

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88
Q

Iatrogenic causes of pneumothorax

A

occurs as a complication of medical procedures, such as thoracentesis, central venous catheter placement, ventilation, including non-invasive ventilation or lung biopsy.

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89
Q

tension pneumothorax

A

severe pneumothorax resulting in the displacement of mediastinal structures that may result in severe respiratory distress and haemodynamic collapse.

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90
Q

Catamenial pneumothora

A

3-6% of spontaneous pneumothoraces occurring in menstruating women. It is thought to be caused by endometriosis within the thorax.

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91
Q

Signs and symptoms of pneumothorax

A

Symptoms tend to come on suddenly:
dyspnoea
chest pain: often pleuritic

Signs
hyper-resonant lung percussion
reduced breath sounds
reduced lung expansion
tachypnoea
tachycardia

92
Q

signs and symptoms of tension pneumothorax

A

respiratory distress
tracheal deviation away from the side of the pneumothorax
hypotension

93
Q

Bronchiectasis

A

Bronchiectasis describes a permanent dilatation of the airways secondary to chronic infection or inflammation. There are a wide variety of causes are listed below:

94
Q

features of bronchoectasis

A

persistent productive cough. Large volumes of sputum may be expectorated
dyspnoea
haemoptysis

95
Q

Signs and symptoms of bronchectasis

A

abnormal chest auscultation
coarse crackles
wheeze
clubbing may be present

96
Q

Investigations for bronchectasis

A

High-resolution computed tomography (HRCT) scan of the chest
Chest X-ray
Pulmonary function tests (spirometry)
Sputum culture and analysis
Bronchoscopy

97
Q

causes of bronchectasis

A

Post-infectious (resulting from severe or recurrent respiratory infections)
Cystic fibrosis
Immunodeficiency disorders
Inhalation of toxic gases or fumes
Autoimmune conditions

98
Q

Managment of bronchectasis

A

Antibiotics to treat infections
Chest physiotherapy to help clear mucus from the airways
Bronchodilators to improve airflow
Inhaled corticosteroids to reduce inflammation
Surgical intervention in severe cases (such as lung resection or bronchial artery embolization)

99
Q

complications of bronchectasis

A

Respiratory failure
Recurrent pneumonia
Atelectasis (lung collapse)
Hemoptysis
Cor pulmonale (right-sided heart failure)

100
Q

Managment of bronchectasis

A

Regular monitoring by a pulmonologist
Pulmonary rehabilitation
Vaccinations (such as influenza and pneumococcal vaccines)
Smoking cessation
Avoidance of respiratory irritants and pollutants

101
Q

COPD

A

COPD is an umbrella term encompassing the older terms chronic bronchitis and emphysema. In the vast majority of cases, COPD is caused by smoking

102
Q

Risk factors of COPD

A

Smoking (primary cause)
Environmental exposure to pollutants (such as air pollution, secondhand smoke, and occupational dust or chemicals)
Genetic factors
Respiratory infections
Aging

103
Q

Types of COPD

A

Chronic bronchitis: Involves inflammation and narrowing of the bronchial tubes, leading to excessive mucus production and cough.
Emphysema: Involves damage to the alveoli (air sacs) in the lungs, impairing their ability to exchange oxygen and carbon dioxide.

104
Q

Investigations in COPD

A

post-bronchodilator spirometry to demonstrate airflow obstruction: FEV1/FVC ratio less than 70%
chest x-ray
hyperinflation
bullae: if large, may sometimes mimic a pneumothorax
flat hemidiaphragm
also important to exclude lung cancer
full blood count: exclude secondary polycythaemia
body mass index (BMI) calculation

105
Q

Risk factors of COPD

A

Smoking (primary cause)
Environmental exposure to pollutants (such as air pollution, secondhand smoke, and occupational dust or chemicals)
Genetic factors
Respiratory infections
Aging

106
Q

Symptoms of COPD

A

Chronic cough
Excessive sputum production
Shortness of breath (dyspnea), especially during physical exertion
Wheezing
Chest tightness
Fatigue
Weight loss (in advanced stages)

107
Q

Diagnosis of COPD

A

Pulmonary function tests (spirometry) to measure airflow limitation and assess severity (FEV1/FVC ratio <0.7)
Chest X-ray or computed tomography (CT) scan
Arterial blood gas (ABG) analysis
Medical history and physical examination

108
Q

Treatment of COPD

A

Smoking cessation (primary intervention)
Bronchodilators (inhaled or oral) to improve airflow
Inhaled corticosteroids to reduce inflammation
Pulmonary rehabilitation to improve exercise tolerance and quality of life
Oxygen therapy for patients with severe hypoxemia
Vaccinations (such as influenza and pneumococcal vaccines) to prevent respiratory infections
Surgical interventions (such as lung volume reduction surgery or lung transplantation) in select cases

109
Q

Complication of COPD

A

Respiratory failure
Acute exacerbations (flare-ups) leading to hospitalization
Cor pulmonale (right-sided heart failure)
Pneumonia
Depression and anxiety
Decline in overall quality of life

110
Q

Pneumonia blood test findings

A

FBC: raised white cell count indicates infection
U&E: urea for the CURB-65 score
CRP: raised in inflammation. Monitoring is recommend for admitted patients to help determine response to treatment
Blood cultures

111
Q

chest X ray findings (pneumonia)

A

Chest X-ray
typically shows consolidation (opacity on the X-ray film) in the area of infection
may also show effusion

112
Q

Signs and symptoms of pneumonia

A

Symptoms:
A cough with purulent sputum (rust coloured/bloodstained)
Dyspnoea
Chest pain (may be pleuritic in nature)
Fever
Malaise

Signs:
Signs of systemic infection: High temperature, tachycardia, hypotension, confusion
Tachypnoea
Low oxygen saturation (below 95% or below 88% in patients with COPD)
On auscultation, there may be reduced breath sounds, bronchial breathing, and crepitations/crackles
Dullness on percussion (fluid)

113
Q

Risk factors of pneumonia

A

Aged under 5 or over 65-years-old
Smoking
Recent viral respiratory tract infection
Chronic respiratory diseases: e.g. cystic fibrosis and COPD
Immunosuppression: e.g. cytotoxic drug therapy and HIV
Patients at risk of aspiration: e.g. those with neurological diseases such as Parkinson’s disease or those with oesophageal obstruction
IV drug users
Other non-respiratory co-morbidities: e.g. diabetes and cardiovascular disease

114
Q

Pneumonia

A

Pneumonia is a common inflammatory condition affecting the alveoli in the lungs. It occurs as a result of pathogens entering the lower respiratory tract and causing infection. Causative pathogens include:
Bacteria: e.g Streptococcus pneumoniae - the most common cause of community acquired pneumonia (CAP)
Virus
Fungus (e.g. Pneumocystis jiroveci

115
Q

Chickenpox

A

Fever initially
Itchy, rash starting on head/trunk before spreading. Initially macular then papular then vesicular
Systemic upset is usually mild

116
Q

Measles

A

Prodrome: irritable, conjunctivitis, fever
Koplik spots: white spots (‘grain of salt’) on buccal mucosa
Rash: starts behind ears then to whole body, discrete maculopapular rash becoming blotchy & confluent

117
Q

Mumps

A

Fever, malaise, muscular pain
Parotitis (‘earache’, ‘pain on eating’): unilateral initially then becomes bilateral in 70%

118
Q

Rubella

A

Rash: pink maculopapular, initially on face before spreading to whole body, usually fades by the 3-5 day
Lymphadenopathy: suboccipital and postauricular

119
Q

Erythema infectiosum

A

Also known as fifth disease or ‘slapped-cheek syndrome’
Caused by parvovirus B19
Lethargy, fever, headache
‘Slapped-cheek’ rash spreading to proximal arms and extensor surfaces

120
Q

Scarlet fever

A

Reaction to erythrogenic toxins produced by Group A haemolytic streptococci
Fever, malaise, tonsillitis
‘Strawberry’ tongue
Rash - fine punctate erythema sparing the area around the mouth (circumoral pallor)

121
Q

Hand, foot and mouth disease

A

Caused by the coxsackie A16 virus
Mild systemic upset: sore throat, fever
Vesicles in the mouth and on the palms and soles of the feet

122
Q

managment of chickenpox

A

Symptomatic relief: paracetamol
Antiviral medications (such as acyclovir) may be prescribed for severe cases, immunocompromised individuals, or adults at risk of complications if started early in the course of the illness.
Calamine lotion or oatmeal baths to relieve itching
Avoid scratching to prevent bacterial superinfection and scarring

123
Q

chickenpox complications

A

Secondary bacterial infections of the skin (cellulitis)
Pneumonia
Encephalitis (inflammation of the brain)
Reye’s syndrome (a rare but serious complication, especially in children who take aspirin during infection)
Shingles (reactivation of the virus later in life)

124
Q

cystic fibrosis

A
125
Q

Mitral stenosis

A

Dyspnoea
Atrial fibrillation
Malar flush on cheeks
Mid-diastolic murmur

126
Q

Lung cancer

A

History of smoking
Symptoms of malignancy: weight loss, anorexia

127
Q

Pulmonary oedema

A

Dyspnoea
Bibasal crackles and S3 are the most reliable signs

128
Q

Tuberculosis

A

Fever, night sweats, anorexia, weight loss

129
Q

PE

A

Pleuritic chest pain
Tachycardia, tachypnoea

130
Q

Lower RTI

A

Usually acute history of purulent cough

131
Q

Bronchiectasis

A

Usually long history of cough and daily purulent sputum production

132
Q

Aspergilloma

A

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

133
Q

Granulomatosis with polyangiitis

A

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

134
Q

Goodpasture’s syndrome

A

Haemoptysis
Systemically unwell: fever, nausea
Glomerulonephritis

135
Q
A
136
Q

Bronchiolitis

A

characterised by acute bronchiolar inflammation. Respiratory syncytial virus (RSV) is the pathogen in 75-80% of cases. NICE released guidelines on bronchiolitis in 2015. Please see the link for more details.

137
Q

Epidemiology of Bronchiolitis

A

most common cause of a serious lower respiratory tract infection in < 1yr olds (90% are 1-9 months, with a peak incidence of 3-6 months). Maternal IgG provides protection to newborns against RSV
higher incidence in winter

138
Q

Basics of Bronchiolitis

A

respiratory syncytial virus (RSV) is the pathogen in 75-80% of cases
other causes: mycoplasma, adenoviruses
may be secondary bacterial infection
more serious if bronchopulmonary dysplasia (e.g. Premature), congenital heart disease or cystic fibrosis

139
Q

Features of Bronchiolitis

A

coryzal symptoms (including mild fever) precede:
dry cough
increasing breathlessness
wheezing, fine inspiratory crackles (not always present)
feeding difficulties associated with increasing dyspnoea are often the reason for hospital admission

140
Q

When referral needed for Bronchiolitis (MUST)

A

immediate referral (usually by 999 ambulance) if they have any of the following:
apnoea (observed or reported)
child looks seriously unwell to a healthcare professional
severe respiratory distress, for example grunting, marked chest recession, or a respiratory rate of over 70 breaths/minute
central cyanosis
persistent oxygen saturation of less than 92% when breathing air.

141
Q

when consider a referral for Bronchiolitis?

A

a respiratory rate of over 60 breaths/minute
difficulty with breastfeeding or inadequate oral fluid intake (50-75% of usual volume ‘taking account of risk factors and using clinical judgement’)
clinical dehydration.

142
Q

investigations for bronchiolitis

A

immunofluorescence of nasopharyngeal secretions may show RSV

143
Q

Managment of Bronchiolitis

A

humidified oxygen is given via a head box and is typically recommended if the oxygen saturations are persistently < 92%
nasogastric feeding may be needed if children cannot take enough fluid/feed by mouth
suction is sometimes used for excessive upper airway secretions

144
Q

cystic fibrosis

A

autosomal recessive disorder causing increased viscosity of secretions (e.g. lungs and pancreas). It is due to a defect in the cystic fibrosis transmembrane conductance regulator gene (CFTR), which codes a cAMP-regulated chloride channel

145
Q

What organisms would colonsie in patients with CF?

A

Staphylococcus aureus
Pseudomonas aeruginosa
Burkholderia cepacia
Aspergillus

146
Q

causes of false positve sweat tests

A

malnutrition
adrenal insufficiency
glycogen storage diseases
nephrogenic diabetes insipidus
hypothyroidism, hypoparathyroidism
G6PD
ectodermal dysplasia

147
Q

diagnostic sweat tests

A

patient’s with CF have abnormally high sweat chloride
normal value < 40 mEq/l, CF indicated by > 60 mEq/l

148
Q

Most common cause for false negative sweat test

A

skin oedema, often due to hypoalbuminaemia/ hypoproteinaemia secondary to pancreatic exocrine insufficiency.

149
Q

features of CF

A

neonatal period (around 20%): meconium ileus, less commonly prolonged jaundice
recurrent chest infections (40%)
malabsorption (30%): steatorrhoea, failure to thrive
other features (10%): liver disease
short stature
diabetes mellitus
delayed puberty
rectal prolapse (due to bulky stools)
nasal polyps
male infertility, female subfertility

150
Q

Managment of CF

A

regular (at least twice daily) chest physiotherapy and postural drainage. Parents are usually taught to do this. Deep breathing exercises are also useful
high calorie diet, including high fat intake*
patients with CF should try to minimise contact with each other to prevent cross infection with Burkholderia cepacia complex and Pseudomonas aeruginosa
vitamin supplementation
pancreatic enzyme supplements taken with meals
lung transplantion
chronic infection with Burkholderia cepacia is an important CF-specific contraindication to lung transplantation

151
Q

Lumacaftor/Ivacaftor (Orkambi)

A

is used to treat cystic fibrosis patients who are homozygous for the delta F508 mutation
lumacaftor increases the number of CFTR proteins that are transported to the cell surface
ivacaftor is a potentiator of CFTR that is already at the cell surface, increasing the probability that the defective channel will be open and allow chloride ions to pass through the channel pore

152
Q

what drugs cause lung fibrosis?

A

amiodarone
cytotoxic agents: busulphan, bleomycin
anti-rheumatoid drugs: methotrexate, sulfasalazine
nitrofurantoin
ergot-derived dopamine receptor agonists (bromocriptine, cabergoline, pergolide)

153
Q

Idiopathic lung fibrosis

A

progressive fibrosis of the interstitium of the lungs. Whilst there are many causes of lung fibrosis (e.g. medications, connective tissue disease, asbestos) the term IPF is reserved when no underlying cause exists.

154
Q

features of IPF

A

progressive exertional dyspnoea
bibasal fine end-inspiratory crepitations on auscultation
dry cough
clubbing

155
Q

Diagnositic IPF

A

spirometry: classically a restrictive picture (FEV1 normal/decreased, FVC decreased, FEV1/FVC increased)
impaired gas exchange: reduced transfer factor (TLCO)
imaging: bilateral interstitial shadowing (typically small, irregular, peripheral opacities - ‘ground-glass’ - later progressing to ‘honeycombing’) may be seen on a chest x-ray but high-resolution CT scanning is the investigation of choice and required to make a diagnosis of IPF
ANA positive in 30%, rheumatoid factor positive in 10% but this does not necessarily mean that the fibrosis is secondary to a connective tissue disease. Titres are usually low

156
Q

Managment of IPF

A

pulmonary rehabilitation
very few medications have been shown to give any benefit in IPF. There is some evidence that pirfenidone (an antifibrotic agent) may be useful in selected patients (see NICE guidelines)
many patients will require supplementary oxygen and eventually a lung transplant

157
Q

Lung fibrosis conditions associated with UPPER zones

A

hypersensitivity pneumonitis (also known as extrinsic allergic alveolitis)
coal worker’s pneumoconiosis/progressive massive fibrosis
silicosis
sarcoidosis
ankylosing spondylitis (rare)
histiocytosis
tuberculosis
radiation-induced pulmonary fibrosis
may develop following radiotherapy for breast or lung cancer
typically seen between 6 and 12 months following completion of radiotherapy course

158
Q

Lung fibrosis lower zone

A

idiopathic pulmonary fibrosis
most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
drug-induced: amiodarone, bleomycin, methotrexate
asbestosis

159
Q

CHARTS upper zone

A

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

160
Q

Investigation of Lung cancer?

A

-CXR
-CT (main choice)
Bronchoscopy
this allows a biopsy to be taken to obtain a histological diagnosis sometimes aided by endobronchial ultrasound
- blood test shows RAISED PLATELETS

—————————————-PET scanning
is typically done in non-small cell lung cancer to establish eligibility for curative treatment
uses 18-fluorodeoxygenase which is preferentially taken up by neoplastic tissue
has been shown to improve diagnostic sensitivity of both local and distant metastasis spread in non-small cell lung cancer

161
Q

What are the three types of lung cancer?

A
  • squamous cell lung cancer
    -adenocarcinoma
    -Large cell lung carcinoma
162
Q

Sqaumous cell cancer

A

typically central
associated with parathyroid hormone-related protein (PTHrP) secretion → hypercalcaemia
strongly associated with finger clubbing
cavitating lesions are more common than other types
hypertrophic pulmonary osteoarthropathy (HPOA)

163
Q

Adenocarcinoma

A

typically peripheral
most common type of lung cancer in non-smokers, although the majority of patients who develop lung adenocarcinoma are smokers

164
Q

Large cell Lung carcinoma

A

typically peripheral
anaplastic, poorly differentiated tumours with a poor prognosis
may secrete β-hCG

165
Q

Managment of non-small cell managment

A

only 20% suitable for surgery
mediastinoscopy performed prior to surgery as CT does not always show mediastinal lymph node involvement
curative or palliative radiotherapy
poor response to chemotherapy

166
Q

Surgical contradictions of non-small cell lung cancer

A

assess general health
stage IIIb or IV (i.e. metastases present)
FEV1 < 1.5 litres is considered a general cut-off point*
malignant pleural effusion
tumour near hilum
vocal cord paralysis
SVC obstruction

167
Q

adenocarcinoma paraneoplastic feature

A

gynaecomastia
hypertrophic pulmonary osteoarthropathy (HPOA)

168
Q

Small cell cancer paraneoplastic features

A

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

169
Q

Squamous cell paraneoplastic feautres

A

parathyroid hormone-related protein (PTH-rp) secretion causing hypercalcaemia
clubbing
hypertrophic pulmonary osteoarthropathy (HPOA)
hyperthyroidism due to ectopic TSH

170
Q

2WW lung cancer referral

A

have chest x-ray findings that suggest lung cancer
are aged 40 and over with unexplained haemoptysis

171
Q

offer 2ww if have 2 of following or ever smoked

A

cough
fatigue
shortness of breath
chest pain
weight loss
appetite loss

172
Q

Consider an urgent chest x-ray (to be performed within 2 weeks) to assess for lung cancer in people aged 40 and over with any of the following:

A

persistent or recurrent chest infection
finger clubbing
supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
chest signs consistent with lung cancer
thrombocytosis

173
Q

Features of SCLC

A

usually central
arise from APUD* cells
associated with ectopic ADH, ACTH secretion
ADH → hyponatraemia
ACTH → Cushing’s syndrome
ACTH secretion can cause bilateral adrenal hyperplasia, the high levels of cortisol can lead to hypokalaemic alkalosis
Lambert-Eaton syndrome: antibodies to voltage gated calcium channels causing myasthenic like syndrome

174
Q

Managment of SCLC

A

usually metastatic disease by time of diagnosis
patients with very early stage disease (T1-2a, N0, M0) are now considered for surgery. NICE support this approach in their 2011 guidelines
however, most patients with limited disease receive a combination of chemotherapy and radiotherapy
patients with more extensive disease are offered palliative chemotherapy

175
Q

What is this CT showing?

A

CT scan showing small cell lung cancer with multiple pulmonary nodules and extensive mediastinal nodal metastases.

176
Q

what is assoicaited with occupational asthma

A

isocyanates - the most common cause
example occupations include spray painting and foam moulding using adhesives
platinum salts
soldering flux resin
glutaraldehyde
flour
epoxy resins
proteolytic enzymes

177
Q

Black lung disease

A

long term exposure to coal dust particles. It is most commonly experienced by those who have been involved in the coal mining industry and severity is linked to the extent of exposure. Often there is a long lead time between the first exposure and the development of the disease.

178
Q

Epidemiology of SCLC

A

Prevalence is higher in populations with higher levels of exposure - e.g. areas with large coal mining industries.
Most individuals are male due to their prevalence in the coal mining industry.
Coal worker’s pneumoconiosis makes up around 7% of all Pneumoconiosis.
Diagnosis is usually 15-20 years after initial exposure to the coal dust.

179
Q

Pathophysiology of black lung disease

A

Coal dust (2-5 μm in size) is inhaled and enters the lungs.
The dust reaches the terminal bronchioles and there it is engulfed by alveolar and interstitial macrophages.
The dust particles are then moved by the macrophages via the mucociliary elevator and removed from the body as mucus.
In coal miners who are exposed over many years, the system is overwhelmed and the macrophages begin to accumulate in the alveoli, which starts an immune response, causing damage to the lung tissue.

180
Q

Simple pneumoconiosis:

A

Is the commonest type of pneumoconiosis.
Patients are often asymptomatic.
Its presence increases the risk of lung diseases such as COPD.
Simple pneumoconiosis may lead to Progressive Massive Fibrosis (PMF), occurring in around 30% of those with stage 3 grading.

181
Q

Black lung disease investigations

A

Chest x-ray: upper zone fibrosis
Spirometry: restrictive lung function tests - a normal or slightly reduced FEV1 and a reduced FVC

182
Q

Managment of Black lung disease

A

Avoid exposure to coal dust and other respiratory irritants (e.g. Smoking).
Manage symptoms of chronic bronchitis
Patients may be eligible for compensation via the Industrial Injuries Act.

183
Q

Progressive Massive Fibrosis

A

Dust exposure causes patients to develop round fibrotic masses which can be several centimetres in diameter.
These are most commonly in the upper lobes.
The exact pathogenesis is not known.
Patients are often symptomatic and have both breathlessness on exertion and cough, some may have black sputum.
Lung function testing shows a mixed obstructive/restrictive picture.

184
Q

occupational causes of silicosis

A

mining
slate works
foundries
potteries

185
Q

Silicosis

A

Silicosis is a fibrosing lung disease caused by the inhalation of fine particles of crystalline silicon dioxide (silica). It is a risk factor for developing tuberculosis (silica is toxic to macrophages).

186
Q

Features of silicosis

A

upper zone fibrosing lung disease
‘egg-shell’ calcification of the hilar lymph nodes

187
Q

what is this?

A

Chest x-ray from a patient with silicosis. Note the bilateral diffuse upper lobe reticular shadowing superimposed with occasional scattered mass like opacities. These features are in keeping with silicosis and progressive massive fibrosis (PMF)

188
Q

What is this?

A

CT scan from a patient with silicosis showing upper zone predominant mass-like scarring with calcification and volume loss. Hilar and mediastinal lymph node calcification also noted. No cavitary changes are seen. There is a left pleural effusion.

189
Q

Features of leigonella

A

flu-like symptoms including fever (present in > 95% of patients)
dry cough
relative bradycardia
confusion
lymphopaenia
hyponatraemia
deranged liver function tests
pleural effusion: seen in around 30% of patients

190
Q

investigations of legionella

A

diagnositic test of choice:urinary antigen
chest x-ray findings are non-specific but may include:
a mid-to-lower zone predominance of patchy consolidation
pleural effusions in around 30%

191
Q

Managment of legionella

A

treat with erythromycin/clarithromycin

192
Q

Legionnaire’s disease

A

Legionella pneumophilia. It typically colonizes water tanks and hence questions may hint at air-conditioning systems or foreign holidays. Person-to-person transmission is not seen`

193
Q

Mycoplasma pneumoniae

A

atypical pneumonia which often affects younger patients.
Epidemics of Mycoplasma pneumoniae classically occur every 4 years. It is important to recognise atypical pneumonia as it may not respond to penicillins or cephalosporins due to it lacking a peptidoglycan cell wall.

194
Q

Features of mycoplasma pneumoniae

A

the disease typically has a prolonged and gradual onset
flu-like symptoms classically precede a dry cough
bilateral consolidation on x-ray
complications may occur as below

195
Q

Complications of mycoplasma pneumonia

A

cold agglutins (IgM): may cause an haemolytic anaemia, thrombocytopenia
erythema multiforme, erythema nodosum
meningoencephalitis, Guillain-Barre syndrome and other immune-mediated neurological diseases
bullous myringitis: painful vesicles on the tympanic membrane
pericarditis/myocarditis
gastrointestinal: hepatitis, pancreatitis
renal: acute glomerulonephritis

196
Q

Investigations of Mycoplasma pneumonia

A

diagnosis is generally by Mycoplasma serology
positive cold agglutination test → peripheral blood smear may show red blood cell agglutination

197
Q

Managment of Mycoplasma Pneumonia

A

doxycycline or a macrolide (e.g. erythromycin/clarithromycin)

198
Q

Klebsiella pneumoniae

A

seen in alcoholics

199
Q

Streptococcus pneumoniae (pneumococcus)

A

Accounts for 80% of cases
Particularly associated with high fever, rapid onset and herpes labialis
A vaccine to pneumococcus is available

200
Q

Haemophilus influenzae

A

Particularly common in patients with COPD

201
Q

Staphylococcus aureus

A

Often occurs in patient following influenza infection

202
Q

Pneumocystis jiroveci

A

Typically seen in patients with HIV
Presents with a dry cough, exercise-induced desaturations and the absence of chest signs

203
Q

Idiopathic interstitial pneumonia

A

group of non-infective causes of pneumonia. Examples include cryptogenic organizing pneumonia which describes a form of bronchiolitis that may develop as a complication of rheumatoid arthritis or amiodarone therapy.

204
Q

CAP infective agents

A

Streptococcus pneumoniae (accounts for around 80% of cases)
Haemophilus influenzae
Staphylococcus aureus: commonly after influenza infection
atypical pneumonias (e.g. Due to Mycoplasma pneumoniae)
viruses

205
Q

Characteristic features of pneumococcal pneumonia

A

rapid onset
high fever
pleuritic chest pain
herpes labialis (cold sores)

206
Q

Pneumothorax spontaneous

A

primary spontaneous pneumothorax (PSP): Occurs without underlying lung disease, often in tall, thin, young individuals. PSP is associated with the rupture of subpleural blebs or bullae.
secondary spontaneous pneumothorax (SSP): Occurs in patients with pre-existing lung disease, such as COPD, asthma, cystic fibrosis, lung cancer, Pneumocystis pneumonia. Certain connective tissue diseases such as Marfan’s syndrome are also a risk factor

207
Q

Traumatic pneumothorax

A

traumatic pneumothorax: results from penetrating or blunt chest trauma, leading to lung injury and pleural air accumulation.

208
Q

Iatrogenic pneumothorax

A

occurs as a complication of medical procedures, such as thoracentesis, central venous catheter placement, ventilation, including non-invasive ventilation or lung biopsy.

209
Q

tension pneumothorax

A

escribes a severe pneumothorax resulting in the displacement of mediastinal structures that may result in severe respiratory distress and haemodynamic collapse.

210
Q

Catamenial pneumothorax

A

spontaneous pneumothoraces occurring in menstruating women. It is thought to be caused by endometriosis within the thorax.

211
Q

Signs of pneumothorax

A

hyper-resonant lung percussion
reduced breath sounds
reduced lung expansion
tachypnoea
tachycardia

212
Q

Tension pneumothorax signs

A

respiratory distress
tracheal deviation away from the side of the pneumothorax
hypotension

213
Q

Rifampicin

A

mechanism of action: inhibits bacterial DNA dependent RNA polymerase preventing transcription of DNA into mRNA
potent liver enzyme inducer
hepatitis, orange secretions
flu-like symptoms

214
Q

Isoniazide

A

mechanism of action: inhibits mycolic acid synthesis
peripheral neuropathy: prevent with pyridoxine (Vitamin B6)
hepatitis, agranulocytosis
liver enzyme inhibitor

215
Q

Pyrazinaminde

A

mechanism of action: converted by pyrazinamidase into pyrazinoic acid which in turn inhibits fatty acid synthase (FAS) I
hyperuricaemia causing gout
arthralgia, myalgia
hepatitis

216
Q

Ethambutol

A

mechanism of action: inhibits the enzyme arabinosyl transferase which polymerizes arabinose into arabinan
optic neuritis: check visual acuity before and during treatment
dose needs adjusting in patients with renal impairment

217
Q

TB pathophysiology

A

The macrophages often migrate to regional lymph nodes, the lung lesion plus affected lymph nodes is referred to as a Ghon complex.
This leads to the formation of a granuloma which is a collection of epithelioid histiocytes.
There is the presence of caseous necrosis in the centre.
The inflammatory response is mediated by a type 4 hypersensitivity reaction.
In healthy individuals the disease may be contained, in the immunocompromised disseminated (miliary TB) may occur

218
Q

risk factors of TB

A

having lived in Asia, Latin America, Eastern Europe, or Africa for years
exposure to an infectious TB case
people who are infected with HIV are 20 to 30 times more likely to develop active TB
immunocompromised individuals (diabetics, patients on immunosuppressive therapy, malnourished, or those with haematological malignancies)
silicosis
apical fibrosis

219
Q

Screening of latent TB

A

The Mantoux test is the main technique used to screen for latent tuberculosis. In recent years the interferon-gamma blood test has also been introduced. It is used in a number of specific situations such as:
the Mantoux test is positive or equivocal
people where a tuberculin test may be falsely negative (see below)

220
Q

False negative TB

A

miliary TB
sarcoidosis
HIV
lymphoma
very young age (e.g. < 6 months)

221
Q

Diagnostics of active TB

A

Chest x-ray
upper lobe cavitation is the classical finding of reactivated TB
bilateral hilar lymphadenopathy

Sputum smear
3 specimens are needed
rapid and inexpensive test
stained for the presence of acid-fast bacilli (Ziehl-Neelsen stain)
all mycobacteria will stain positive (i.e. nontuberculous mycobacteria)
the sensitivity is between 50-80%
this is decreased in individuals with HIV to around 20-30%

Sputum culture
the gold standard investigation
more sensitive than a sputum smear and nucleic acid amplification tests
can assess drug sensitivities
can take 1-3 weeks (if using liquid media, longer if solid media)

Nucleic acid amplification tests (NAAT)
allows rapid diagnosis (within 24-48 hours)
more sensitive than smear but less sensitive than culture

222
Q

TB

A

Mycobacterium tuberculosis that most commonly affects the lungs.

223
Q

Primary TB

A

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

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

224
Q

Secondary TB

A
  • host already immunocompromised

Reactivation generally occurs in the apex of the lungs and may spread locally or to more distant sites. Possible causes of immunocompromise include:
immunosuppressive drugs including steroids
HIV
malnutrition

225
Q
A
226
Q

Where is air located in pneumo

A

Visceral and parietal pleura