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FinalMB Part I - Medicine > Respiratory > Flashcards

Flashcards in Respiratory Deck (350)
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1
Q

How common is lung cancer compared to other cancers in the UK?

A
  • Thirst most common<div>- Behind breast (first) and prostate (second)</div>
2
Q

What is by far the biggest cause of lung cancer?

A

Smoking - 80% of lung cancer believed to be preventable

3
Q

What are the two main histological types of lung cancer?

A
  • Non-small cell lung cancer (NSCLC)<div>- Small cell lung cancer (SCLC)</div>
4
Q

Which is the most prevalent histological form of lung cancer?

A
  • Non-small cell lung cancer (<b>NSCLC); 80%</b><div>- Small cell lung cancer (SCLC); 20%<br></br></div>
5
Q

What are the two subtype of Non-small cell lung cancer (NSCLC)?

A
  • Squamous cell carcinoma (35%)<div>- Adenocarcinoma (25%)</div>
6
Q

Why are small-cell lung cancers (SCLC) responsible for many paraneoplastic syndrome?

A

Small cell lung cancer cells contain neurosecretory granules that may release neuroendocrine hormones

7
Q

Outline the signs and symptoms of lung cancer?

A
  • SOB<div>- Cough</div><div>- <b>Haemoptysis</b></div><div>- Finger <b>clubbing</b></div><div>- Recurrent pneumonia</div><div>- Unexplained weight loss</div><div>- Lymphadenopathy; often in the supraclavicular nodes</div>
8
Q

What is the first line investigation in suspected lung cancer?

A

CXR

9
Q

What findings may be present on CXR in a patient with lung cancer?

A
  • Hilar enlargement<div>- Peripheral opacity; visual <b>lesion </b>in the lung field(s)</div><div>- Pleural effision; usually <b>unilateral </b>in cancer</div><div>- Lung collapse</div>
10
Q

Once lung cancer has been diagnosed on CXR, what further investigations are required?

A
  • <b>Staging CT Scan</b>; contrast enhanced, checking for lymph node involvement and metastasis<div>- PET-CT; useful in identifying metastasis through ares of increased metabolic activity</div><div>- <b>Bronchoscopy </b>with <b>endobronchial ultrasound </b>(EBUS); useful for detailed assessment of the tumour and US-guided biopsy</div><div>- Histololgical diagnosis; using biopsy obtained from EBUS or percutaneously</div>
11
Q

How are treatment options identified in lung cancers

A

Must be discussed at lung MDT meeting

12
Q

What are the broad options for lung cancer treatment?

A
  • <b>Surgery;</b>lobectomy or segmentectomy/wedge ressection<div><b>- Radiotherapy; </b>curative in NSCLC</div><div><b>- Chemotherapy;</b>adjuvant or palliative</div><div><b>- Endobronchial treatments</b>; stents or debulking, palliative</div>
13
Q

What is the first line treatment offered in NSLC if the disease is confined to a single area?

A

<b>Surgery</b><div>- Lobectomy; first line</div><div>- Segmentectomy or wedge resection; secondary option</div>

14
Q

What medical treatment can be given in patients with NSCLC?

A

<b>- Radiotherapy;</b> can be curative<div><b>- Chemotherapy;</b> used as an adjuvant to radiotherapy or as palliative treatment to improve survival/quality of life</div>

15
Q

Outline the treatment options in SCLC?

A

Usually a combination therapy of both radiotherapy and chemotherapy

16
Q

Which kind of lung cancer has the worse prognosis?

A

SCLC

17
Q

Outline the extrapulmonary manifestations/paraneoplastic syndromes associated with lung cancer?

A
  • Recurrent laryngeal nerve palsy<div>- Phrenic nerve palsy</div><div>- Superior vena cava (SVC) obstruction</div><div>- Syndrome of innappropriate ADH (SIADH)</div><div>- Cushing’s syndrome</div><div>- Hypercalcaemia</div><div>- Limbic encephalitis</div><div>- Lambert-Eaton Myasthenic Syndrome (LEMS)</div>
18
Q

How can lung cancer cause recurrent laryngeal nerve palsy?

A

Tumour may compress the recurrent laryngeal nerve as it passes through the mediastinum, resulting in a hoarse voice

19
Q

How can lung cancer cause phrenic nerve palsy?

A

Tumour may compress the phrenic nerve, resulting in shortness of breath

20
Q

How does lung cancer sometimes cause SVC obstruction?

A

Direct compression of the SVC by the tumour

21
Q

How does SVC compression present in patients?

A
  • Swelling of the face<div>- Difficulty breathing</div><div>- Distended neck veins</div><div>- <b>Pemberton’s sign;</b>raising the hands over the head causes facial congestion and cyanosis</div>
22
Q

How does Horner’s syndrome present?

A
  • Ptosis<div>- Miosis</div><div>- Anhydrosis</div>
23
Q

What kinds of lung cancers cause Horner’s syndrome?

A

Pancoast tumours of pulmonary apex; compresses the cervical sympathetic chain

24
Q

Why can lung cancer trigger SIADH?

A

Some SCLCs are neuroendocrine tumours that secrete peptide hormones that mimic the action of ADH

25
Q

How does SIADH present?

A

Hyponatraemia

26
Q

Why can lung cancer trigger Cushing’s syndrome?

A

Some SCLC are neuroendocrine tumours that secrete peptide hormones that mimic the action of ACTH and raise the circulating cortisol levels

27
Q

Why can lung cancer trigger hypercalcaemia?

A

Some SCLCs are neuroendocrine tumours that secrete peptide hormones that mimic the action of PTH and raise circulating calcium levels

28
Q

How can some SCLCs result in limbic encephalitis?

A

Some SCLCs cause the immune system to make antibodies to tissues in the limbic system, causing inflammation. This causes symptoms such as short term memory impairment, hallucinations, confusion and seizures. It is associated with <b>anti-Hu antibodies</b>

29
Q

What is Lambert-Eaton Myasthenic Syndrome (LEMS)?

A
  • Result of antibodies against voltage-gated Ca2+ channels in presynaptic terminals of motor neurones<div>- Similar to myasthenia gravis</div>
30
Q

How can some lung cancers cause Lambert-Eaton Myasthenic Syndrome (LEMS)?

A
  • Some SCLCs can produce antibodies against the voltage-gated Ca2+ channels<div>- More common in older patients; consider SCLC in elderly smokers presenting with new onset LEMS</div>
31
Q

What are the symptoms of Lambert-Eaton Myasthenic Syndrome (LEMS)?

A
  • Weakness in proximal muscles<div>- Also affects intraocular muscles</div><div>- Diplopia</div><div>- Ptosis</div><div>- Slurred speach</div><div>- Dysphagia</div><div>- Weakness worsens with prolonged use</div>
32
Q

What is mesothelioma?

A
  • Lung cancer of the mesothelial cells that line the pleural membranes<div>- Strongly-linked to asbestos inhalation</div><div>- Long latent period</div><div>- Poor prognosis</div>
33
Q

What is the definition of pneumonia?

A

Infection of the lung tissue causing inflammation and sputum filling the airways and alveoli

34
Q

How can pneumonia be seen on CXR?

A

Consolidation

35
Q

Outline the relationship between chest infections, bronchitis and pneumonia?

A

”- Chest infection is an non-specific umbrella term that covers both bronchitis and pneumonia<div>- Pneumonia and bronchitis have overlapping symptoms but may be distinguised by subtle differences</div><div><img></img><br></br></div>”

36
Q

Outline the different classifications of pneumonia?

A

<b>- Community Acquired Pneumonia (CAP);</b> pneumonia that has developed outside of hospital OR <48hrs after admission<div><b>- Hospital Acquired Pneumonia (HAP); </b>pneumonia that has developed >48hrs after admission to hospital</div><div><b>- Aspiration Pneumonia;</b> pneumonia that has developed following clear evidence/indication of aspiration/inhalation of foreign materal</div>

37
Q

How may patients present with pneumonia?

A
  • SOB<div>- Cough; with productive sputum</div><div>- Haemoptysis</div><div>- <b>Pleuritic chest pain</b>; sharp chest pain that is worse on inspiration</div><div>- Delirium; acute confusion associated with an infeciton</div>
38
Q

What signs may indicate sepsis secondary to pneumonia?

A
  • Tachypneoa<div>- Tachycardia</div><div>- Hypotension</div><div>- Fever</div><div>- Confusion</div><div>- Hypoxia</div>
39
Q

Outline the characteristic chest signs of pneumonia?

A

<b>- Bronchial breath sounds;</b> harsh breath sounds equally loud on inspiration and expiration<div><b>- Focal coarse crackles; </b>due to air passing through the sputum</div><div>-<b> Dullness to percussion;</b> due to collapse and/or consolidation</div>

40
Q

What scoring system is used out of hospital/in general practise when considering admission for a patient with suspected pneumonia?

A

<b>CRB-65 Score; </b>any score greater than 0 requires referral to the hospital

41
Q

Outline the CRB-65 score for suspected pneumonia requiring hospital referral/admission?

A

“<div><b><u>CRB-65 Score</u>;</b><b></b>>1 Requires Hospital Referral/Admission</div><b>- <u>C</u>onfusion; </b>disorientation in <u>p</u>ersonal, <u>p</u>lace or <u>t</u>ime = 1<div>- <b><u>R</u>espiratory rate </b>> 30 = 1</div><div><b>- <u>B</u>lood pressure </b><90 systolic and/or <60 diastolic = 1</div><div>- <b><u>65</u>;aged over 65</b> = 1</div>”

42
Q

What scoring system is used in hospital to predict mortality in patients with suspected pneumonia?

A

“<b><u>CURB-65 Score</u></b>”

43
Q

How is the CURB-65 score used in hospitals to guide admission in patients with suspected pneumonia?

A

“<b><u>CURB-65 Score</u></b><div><b>- Score 0-1;</b> consider home treatment (no admission)</div><div>- <b>Score 2; </b>consider hospital admission</div><div><b>- Score >3;</b> consider intensive care assessment</div>”

44
Q

Outline the CURB-65 scoring used to guide patient admission in the hospital?

A

“<b><u>CURB-65;</u></b><div>- <b><u>C</u>onfusion</b>; new disorientation in person, place or time = 1</div><div>- <b><u>U</u>rea</b>; greater than 7 = 1</div><div>- <b><u>R</u>espiratory rate </b>>30 = 1</div><div>- <b><u>B</u>lood pressure</b> <90 systolic and/or <60 diastolic = 1</div><div>- <b><u>65</u>;</b> aged 65 or over = 1</div>”

45
Q

What are the most common organims that cause community acquired pneumonia (CAP)?

A
  • <i>Streptoccocus pneumoniae </i>(50%)<div>-<i> Haemophilius influenzae </i>(20%)</div>
46
Q

What are the most common organims that cause hospital acquired pneumonia (HAP)?

A
  • <i>Gram negative bacilli</i>; pseudomonas aerunginosa<div>- <i>Staphylococcus aureus</i></div><div>- <i>Legionella pneumophilia</i></div>
47
Q

Which organism is often responsible for pneumonia in immunocompromised patients or those with chronic pulmonary disease?

A

<i>Moraxella catarrhalis</i>

48
Q

Which organism is often responsible for pneumonia in patients with cystic fibrosis or bronchiectasis?

A

<i>Pseudomonas aerunginosa</i>

49
Q

Which organisms are often responsible for pneumonia in patients with cystic fibrosis?

A
  • <i>Pseudomonas aerunginosa</i><div>- <i>Staphylococcus aureas</i></div>
50
Q

Which conditions are particularly associated with aspiration pneumonias?

A
  • Reduced conscious level<div>- Neuromuscular diseases</div><div>- Oesophageal conditions</div><div>- Mechanical interventions such as endotracheal tubes</div>
51
Q

What is meant by atypical pneumonia?

A
  • An atypical pneumonia is any pneumonia caused by an organism that <b>cannot be cultured</b> in the normal way or detected using a gram stain<div>- These often present primarily with <b>extrapulmonary systems </b>as opposed to the classical pulmonary symptoms (cough, dyspnoea)</div>
52
Q

What types of antimicrobials can be used in the treatment of atypical pneumonias?

A

<b>- </b>Macrolides; <b>clarithromycin</b><div>- Fluoroquinolones; levofloxacin</div><div>- Tetracyclines; <b>doxycycline</b></div>

53
Q

How can organisms causing atypical pneumonias be subclassified?

A

<b>Non-zoonotic; </b>mycoplasma pneumoniae, legionella pneumophilia, chlamydophilia pneumoniae<div><b>Zoonotic; </b>chlamydophilia psittaci (psittacosis), coxiella burnetii (Q fever), francisella tularensis (tularemia)</div>

54
Q

What is Legionnaires’ disease?

A
  • Atypical pneumonia caused by <i>legionella pneumophilia</i><div>- Typically contracted from infected water supplies or air conditioning</div><div>- Causes an SIADH that results in hyponatraemia</div>
55
Q

How can you distinguish mycoplasma pneumoniae infections in atypical pneumonia?

A
  • Rash called erythema multiforme<div>- Target lesions; pink rings with pale centres</div><div>- Neurological symptoms in young patients</div>
56
Q

Which patients often present with an atypical pneumonia caused by chlamydophilia pneumoniae?

A
  • School-aged children<div>- Mild to moderate chronic pneumonia and wheeze</div>
57
Q

What is Q fever?

A
  • An atypical pneumonia caused by coxiella burnetii<div>- Associated with exposure to animals and their bodily fluids</div>
58
Q

Which patients are likely to contract atypical pneumonias caused by chlamydia psittaci (sit-a-see)?

A

Those who keep birds as pets

59
Q

What are the 5 causes of atypical pnemonia?

A

“<b><u>Legions of psittaci MCQs;</u></b><div><b>- <u>L</u>egionella pneumophilia</b></div><div><b>- Chlamydia <u>psittaci </u></b>(sit-a-see)</div><div><b>- <u>M</u>ycoplasma pneumoniae</b></div><div><b>- <u>C</u>hlamydia pneumoniae</b></div><div>- <b><u>Q</u> fever</b> (<b>coxiella burnetii</b>)</div>”

60
Q

Which organisms can cause fungal pneumonia in immunocompromised patients?

A

<b>Pneumocystis jiroveci </b>(PCP)

61
Q

Which patients are particularly at risk to fungal pneumonias?

A

HIV Patients with a low CD4+ count

62
Q

How do fungal pneumonias often present?

A
  • Subtle presentation<div>- Dry cough; <b>without sputum</b></div><div>- SOBOE</div><div>- <b>Night sweats</b></div>
63
Q

How are fungal pneumonias treated?

A

<b>Co-trimoxazole </b>(SeptrinTM);trimethoprin + sulfamethoxazole

64
Q

Outline the investigations for patients with a CRB-65 score of 0-1?

A

<b>Point-of-care testing;</b> bloods specifically CRP and WCC

65
Q

Outline the investigations for patients presenting to hospital with suspected pneumonia and a CURB-65 between 0 and 1?

A
  • CXR<div>- FBC</div><div>- U&Es</div><div>- CRP</div>
66
Q

Outline the additional investigations required in patients presenting to hospital with suspected pneumonia and a CURB-65 greater than 1?

A
  • Sputum cultures<div>- Blood cultures</div><div>- Legionella and pneumococcal urinary antigens</div>
67
Q

Why might inflammatory markers not be raised in patients with suspected pneumonia?

A

If they are immunocompromised they may not show an inflammatory response and hence wont have elevated inflammatory markers

68
Q

Which antibiotic regimine should be used in a mild CAP?

A

5 day course of oral antibiotics; often amoxicillin or macrolide

69
Q

Which antibiotic regimine should be used in a moderate to severe CAP?

A

7-10 day coruse of dual antibiotics; usually amoxicillin plus a macrolide

70
Q

What are the complications that can arise secondary to pneumonia?

A

<div><b><u>Pulmonary Complications;</u></b></div>

<div>- Pleural effusion</div>

<div>- Empyema; pus in the pleural space</div>

<div>- Lung abscess</div>

<div>- Pneumothorax</div>

<div><b><u><br></br></u></b></div>

<div><b><u>Extrapulmonary Complications;</u></b></div>

<div>- Sepsis<br></br></div>

<div>- Death</div>

71
Q

What are lung function tests used for?

A
  • Make diagnoses in lung disease<div>- Distinguish between <b>obstructive </b>and <b>restrictive </b>lung diseases</div>
72
Q

What spirometry finding is usefull when distinguishing between obstructive lung diseases?

A
  • Reversibility<div>- Improvement post-bronchodilator therapy indicates asthma over COPD</div>
73
Q

What is meant by the FEV1?

A

Forced expiratory volume in 1 second

74
Q

What happens to the FEV1value in obstructive lung disease?

A

It will be reduced

75
Q

What is meant by the FVC value?

A

Forced vital capacity; the maximum amount of air exhaled <b>after a full inspiration</b>

76
Q

What happes to the FVC value in restrictive lung disease?

A

It will be reduced

77
Q

What value is primarily used in spirometry to diagnose obstructive/restrictive lung disease?

A

FEV1/FVC

78
Q

Outline the spirometry findings that would be expected in a restrictive airway disease?

A
  • FVC; reduced<div>- FEV1; reduced</div><div>- <b>FEV1/FVC; >0.7</b> (70%)</div>
79
Q

Outline the spirometry findings that would be expected in a obstructive airway disease?

A
  • FVC; may be normal but often reduced due to air trapping<div>- FEV1; reduced</div><div><b>- FEV1/FVC; <0.7</b> (70%)</div>
80
Q

What lung function test is useful as an addition to spirometry in obstructive airway disease?

A

<b>Peak Flow</b> - meaures the peak expiratory flow rate (PEFR)

81
Q

How can peak flow be used to guide diagnosis in obstructive lung disease?

A

”- Particularly in asthma<div>- Take 3 readings; record <b>best result</b></div><div>- Compare with predicted PEFR</div><div>- Use % of predicted</div><div><img></img><br></br></div>”

82
Q

Give examples of obstructive airway diseases

A

“<div><b><u>ABCDE;</u></b></div><div>- <b><u>A</u>sthma</b><br></br></div><div>- <b><u>B</u>ronchiectasis</b>, bronchiolitis<div>- <b><u>C</u>ystic fibrosis</b></div><div>- <b>α1-antitryspin <u>D</u>eficiency</b></div><div>- <b><u>E</u>mphysema</b>; <b>COPD</b> = emphysema + chronic bronchitis</div></div>”

83
Q

Give examples of restrictive airway diseases

A
  • Pulmonary fibrosis<div>- Neuromuscular disorders</div><div>- Congestive cardiac failure</div><div>- Sarcoidosis</div><div>- Obesity</div>
84
Q

What is asthma?

A

Asthma is a chronic inflammatory disorder of the airways

85
Q

What three features are characteristic of asthma?

A
  • <b>Reversible</b> airflow limitation<div>- Airway <b>hyper-responsiveness</b></div><div>- Inflammation of the <b>bronchi</b></div>
86
Q

What is the main pathophysiology of asthma?

A

“<div><b><u>HBO;</u></b></div><b>Hyper-responsiveness</b> of the airways causes <b>bronchoconstriction</b> and subsequent airway <b>obstruction</b>”

87
Q

Outline some of the triggers associated with asthma?

A
  • Infection<div>- Night time or early morning</div><div>- Exercise</div><div>- Animals; allergy</div><div>- Cold/damp environments</div><div>- Dust</div><div>- Strong emotions</div>
88
Q

What is meant by atopy and how does this relate to asthma?

A

”- Atopy is a <b>genetic predisposition </b>to<b> IgE-mediated </b>allergen <b>sensitivity</b><div>- Atopy prediposes an individual to three main conditions</div><div> o <b>Allergic asthma</b></div><div> o <b>Atopic dermatitis</b></div><div> o <b>Allergic rhinitis</b></div>”

89
Q

What are the five main proposed aetiologies for the development of asthma?

A
  • Atopy<div>- Hygiene hypothesis</div><div>- Aspirin-induced hypersensitivity</div><div>- Occupational asthma</div><div>- Exercise-induced asthma</div>
90
Q

What is meant by the hygiene hypothesis of asthma?

A

“<span>- Postulates that r<b>educed exposure to infectious pathogens</b> at a young age predisposes individuals to such diseases</span><div>- The environment is thought to encourage <b>TH2 predominant response</b>- this is the one that <b>produces IgE</b></div>”

91
Q

What is meant by Samter’s triad?

A
  • Triad of symptoms that occur in patients with aspirin-induced asthma<div> o Asthma</div><div> o Aspirin sensitivity</div><div> o Nasal polyps</div>
92
Q

Which compounds are associated with an occupational risk of developing asthma?

A
  • High molecular weight; flour, latex<div>- Low molecular weigh; isocyanates, wood dust</div>
93
Q

Outline the key presentation of a patient with asthma?

A
  • Episodic symptoms<div>- Diurnal variability; typically worse at night</div><div>- Dry cough; with wheeze +/- SOB</div><div>- History of other atopic conditions; eczema, hayfever, food allergies</div><div>- Family history</div><div><b>- Bilateral widespread polyphonic wheeze</b></div>
94
Q

Outline the BTS/Sign Guidelines for diagnosis of asthma?

A

<b>- High probabililty;</b>make clinical diagnosis and try treatment<div><b>- Intermediate probability;</b> perform spirometry with reversibility testing to confer diagnosis</div><div><b>- Low probability;</b> investigate differentials and consider referrals</div>

95
Q

Outline the NICE Guidelines for diagnosis of asthma?

A

<b><u>First Line;</u></b><div>- Fractional Exhaled Nitric Oxide (FeNO)</div><div>- Spirometry with reversibility testing</div><div><br></br></div><div><b><u>Second Line;</u></b> diagonistic uncertainty following first line</div><div>- Peak Flow Variability; PEFR several times a day for 2-4 weeks</div><div>- Direct Bronchial Challenge Test; administration of histamine or methylcholine</div>

96
Q

Outline how the fractional exhaled nitric oxide (FeNO) test can be used to aid in the diagnosis of asthma?

A

-<b> FeNO >40ppb</b> (parts per billion); supports diagnosis of <b>asthma</b><div><b>- FeNO 25-39ppb; </b>is<b>suggestive</b> of asthma diagnosis, use PEFR variability to aid</div><div>- <b>FeNO <25ppb</b>; is<b>not supportive</b> of asthma diagnosis</div>

97
Q

When the diagnosis of asthma is unclear, what criteria are required for specialist referral?

A
  • Diagnosis unclear<div>- Suspected occupational asthma</div><div>- Poor response to treatment</div><div>- Severe/life-threatening attack</div>
98
Q

What concomitant findings in suspected asthma are suggestive of an alternative diagnosis?

A
  • Systemic features; myalgia, fever, weight loss<div>- Unexpected clinical findings; clubbing, cyanosis, cardiac disease, stridor/monophonic wheeze</div><div>- Persistent non-variable breathlessness</div><div>- Chronic sputum production</div><div>- Restrictive pattern on spirometry</div><div>- CXR abnormalilies</div>
99
Q

What is the definition of controlled asthma?

A

<b>- Clinical Control</b>; no daytime symptoms, night-time waking or activity limitation<div><b>- Acute Control</b>; no asthma attacks and no need for rescue medication</div><div><b>- Medications</b>; no need for rescue medication and minimal side effects</div><div><b>- Lung function</b>; normal PEFR/FEV1</div>

100
Q

Outline the BTS/SIGN Guidelines for the medical management of asthma?

A

<div><b><u>Step 1;</u></b></div>

  • SABA reliever (salbutamol); PRN<div>- ICS preventer (fluticasone/beclomethasone); OD</div><div><br></br></div><div><b><u>Step 2;</u></b></div><div>- Add LABA (salmeterol)</div><div><br></br></div><div><b><u>Step 3;</u></b></div><div>- Increased ICS dose</div><div>- OR add luekotriene receptor antagonist (monteleukast)</div><div><br></br></div><div><b><u>Step 4;</u></b></div><div>- Refer to specialist</div>
101
Q

What indication is there for going up a stage in the long-term management of asthma?

A

If the patient is <b>taking their SABA > 3 times per week</b> alongside any of their other asthma medication then they need to be moved up to the next stage of treatment

102
Q

What are the two main categories of single drug inhalers used in the management of asthma?

A

<b>- Multi-dose inhalers (MDIs);</b> pressurised aerosol dispensers, require coordination, can be used with spacers, requires low flow rate<div><b>- Dry powder inhalers (DPIs);</b> single dose devices, breath actuated, require high flow rates</div>

103
Q

What is meant by maintenance and reliever therapy (MART)?

A
  • MART refers to a combined inhaler which contains both a reliever and an ICS preventer<div>- Fostair; formoterol + beclomethasone</div>
104
Q

Outline the acute management for a patient having an asthma attack?

A

<div><b><u>Step 1;</u></b><br></br></div>

<div>- <b>Salbutamol </b>nebuliser (2.5-5mg); every 15-30mins</div>

<div>- <b>Ipratropium</b> nebuliser (0.5mg); every 4-6hrs</div>

<div>- <b>Oxygen</b>; titrate SpO2 to 94-98%</div>

<div>- <b>Steriods</b>; prednisolone (40-50mg, orally), hydrocortisone (100mg, IV, 6 hourly)</div>

<div><br></br></div>

<div><b><u>Step 2;</u></b></div>

<div><b>- Magnesium sulfate</b> (1.2-2g IV); over 20mins</div>

<div><br></br></div>

<div><b><u>Step 3;</u></b></div>

<div>- Senior review</div>

<div>- Consider IV aminophyline</div>

<div>- Consider β2agonist IV</div>

<div>- HDU/ITU review</div>

105
Q

What is the first-line management for a patient experiencing a moderate acute asthma attack?

A

“<b><u>I Am Short Of Breath;</u></b><div><b><span>- </span><u>I</u>pratropium bromide</b>; (Nebuliser, 0.5mg, 4-6hrly)</div><div>- <u><b>A</b></u><b>ntibiotic</b>s; if clear evidence of bacterial infection</div><div><b>- </b><b>S</b><b>teriods</b>; prednisolone (PO, 40-50mg, daily), hydrocortisone (IV, 100mg, 6hrly)</div><div><b>- </b><b>O</b><b>xygen</b>; get SpO2 92-98%</div><div>- <b><u>β</u>2 agonist</b>; salbutamol (Nebuliser, 2.5-5mg, every 15-30mins)</div>”

106
Q

What additional long-term management is required for asthma?

A
  • Asthma self-management programme<div>- Yearly flu jabs</div><div>- Yearly asthma reviews</div><div>- Advise on exercise and smoking</div>
107
Q

Outline the discharge criteria for a patient presenting with asthma?

A
  • Early discharge at <b>20mins</b>; if patient stable, no life-threatening or severe features AND <b>PEFR >75%</b> of best/predicted<div>- Discharge at <b>60mins</b>; if patient recovering, no signs of life-threatening or severe features AND <b>PEFR >75%</b> of best/predicted</div><div><div>- Discharge at <b>120mins</b>; if patient recovering, no signs of life-threatening or severe features, <b>PEFR >50% </b>of best/predicted</div></div><div>- <b>Admission</b>; if any features of <b>life-threatening</b> asthma, ongiong features of <b>severe</b> asthma and/or <b>PEFR <50% </b>best/predicted</div>
108
Q

What are the follow-up criteria for a patient discharged following an acute presentation of asthma?

A
  • <b>PEFR < 50% best/predicted</b>; require prenisolone 40-50mg/day for 5+ days<div>-<b> Check inhaler technique </b>and ensure adequate supply</div><div>- <b>GP Follow up</b>; withing two days of discharge</div><div>- <b>Specialist clinic referral</b>; within four weeks if admitted to hospital</div>
109
Q

How do acute exacerbations of asthma usually present?

A
  • Progressively worsening SOB<div>- Use of accessory muscles of respiration</div><div>- Tachypnoea</div><div>- Symmetrical expiratory wheeze</div><div>- Chest sounds tight with reduced air entry</div>
110
Q

Outline the grading criteria for acute exacerbations of asthma?

A

<b>Moderate;</b><div>- PEFR 50-70% of predicted</div><div><br></br></div><div><b>Severe;</b></div><div>- PEFR 33-50% of predicted</div><div>- Respiratory rate >25</div><div>- Heart rate >110bpm</div><div>- Unable to complete sentences</div><div><b><br></br></b></div><div><b>Life-threatening;</b></div><div>- SpO2< 92%</div><div>- Becoming tired</div><div>- Silent chest; no wheeze, airways so tight that there is no air entry/movement at all</div><div>- Haemodynamically unstable</div>

111
Q

In addition to the first-line management, what add-on therapies can be used for a patient experiencing a severe acute asthma attack?

A
  • Oxygen is required to maintain SpO2 94-98%<div>- Aminophylline infusion</div><div>- IV salbutamol</div>
112
Q

In addition to the first-line management, what add-on therapies can be used for a patient experiencing a life-threatening acute asthma attack?

A
  • Oxygen is required to maintain SpO294-98%<div>- Aminophylline infusion</div><div>- IV salbutamol</div><div>- IV magnesium sulfate</div><div>- Admission to HDU/ITU</div><div>- Intubation in worst cases; needs to be done early as can be difficult in severe bronchoconstriction</div>
113
Q

What kind of acid base disorder would you expect to see in a patient presenting wtih an acute exacerbation of asthma?

A

<b>Respiratory alkalosis</b>; hyperventilation due to bronchoconstriction will drive pCO2 down

114
Q

What kind of acid base disorder may be seen in a patient presenting with a life-threatening acute exacerbation of asthma?

A

<b>- Respiratory acidosis; </b>normal pO2 or hypoxia also extremely concerning

115
Q

What variables can be monitored to determine if a patient experiencing an acute exacerbation of asthma is responding to treatment?

A
  • Respiratory rate<div>- Respiratory effort</div><div>- PEFR</div><div>- SpO2</div><div>- Chest auscultation</div>
116
Q

Why is it important ot monitor serum potassium in patients whom you are treating for an acute exacerbation of asthma?

A
  • Salbutamol can cause hypokalaemia
117
Q

What are the discharge criteria for a patient following an acute exacerbation of asthma?

A

<b>- Asthma action plan</b>; may include prescription of asthma rescue pack<div>- <b>PEFR < 50% best/predicted</b>; require prenisolone 40-50mg/day for 5+ days</div><div>-<b>Check inhaler technique</b>and ensure adequate supply</div><div>-<b>GP Follow up</b>; withing two days of discharge</div><div>-<b>Specialist clinic referral</b>; within four weeks if admitted to hospital</div>

118
Q

Broadly speaking, what is COPD?

A

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

119
Q

What are the main components of the disease in COPD?

A
  • <b>Chronic bronchitis</b>; chronic productive cough for at least 3 months over two consecutive yearts<div>- <b>Emphysema</b>; abnormal airspace enlargement distal to terminal bronchioles with alveolar destruction with no obvious fibrosis</div>
120
Q

What is the clinical definition of chronic bronchitis?

A

Chronic <b>productive cough</b> lasting for >3months over two or more consecutive years<br></br>

121
Q

What is meant by the pathological term, emphysema?

A
  • Abnormal airspace enlargement occuring distal to the terminal bronchioles<div>- Evidence of alveolar destruction with no obvious fibrosis</div>
122
Q

What causes of chronic cough need to be exlcuded before a diagnosis of chronic bronchitis can be made?

A

Bronchiectasis

123
Q

Why is COPD extremely common?

A

Occurs almost exclusively as a result of smoking-related lung damage

124
Q

How may COPD be distinguished from asthma?

A
  • In COPD there will be a lack of reversibility with bronchodilators<div>- Flow will not improve post-salbumatol nebuliser</div>
125
Q

What is meant by an acute exacerbation of COPD?

A

A sustained worsening of a patients clinical symptoms and/or lung function above and beyond the normal day-to-day variation

126
Q

What causes exacerbations of COPD?

A
  • Most often these are caused by infections<div>- Obstruction of the airways prevents effective ventilation and clearance of pathogens</div><div>- Hence pathogens remain in the airways causing <b>infective exacerbations </b>(IECOPD)</div>
127
Q

What is the most important aetiological risk factor in the development of COPD?

A

Smoking

128
Q

Outline the common symptoms and signs seen in a presentation of COPD?

A
  • Chronic breathlessness<div>- Chronic cough</div><div>- Sputum productive</div><div>- Wheeze</div><div>- Recurrent respiratory infections</div>
129
Q

Which respiratory symptoms do <b>NOT </b>correspond with a COPD presentation and thus need to be investigated separately?

A
  • <b>Haemoptysis</b>; consider lung cancer etc.<div>- <b>Clubbing</b>; consider lung cancer etc.</div><div>- <b>Chest pain</b>; consider fibrosis, heart failure, PE etc.</div>
130
Q

Outline the MRC Dyspnoea Scale that is used to assess the impact of a patients’ breathlessness?

A
  • Grade 1; breathlessness on <b>strenuous exercise</b><div>- Grade 2; breathlessness on walking <b>uphill/stairs</b><br></br></div><div>- Grade 3; breathlessness that <b>slows walking</b> on the <b>flat</b><br></br></div><div>- Grade 4; patient stops to <b>catch their breath </b>after walking<b> 100m</b> on the flat<br></br></div><div>- Grade 5; <b>unable </b>to<b> leave </b>the <b>house</b> due to breathlessness<br></br></div>
131
Q

How is a diagnosis of COPD made?

A

Based on <b>clinical presentation plus spirometry</b> to confirm

132
Q

What spirometry findings would be consistent with COPD?

A
  • FEV1/FVC <0.7<div>- No significant improvement post-bronchodilator therapy</div>
133
Q

a8ee8b310daa4f6bbd7422bf6237dba8-ao-1

A

Stage of COPD

134
Q

a8ee8b310daa4f6bbd7422bf6237dba8-ao-2

A

Stage of COPD

135
Q

a8ee8b310daa4f6bbd7422bf6237dba8-ao-3

A

Stage of COPD

136
Q

a8ee8b310daa4f6bbd7422bf6237dba8-ao-4

A

Stage of COPD

137
Q

How is the severity of COPD classified?

A

”- Depending on the <b>FEV1% compared to predicted</b><div>- FEV1% = FEV1 recorded / FEV1 predicted</div>”

138
Q

Which investigations are required at the time of diagnosis of COPD?

A
  • <b>CXR</b>; exlude other pathologies<div>- <b>FBC</b>; polycythaemia or anaemia</div><div>- <b>BMI</b>; assess baseline to identify weight loss (severe COPD/lung cancer) or weight gain (ICS)</div><div>- <b>Sputum culture</b>; assess for IECOPD or chronic infections (pseudomonas)</div><div>- <b>ECG</b>; assess heart function if cor pulmonale suspected</div><div>- <b>ABG</b>; if hypoxia or hypercapnia suspected</div><div>- CT thorax; if alternate diagnosis suspected</div><div>- Serum α1-antitrypsin; look for α1-antitrypsin deficiency (AAT) in younger patients or those with severe/early onset</div><div>- Transfer factor for carbon monoxide (TLCO); give an indication of severity of the disease</div>
139
Q

Outline the component parts of COPD management?

A
  • Education<div>- Smoking cessation</div><div>- Vaccination; influenzae and pneumococcal</div><div>- Pulmonary rehabilitation</div><div>- Self-management plans</div><div>- Management of co-mobidities</div><div>- Pharmacotherapy</div>
140
Q

What are the three types of drugs used in the pharmacological management of COPD?

A
  • β2AR agonists<div>- Muscarinic antagonists</div><div>- Inhaled corticosteroids</div>
141
Q

What are the three different types of inhalers used in the management of COPD?

A
  • <b>Metered Dose Inhalers</b> (MDIs); aerosolised drug, require coordination and good technique<div>- <b>Dry Power Inhalers</b> (DPIs); powered drug, need good force of inhalation</div><div>- <b>Soft Mist Inhalers</b> (SMIs); liquid drug, requires less coordination</div>
142
Q

What delivery device modifications can be used to aid administration of drug in patients who struggle to use inhalers?

A

<b>- Spacers</b>; typically used with an MDI inhaler, reduce need for good coordination<div>- <b>Nebulisers</b>; convert drug to liquid form with compressed air, used in acute exacerbations</div>

143
Q

What additonal oral add-on therapies can be used in pateints with COPD?

A

<b>- Corticosteroids;</b> used mainly in acute exacerbations<div><b>- Theophyline;</b> PDE inhibitor used to cause bronchodilation</div><div><b>- Mucolytics</b> (carbocisteine); used to reduce frequency of chronic productive cough</div><div><b>- Antibiotics</b>; including azithromycin, used in acute exacerbations</div>

144
Q

What treatment can be given in patients with COPD who are still experiencing acute exacerbations despite optimal inhaled therapy?

A

Long-term oxygen therapy (LTOT)

145
Q

What indications are there for long-term oxygen therapy (LTOT) in COPD?

A
  • Chronic hypoxia<div>- Polycythaemia</div><div>- Cyanosis</div><div>- Cor pulmonale; heart failure secondary to pulmonary hypertension</div>
146
Q

When can long-term oxygen therapy not be used in COPD?

A

If they are continuing to smoke as it poses a severe fire risk

147
Q

What surgical interventions can be offered in severe COPD?

A
  • Lung reduction<div>- Bullectomy</div><div>- Lung transplantation</div>
148
Q

Outline some of the common clinical features of an acute exacerbation of COPD?

A
  • Worsening breathlessness<div>- Worsening cough</div><div>- Increased sputum production</div><div>- Change in sputum colour</div>
149
Q

What considerations need to be taken into account when deciding whether to admit a patient experiencing an acute exacerbation of COPD for inpatient hospital treatment?

A
  • Ability/inability to cope at home<div>- Severity of clinical symptoms</div><div>- Severe co-mobidities</div><div>- Poor levels of activity</div><div>- Already receiving LTOT</div><div>- Chest radiograph changes</div>
150
Q

What investigations should be carried out in patients presenting with an acute exacerbation of COPD?

A

“<div><b><u>ABCDE;</u></b></div><div>- <b><u>A</u>BG</b><br></br></div><div>- <b><u>B</u>loods</b>; FBC, U&Es, CRP, cultures if pyrexial<br></br></div>- <b><u>C</u>XR</b><div>- <b><u>D</u>rug Levels</b>; <b>theophylline</b> if part of admission medications</div><div>- <b><u>E</u>CG</b><br></br></div><div><img></img><b><br></br></b></div>”

151
Q

What acid-base status disorder are patients with an acute exacerbation of COPD likely to be experiencing

A

Respiratory acidosis

152
Q

What treatments are given in an acute exacerbation of COPD?

A

“<div><b><u>Oh! ABC;</u></b></div>- Controlled <b><u>O</u>xygen</b>; maintain SpO288-92%<div>- <b><u>A</u>ntibiotics; </b>co-amoxiclav or doxcycline<br></br></div><div>- <b><u>B</u>ronchodilators; </b>salbutamol or ipratropium</div><div><b>- <u>C</u>orticosteroids; </b>oral prednisolone or IV hydrocortisone</div><div><img></img><br></br></div>”

153
Q

Why do we need to be careful when using oxygen therapy in patients presenting with an acute exacerbation of COPD?

A

Too much oxygen in someone who is retaining CO2as in the case of COPD, can depress respiratory drive. This would result in a decrease in breathing rate and effort that results in further CO2 retention

154
Q

What oxygen delivery devices can be used to carefully control oxygen delivery to patients experiencing an acute exacerbation of COPD?

A

“Venturi(TM) Masks - allow careful controlling of the fraction of inspired oxygen FiO2<div><img></img><br></br></div>”

155
Q

Whad indication is there for controlled oxygen delivery in exacerbations of COPD?

A

Evidence of CO2 retention<div>- High PACO2 (acute)</div><div>- High HCO3- (compensated)</div>

156
Q

What is the target oxygen saturation in patients who are retaining CO2during an exacerbation of COPD?

A

88-92%

157
Q

What is the target oxygen saturation in patients who are not retaining CO2 during an exacerbation of COPD?

A

> 94%

158
Q

What is the definition of type I respiratory failure?

A

“<b>- Hypoxaemia; PAO2 < 8kPa</b> (this can any value greater than 8kPa lower than the oxygen inspired, it depends on whether the patient is on room air or oxygen)<div>- <b>Normocapnia/hypocapnia</b>; <b>PACO2 < 6.7kPa</b></div>”

159
Q

What often causes type I respiratory failures?

A

Ventilation/perfusion mismatches

160
Q

What is the definition of type II respiratory failure?

A

“<b>- Hypoxaemia;PAO2< 8kPa</b>(this can any value greater than 8kPa lower than the oxygen inspired, it depends on whether the patient is on room air or oxygen)<div>-<b>Hypercapnia</b>;<b>PACO2> 6.7kPa</b></div>”

161
Q

What is the primary cause of type II respiratory failure?

A

Secondary to reduced air flow with alveolar hypoventilation that results in CO2 retention

162
Q

Which kind of respiratory failure are patients with COPD at significant risk of developing during an exacerbation?

A

“<b><u>Type II Repiratory Failure (T2RF);</u></b><div>- <b>Hypoxia</b>; PAO2 < 8kPa</div><div>- <b>Hypercapnia</b>; PACO2 > 6.7kPa</div>”

163
Q

What is the initial management for a patient presenting with E-COPD who is found to be in type II respiratory failure?

A
  • <b>Ventri Mask for 1hr</b>; maintaining SpO2at 88-92%<div>- <b>Repeat ABG</b></div>
164
Q

What is BiPAP?

A

Bilevel Positive Airway Pressure; helps patients blow off excess CO2 and normalise their pH

165
Q

What are the indications for BiPAP in patients in an exacerbation of COPD?

A
  • <b>Acute or acute-on-chronic hypercapnic respiratory failure</b>; pH < 7.35, PCO2 > 6kPa, Increased RR despite optimisation of oxygen therapy<div>- <b>Cardiogenic pulmonary oedema</b></div><div>-<b> Type I Respiratory failure and clinically tiring</b></div><div>- <b>Weaning from mechanical ventilation</b></div>
166
Q

What are the indications for long-term oxygen therapy (LTOT) in patients with COPD?

A
  • Arterial <b>PAO2 < 7.3kPa</b><div><br></br></div><div><b><u>OR</u></b></div><div><br></br></div><div>- Arterial <b>PAO2< 8kPa PLUS</b> either;</div><div> o Pulmonary hypertension</div><div> o Peripheral oedema</div><div> o Secondary polycythaemia</div>
167
Q

Outline the medical treatment for E-COPD that can be managed at home?

A
  • Prednisolone (30mg); oral, OD, 7-14 days<div>- Regular inhalers or home nebulisers</div><div>- Antibiotics if evidence of IE-COPD</div>
168
Q

What is the treatment dose of prednisolone used to treat E-COPD at home?

A

Prednisolone (30mg), OD, PO, 7-14 days

169
Q

Outline the medical treatment for E-COPD that is given to inpatients in hospital?

A
  • <b>Nebulised bronchodilators</b>; salbutamol (5mg/4hr) AND ipratropium (500μg/6hr)<div>- <b>Steriods</b>; prednisolone (PO, 30-40mg, OD) OR hydrocortisone (IV, 200mg)</div><div>- <b>Antibiotics</b> (if IE-COPD); co-amoxiclav or doxycycline</div><div>- <b>Physiotherapy</b>; to help clear sputum</div>
170
Q

What are the treatment doses of nebulised bronchodilators used to treat E-COPD at in hospital?

A
  • Salbutamol; <b>2.5-5mg</b> up to <b>6 times a day</b><div>- Ipratropium; <b>500μg</b> upto <b>4 times a day</b></div>
171
Q

What is the treatment doses of corticosteroids used to treat E-COPD in hospital?

A
  • Prednisolone; <b>30mg</b>, PO, OD for 5 days<div>- Hydrocortisone; <b>200mg</b>, IV, OD</div>
172
Q

Outline some add-on therapies that may be tried in patients who arent responding to first-line therapy in the treatment of E-COPD?

A
  • Aminophylline; IV<div>- NIV</div><div>- Intubation and ventilation; requiring ITU admission</div><div>- Doxapram; IV, respiratory stimulant</div>
173
Q

Outline some of the complications of COPD that are often seen?

A
  • <b>Spontaneous pneumothorax</b>; due to rupture of emphysematous bullae<div>- Recurrent pneumonia; due to minimal airflow and clearance of pathogens</div><div>- Respiratory failure; due to hypoxia +/- hypercapnia</div><div>- Polycythaemia or anaemia; due to chronic compensation</div><div>- Depression</div>
174
Q

What is non-invasive ventilation (NIV)?

A

An alternative to full intubation used to support the lungs in respiratory failure

175
Q

When is non-invasive ventilation used?

A

In cases of respiratory failure due to obstructive lung disease

176
Q

What is involved in delivering NIV?

A

Tight fitting facemask that forecfully blows air into the lungs to ventilate them without having to intubate

177
Q

What are the two different types of non-invasive ventilation?

A
  • <b>BiPAP</b>; bilevel positive airway pressure<div>- <b>CPAP</b>; continuous positive airway pressure</div>
178
Q

What is bilevel positive airway pressure (BiPAP)?

A

Involves a cycle of high and low pressure corresponding to inspiration and expiration respectively

179
Q

When is BiPAP used?

A

BiPAP is used in type 2 respiratory failure often due to COPD

180
Q

What criteria need to be met in order for BiPAP to be considered?

A

Respiratory acidosis (pH <7.35 and PACO2 >6kPa) despite adequate medical treatment

181
Q

What are the main contraindications for BiPAP?

A
  • Untreated pneumothorax<div>- Structural abnormalities; affecting the face, airway or GI traction</div>
182
Q

What investigation should a patient have before being considered for BiPAP?

A

CXR to look for pneumothorax

183
Q

What are the two different sub-types of BiPAP?

A

-<b> IPAP</b>; inspiratory positive airway pressure where air is forced into the lungs<div>- <b>EPAP</b>; expiratory positive airway pressure which prevents collapse during expiration in patients with obstructive lung disease</div>

184
Q

What factors influence ghe initial pressures used in BiPAP?

A

The body mass of the patient

185
Q

What are the rough pressures used for IPAP and EPAP in the average male patient?

A
  • IPAP; 16-20cmH2O<div>- EPAP; 4-6cmH2O<br></br></div>
186
Q

What investigation is required 1hr after a patient is started on BiPAP?

A

Repeat ABG

187
Q

What is CPAP?

A

Continuous airway pressure provides continuous air being blown into the lungs in order to keep them expanded

188
Q

When is CPAP used?

A

To maintain the patients’ airway in conditions where it is prone to collapse

189
Q

What are the indications for CPAP?

A
  • Obstructive sleep apnoea<div>- Congestive cardiac failure</div><div>- Acute pulmonary oedema</div>
190
Q

What is meant by interstitial lung disease?

A

Interstitial lung disease is an umbrella term used to describe conditions that affect the lung parenchyma

191
Q

What are the characteristic features of interstitial lung diseases?

A
  • Inflammation<div>- Fibrosis</div>
192
Q

Give some examples of interstitial lung diseases?

A

“<div><b><u>CHAP;</u></b></div><div>- <b><u>C</u>ryptogenic</b> organising pneumonia<br></br></div><div><div>- <b><u>H</u>ypersensitivity</b> pneumonitis (extrinsic allergic alveolitis)</div><div>- <b><u>A</u>sbestosis</b></div></div>- <b><u>P</u>ulmonary fibrosis</b>”

193
Q

What two features are used to inform a diagnosis of interstitial lung disease?

A
  • Clinical features<div>- High resolution CT (HRCT)</div>
194
Q

What is the key investigation used in the diagnosis of interstitial lung disease?

A

High resolution CT (HRCT)

195
Q

What key feature is seen in CT in patients with interstitial lung disease?

A

”- Ground-glass opacities<div><img></img><br></br></div>”

196
Q

What additional test can be used to confirm a diagnosis of interstitial lung disease if it is unclear following HRCT?

A

Lung biopsy and histological investigation

197
Q

Outline the prognosis of interstitial lung diseases?

A

Prognoses are poor and the damage is often irreversible, hence management tends to be supportive

198
Q

Outline some of the management options in intersitial lung diseases?

A
  • Remove or treat the underlying cause<div>- Home oxygen where they are hypoxic at rest</div><div>- Smoking cessation</div><div>- Physiotherapy and pulmonary rehabilitation</div><div>- Pneumococcal and influenzae vaccinations</div><div>- Advanced care planning and palliative care where appropriate</div><div>- Lung transplant</div>
199
Q

How do patients with idiopathic pulmonary fibrosis often present?

A
  • Usually over 50<div>- Insidious onset SOB</div><div>- Dry cough for longer than 3 months</div>
200
Q

What examination findings are often seen in patients with idiopathic pulmonary fibrosis?

A
  • Bibasal fine inspiratory crackles<div>- Finger clubbing</div>
201
Q

Which medications can be used to prevent the progression of idiopathic pulmonary fibrosis?

A

<b>- Pirfenidone;</b> anti-fibrotic and anti-inflammatory<div><b>- Nintedanib; </b>monoclonal antibody that inhibits non-receptor tyrosine kinases (nRTKs)</div>

202
Q

Which drugs are known to induce pulmonary fibrosis?

A

“<b><u>MANC;</u></b><div><b>- <u>M</u>ethotrexate</b></div><div><b>- <u>A</u>miodarone</b></div><div><b>- <u>N</u>itrofuratoin</b></div><div><b>- <u>C</u>yclophospamide</b></div>”

203
Q

Which conditions can cause secondary pulmonary fibrosis

A

“<div><b><u>SARS;</u></b></div><div>- <b><u>S</u></b>ystemic lupus erythematosis (SLE)<br></br></div>- <b><u>α</u></b>1antitrypsin deficiency<div>- <b><u>R</u></b>heumatoid arthritis</div><div>- <b><u>S</u></b>ystemic sclerosis</div>”

204
Q

What types of hypersensitivity reaction is hypersensitivity pneumonitis?

A

Type III Hypersensitivity Reaction

205
Q

What causes hypersensitivity pneumonitis?

A

Environmental allergen that causes parenchymal inflammation

206
Q

What investigation can be used to diagnose hypersensitivty pneumonitis?

A

<b>Broncoalveolar lavage</b>; bronchoscopy combined with cell collection from the ariways and subsequent testing

207
Q

What is seen in the cellular fluid collected from the airways during bronchoscopy in patients with hypersensitivity pneumonitis?

A

Raised lymphocytes and mast cells

208
Q

Give some examples of specific hypersensitivity pneumonitis conditions?

A

<b>- Bird-fanciers lung</b>; allergen found in bird droppings<div><b>- Farmers lung;</b> allergen is mouldy spores found in hay</div><div><b>- Mushroom workers lung;</b> reaction to specific mushroom antigens</div><div><b>- Malt workers lung;</b> reaction to mould on barley</div>

209
Q

What is the other name for cryptogenic organising pneumonia (COP)?

A

Bronchiolitis obliterans organising pneumonia (BOOP)

210
Q

What can cause cryptogenic organising pneumonia?

A
  • Idiopathic<div>- Infection</div><div>- Inflammatory disorders</div><div>- Medications</div><div>- Radtion</div><div>- Environmental toxins or allergens</div>
211
Q

How does cryptogenic organising pneumonia present?

A

Similar to infectious pneumonias; SOB, cough, fever, lethargy, focal consolidation on CXR

212
Q

What is the definitive investigation used in the diagnosis of cryptogenic organising pneumonia?

A

Lung biopsy

213
Q

How is cryptogenic organising pneumonia treated?

A

Systemic corticosteroids

214
Q

How does asbestos cause interstitial lung disease?

A

Asbestos is fibrogenic and oncogenic and can result in asbestosis

215
Q

What problems can arise as a result of asbestos inhalation?

A
  • Lung fibrosis<div>- Pleural thickening and pleural plaques (seen on CXR)</div><div>- Adenocarcinoma</div><div>- Mesothelioma</div>
216
Q

What do patients diagnosed with asbestosis need to be informed of?

A

That they may be eligable for compensation

217
Q

What needs to be done in all patients that die of asbestosis?

A

Referral to the coroner

218
Q

What is a pleural effusion?

A

Collection of fluid in the pleural cavity

219
Q

What are the two different types of pleural effusion?

A

<b>- Exudative</b>; high protein content (>3g/dL)<div><b>- Transudative</b>; low protein content (<3g/dL)</div>

220
Q

What broad process causes exudative pleural effusions?

A

Inflammation; resulting in protein leakage out of the tissues and into the pleural space

221
Q

What inflammatory causes can lead to exudative pleural effusion?

A
  • Lung cancer<div>- Pneumonia</div><div>- Rheumatoid arthritis</div><div>- Tuberculosis</div>
222
Q

What is the process underlying transudative pleural effusion?

A

Fluid moving accross the blood vessel walls into the pleural space

223
Q

What are some of the causes of transudative pleural effusions?

A
  • Congestive heart failure<div>- Hypoalbuminaemia</div><div>- Hypothyroidism</div><div>- Meig’s Syndrome; right sided pleural effusion associated with ovarian malignancy</div>
224
Q

What is Meig’s Syndrome?

A
  • Right sided pleural effusion that is associated with an underlying ovarian malignancy
225
Q

How do pleural effusions often present?

A
  • SOB<div>- Dullness to percussion over the area of the effusion</div><div>- Reduced breath sounds on auscultation</div><div>- Tracheal deviation; <b>away</b> from the side of the effusion</div><div>- Mediastinal shift; away from the side of the effusion</div>
226
Q

What investigation is key in diagnosing a pleural effusion?

A

CXR

227
Q

What signs may be seen in CXR in patients with a pleural effusion?

A

”- Blunting of costophrenic angles<div>- Fluid in the lung fissures</div><div>- Menisci; upward curvings where lung fields meet mediastinum/chest wall, seen in large effusions</div><div>- Tracheal deviation; in large effusions</div><div>- Mediastinal deviation; in large effusions</div><div><img></img><br></br></div>”

228
Q

What are the three different treatment approaches considered in pleural effusions?

A
  • Conservative managements; used in small effusions<div>- Pleural aspiration; sticking a needle into the chest and aspirating the fluid<br></br></div><div>- Chest drain; used in larger effusions</div>
229
Q

What is mean by empyema?

A

Empyema is an infected pleural effusion

230
Q

When is empyema suspected?

A

Patients with improving pneumona with a new or ongoing fever

231
Q

How can empyema be diagnosed?

A

Aspiration of pleural fluid and analysis indicates pus<div>- Acidic pH (pH <7.2)</div><div>- Low glucose</div><div>- High LDH</div>

232
Q

How can empyema be treated?

A
  • Chest drain<div>- Antibiotics</div>
233
Q

What is a pneumothorax?

A

A collection of air within the pleural space

234
Q

What are the broad categories of pneumothorax?

A

<b>- Traumatic pneumothorax</b>; following trauma to the chest wall<div><b>- Spontaneous pneumothorax</b>; in elderly patients and young men who are tall and slim</div><div><b>- Secondary pneumothorax</b>; secondary to medical interventions or lung pathology</div>

235
Q

What is the typical presentation of a spontaneous pneumothorax?

A

Tall, thin, young male with sudden onset SOB and pleuritic chest pain that often occurs whilst playing sport

236
Q

What are the four causes of pneumothoraces?

A
  • Spontaneous<div>- Traumatic</div><div>- Iatrogenic; following lung biopsy, mechanical ventilation or central line insertion</div><div>- Lung pathology; infection, asthma or COPD</div>
237
Q

What is the most suitable investigation in suspected pneumothorax?

A

Erect CXR

238
Q

How can a pneumothorax be seen on CXR?

A

“Loss of lung markings<div><img></img><br></br></div>”

239
Q

How can you measure the size of a pneumothorax (BTS Guidelines)?

A

“Measuring horizontally from the lung edge to the inside of the chest wall at the level of the hilum<div><img></img><br></br></div>”

240
Q

What other investigation(s) can be used to diagnose a pneumothorax that is too small to pick up on CXR?

A

CT thorax

241
Q

Outline the treatment for a pneumothorax <b>< 2cm</b> in size in a patient <b>without SOB</b>?

A

Consider discharge and outpatient follow-up in 2-4 weeks

242
Q

What is the treatment for a pneumothorax <b>> 2cm</b> in size AND/OR<b>with SOB</b>?

A
  • Aspiration<div>- If no improvement following two aspirations, consider chest drain</div>
243
Q

When is a chest drain the immediate management stragety in the treatment of a pneumothorax

A
  • Bilateral pneumothoraces<div>- Secondary pneumothoraces</div><div>- If the patient is unstable</div><div>- Evidence of tension pneumothorax</div>
244
Q

What causes a tension pneumothorax?

A

Tension pneumothoraces are <b>caused by trauma</b> to chest wall that creates a <b>one-way valve</b> that lets air in but not out of the pleural space

245
Q

What is the major risk of a tension pneumothorax?

A

Pressure inside the thorax will build up and cause <b>mediastinal shift</b> that will <b>kink </b>the<b> great vessels</b> resulting in <b>cardiorespiratory arrest</b>

246
Q

What are the signs of a tension pneumothorax?

A
  • Tracheal deviation; away from the affected side<div>- Reduced air entry/breath sounds on affected side</div><div>- Increased resonant percussion on affected side</div><div>- Tachycardia</div><div>- Hypotension</div>
247
Q

Outline the mainstay treatment of a tension pneumothorax?

A

“<div>- Large bore cannula inserted into the 2nd intercostal space at the midclavicular line<br></br></div><div>- Once pressure is relieved, insert chest drain</div><div><img></img><br></br></div>”

248
Q

Outline the position where a chest drain should be inserted in the management of a pneumothorax?

A

“<b><u>Triangle of Safety;</u></b><div>- Horzontal line across the <b>5th intercostal space</b> (inferior nipple line)</div><div>- Vertical line consisting of the <b>mid-axillary line</b> (follows the lateral edge of latissimus dorsi)</div><div>- Diagnonal line consisting of the<b>anterior axillary line </b>(follows the lateral edge of pectoralis major)</div><div><img></img><br></br></div>”

249
Q

Where relative to the rib contained within the triangle of safety should the needle be inserted for a chest drain?

A

Just above the rib to avoid the neurovascular bundle that runs just below the rib

250
Q

What investigation needs to be carried out immediately after the insertion of a chest drain

A

CXR to check the positioning of the drain

251
Q

What is a meant by the term pulmonary embolism?

A

This is a condition where there is a blood clot (thrombus) in the pulmonary arteries that is often the result of a deep vein thrombosis that has developed in the legs and embolised through the venous system and right side of the heart to the lungs

252
Q

What is the effect of pulmonary embolisms on the functioning of the heart?

A

Once lodge in the pulmonary arteries, the backlog of pressure puts strain on the right side of the heart

253
Q

What is the umbrella term used to describe both deep vein thromboses and pulmonary emboli?

A

Venous thromboembolism (VTE)

254
Q

Outline some of the risk factors for developing a VTE?

A
  • Immobility<div>- Recent surgery</div><div>- Long haul flights</div><div>- Pregnancy</div><div>- Hormone therapy with oestrogens</div><div>- Malignancy</div><div>- Polycythaemia</div><div>- Systemic lupus erythematosus</div><div>- Thrombophilia</div>
255
Q

What is done to prevent patients developing VTE in hospital?

A
  • Every patient admitted is assessed for the risk of developing a VTE<div>- Patients at increased risk are given prophylactic doses of a low molecular weight heparin</div>
256
Q

What prophylactic medications can be given to patients at high risk of developing VTE in hopsital?

A

<b><u>Low Molecular Weight Heparins;</u></b><div>- Tinzaparin</div><div>- Enoxaparin</div><div>- Dalteparin</div>

257
Q

What are the contraindications for VTE prophylaxis?

A
  • Active bleeding<div>- Existing anticoagulation</div>
258
Q

What non-pharmacological intervention can also be used in the prophylaxis of VTE?

A

Anti-embolic compression stockings

259
Q

What is the main contraindication for the use of anti-embolic compression stockings?

A

Peripheral arterial disease

260
Q

What features may form part of the initial presentation of a patient with a pulmonary embolism?

A
  • SOB<div>- Cough with or without haemoptysis</div><div>- Pleuritic chest pain</div><div>- Hypoxia</div><div>- Tachycardia</div><div>- Raised respiratory rate</div><div>- Low grade fever</div><div>- Haemodynamic instability causing hypotension</div><div>- Peripheral signs of DVT; leg swelling and/or tenderness</div>
261
Q

What scoring system can be used to assess the risk of a patient presenting with symptoms actually having a DVT or PE?

A

<u><b>Wells Score;</b></u><div>- Signs and symptoms of DVT = 3</div><div>- PE is #1 diagnosis or equally likely = 3</div><div>- Heart rate > 100 = 1.5</div><div>- Immobilised for 3+ days AND/OR sugery within 4 weeks = 1.5</div><div>- Previous VTE = 1.5</div><div>- Haemoptysis = 1</div><div>- Malignancy +/- treatment <6 months or palliative = 1</div>

262
Q

How can the Wells Score for potential PE be used to inform further investigation/management?

A

Wells Score <b>> 4</b>; PE is likely, proceed to CT pulmonary angiography (<b>CTPA</b>)<div>Wells Score <b>< 4</b>; PE is possible but arrange <b>D-Dimer</b> within 4hrs, if positive arange CTPA, if negative exclude PE</div>

263
Q

What investigation can be carried out in patients suspected of PE to aid assessment of alternative causes for their symptoms?

A

CXR

264
Q

How can a D-Dimer blood test be used to inform a diagnosis of PE?

A
  • D-Dimer is a fibrin-degradation product of the breakdown of blood clots<div>- D-Dimer values are raised in VTE</div>
265
Q

What are the caveats to consider when using D-Dimers to confer PE?

A

-<b> High Sensitivity</b>; hence if <b>NOT RAISED</b> then<b> PE</b> can be <b>EXCLUDED</b><div>- <b>Low Specificity</b>; hence if <b>RAISED</b>, this does <b>NOT confer</b> diagnosis of <b>PE</b> (there are a number of causes of raised D-Dimer)</div>

266
Q

What scoring system can be used to determine whether D-Dimer blood testing is required in patients at low risk of having a PE?

A

<b><u>Pulmonary Embolism Rule-out Criteria (PERC);</u></b><div>- Age >50 = 1</div><div>- Heart Rate >100 = 1</div><div>- SpO2 < 95% (room air) = 1</div><div>- Unilateral leg swelling = 1</div><div>- Recent surgery or trauma within 4 weeks = 1</div><div>- Previous VTE = 1</div><div>- Hormone use = 1</div>

267
Q

How can the PERC criteria be used to confer next steps in patients suspected of having a PE?

A
  • PERC Score <b>< 1; PE can be excluded</b> no D-Dimer or CTPA required<div>- PERC Score > 1; PE cannot be excluded consider D-Dimer</div>
268
Q

What is the gold-standard investigation for the diagnosis of PE?

A

“<b><u>CT Pulmonary Angiography (CTPA)</u></b><div>- CT scan with intravenous contrast</div><div><img></img><br></br></div>”

269
Q

What acid-base disorder is often seen in patients with pulmonary embolism upon initial assessment?

A

“<b><u>Respiratory Alkalosis;</u></b><div>- High respiratory rate causes CO2 blow-off</div><div>- Will also have low pO2</div>”

270
Q

Why do patients suffering from a pulmonary embolism often have low pO2?

A

<b><u>Ventilation-perfusion (VA/Q) mismatch</u></b><div>- Clot reduces the perfusion component (Q)</div><div>- Ventilation (VA) remains unaltered or even increases</div><div>- Hence VA/Q ratio increases and not all the blood passing through the lungs is sufficiently oxygenated</div><div>- Hence hypoxia</div>

271
Q

What investigations are important to carry out in patients with a suspected PE where there is suspected right ventricular strain?

A
  • ECG<div>- Echocardiogram</div><div>- Troponin</div>
272
Q

What changes can sometimes been seen in the ECG of patients with a pulmonary embolism?

A

“<u><b>Common;</b></u><div><b>- Sinus tachycardia</b></div><div>- Non-specific ST or T waves abnormalities<div><u><br></br></u></div><div><b><u>Classical;</u></b></div><div><b>- S1Q3T3</b> patterning (deep S waves in lead I, deep Q waves in lead III and T wave inversion in lead III)</div><div><u><br></br></u></div><div><b><u>Right heart strain</u>;</b></div><div>-<b>RBBB</b></div><div>- ST depression and <b>T wave inversion</b> anteriorly (<b>V1-V4</b>) AND/OR inferiorly (<b>II, III </b>and<b> aVF</b>)</div><div><img></img><br></br></div></div>”

273
Q

What imaging can be used in patients suspected of having a PE who are pregnant and/or where CTPA is contraindicated?

A

“V/Q Scan ;<span>involves using radioactive isotopes and a gamma camera to compare the</span>ventilation<span>with the</span>perfusion<span>of the lungs</span>”

274
Q

Outline the process of a ventilation-perfusion (VQ) scan?

A

<div>- Isotopes are inhaled to fill the lungs and a picture is taken to demonstrateventilation</div>

<div>- Next a contrast containingisotopes is injected and a picture is taken to demonstrateperfusion</div>

<div>- The two pictures are then compared</div>

<div>- With a pulmonary embolism there will be a deficit in perfusion as the thrombus blocks blood flow to the lung tissue</div>

<div>- This area of lung tissue will be ventilated but not perfused.</div>

275
Q

What are the contraindications for CTPA?

A
  • Pregnancy<div>- Renal impairment</div><div>- Contrast allergy</div><div>- Radiation risk too high</div>
276
Q

What is Virchow’s triad?

A

This describes the triad of pathophysiological processes that underly the development of a PE<div> o Venous stasis</div><div> o Hypercoaguable state</div><div> o Endothelial injury</div>

277
Q

What is the principle treatment for pulmonary embolism?

A

Anticoagulation

278
Q

How does the status of a patient with a PE inform the acute management?

A
  • Haemodynamically unstable patients or those in shock (hypotensive) need to be moved to resus/HDU/ITU<div>- Haemodynamically stable patients can be managed depending on their PESI score</div>
279
Q

What scoring system is used to guide the management of haemodynamically stable patients with a confirmed diagnosis of PE?

A

“<b><u>PESI Score;</u></b><div>- Predicts <b>30-day outcome</b> of PE</div><div>- Can be used to <b>guide management of inpatients </b>with PE</div><div>- Also used to assess <b>appropriateness of outpatient management</b></div>”

280
Q

What acute management should be considered in patients with a confirmed PE who are haemodynamically unstable?

A

Thombolysis; as per local guidelines

281
Q

What two aspects need to be considered when managing the haemodynamically stable patient with a confirmed diagnosis of PE?

A
  • PESI Score<div>- Evidence of right heart strain</div>
282
Q

Outline the management for a haemodynamically stable patient with a confirmed diagnosis of PE AND a high PESI score AND/OR evidence of right heart strain?

A
  • High risk<div>- Consider transfer to HDU/ITU</div><div>- Initiate anticoagulation</div>
283
Q

Outline the management for a haemodynamically stable patient with a confirmed diagnosis of PE AND a low PESI score and no evidence of right heart strain?

A
  • Low risk<div>- Initiate anticoagulation</div><div>- Consider discharge with anticoagulation follow-up</div>
284
Q

What agents are used in anticoagulation therapy in the management of PE?

A
  • Low molecular weight heparins (LMWH); tinzeparin, dalteparin, enoxaparin<div>- DOACs; apixaban, rivaroxaban, endoxaban</div><div>- Unfractionated heparins (UFH); heparin sodium</div><div>- Vitamin K antagonists (VKA); warfarin</div>
285
Q

What is the <b>first-line choice</b> in the anticoagulation of a stable patient with a PE and no renal impairment/co-morbidities?

A

<b>DOACs</b>; rivaroxaban, apixaban, edoxaban, dabigatran

286
Q

What is the first-line management choice in patients with a PE who are haemodynamically unstable?

A
  • Consider thrombolysis; alteplase, streptokinase, tenecteplase<div>- Unfractionated heparin</div>
287
Q

What is the first-line management choice in patients with a PE who have an active cancer?

A
  • DOACs<div>- If not suitable, consider LMWH for 5 days</div>
288
Q

Outline the acute management in patients with a PE who are also in renal failure?

A

”- <b>Creatinine clearance (CrCl) 15-50ml/min</b>; apixaban/rivaroxaban or LMWH for 5 days then follow up with edoxaban/warfarin<div><b>- Creatine clearance (CrCl) <15ml/min</b>; LMWH/UFH as per local guidelines</div>”

289
Q

Which thrombolytic drugs can be used in the management of PE?

A
  • Alteplase; recombinant t-PA<div>- Tenecteplase; recombinant t-PA</div><div>- Streptokinase; t-PA activator</div>
290
Q

Outline the two ways that thrombolysis can be performed?

A

<b>- Intravenously</b>; through a peripheral cannula<div><b>- Catheter-directed</b>; interventional radiologists administers thrombolysis directly to pulmonary arteries</div>

291
Q

What are the indications for thrombolysis in a PE?

A
  • Cardiac arrest with confirmed or suspected PE<div>- Confirmed PE with deterioration despite anticoagulation</div><div>- Haemodynamic instability AND high suspicion of PE OR confirmed PE within 14 days</div>
292
Q

Outline the long-term management for PE?

A

Continued anticoagulation for a minimum of <b>3 months</b>

293
Q

Outline the long-term management for PE in a patient with an active cancer?

A

Continued anticoagulation for <b>3-6months</b>

294
Q

What features of the PE’s presentation influence the long-term management?

A
  • Provoked or unprovoked PE<div>- Location of PE</div><div>- Bleeding risk</div><div>- Presence of underlying factors</div>
295
Q

What underlying causes should be considered in patients with an unprovoked PE?

A

<b>- Thrombophilia</b>; carry out thombophilia screening<div><b>- Cancer</b>; clinically assess and examine patient for evidence of tumour</div>

296
Q

Outline some of the long-term complications associated with PE?

A
  • Chronic thromboembolic pulmonary hypertension (CTEPH)<div>- Right sided heart failure</div><div>- Recurrance</div><div>- High mortality</div>
297
Q

What score can be used as a predictor of prognostic outcome following a PE?

A

<b><u>PESI Score;</u></b><div>- Age = 1 per year</div><div>- Male sex = 10</div><div>- History of cancer = 30</div><div>- History of heart failure = 10</div><div>- History of chronic lung disease = 10</div><div>- Heart rate >110bpm = 20</div><div>- Systolic blood pressure <100mmHg = 30</div><div>- Respiratory rate >30 = 20</div><div>- Temperature <36ºC = 20</div><div>- Altered mental status = 60</div><div>- SpO2<90% = 20</div>

298
Q

What is meant by pulmonary hypertension?

A

Increased resistance and thus pressure in the pulmonary arteries

299
Q

What is the effect of pulmonary hypertension?

A

Increased strain on the right side of the heart and a subsequent backlog of blood in the systemic venous system

300
Q

What are the 5 different classifications of pulmonary arterial hypertension (PAH)?

A

<b>- Group 1;</b> primary pulmonary arterial hypertension or that occurs as a result of SLE<div><b>- Group 2;</b> PAH due to left heart failure as a result of MI or systemic hypertension</div><div><b>- Group 3;</b> PAH due to chronic lung diseases</div><div><b>- Group 4; </b>PAH due to pulmonary vascular disease such as PE</div><div><b>- Group 5; </b>PAH due to sarcoidosis, glycogen storage disease, haematological disorders etc.</div>

301
Q

Outline the typical signs and symptoms of pulmonary hypertension?

A

<b>- SOB</b><div>- Syncope</div><div>- Tachycardia</div><div>- Rasied JVP</div><div>- Hepatomegaly</div><div>- Peripheral oedema</div>

302
Q

What investigations should be carried out in a patient with suspected pulmonary hypertension?

A
  • <b>ECG</b>; looking for right sided heart strain<div>- <b>CXR</b>; dilated pulmonary arteries and/or RV hypertrophy</div><div>- <b>NT-proBNP</b>; blood marker of atrial stretch that indicates RV failure</div><div>-<b> Echo</b>; used to estimate pulmonary arterial pressure</div>
303
Q

What changes may be seen on the ECG of a patient with pulmonary arterial hypertension?

A
  • <b>Dominant R waves</b>in<b>V1-V3</b>(right sided chest leads); right ventricular hypertrophy<div>- <b>Dominant S waves</b>in V4-V6 (left sided chest leads); right ventricular hypertrophy</div><div>- <b>Right axis deviation</b>; negative QRS in I and positive QRS in II and III/aVF</div><div>- <b>Right bundle branch block</b> (RBBB); rSR’ in V1 and qRs in V6</div>
304
Q

What changes may be seen on CXR in patient with pulmonary arterial hypertension?

A
  • Dilated pulmonary arteries<div>- Right ventricular hypertrophy</div>
305
Q

Outline the prognosis for patients with PAH?

A
  • Prognosis is very poor<div>- 30-40% 5-year survival</div><div>- Can be increased to 60-70% with effective management</div>
306
Q

Outline the treatment of primary pulmonary hypertension?

A
  • <b>IV prostanoids</b>; epoprostenol<div>- <b>Endothelin receptor antagonists</b>; macitentan</div><div>- <b>PDE-5 inhibitors</b>; sildenafil</div>
307
Q

How can secondary pulmonary hypertension be managed?

A

Treating the underlying cause sich as PE or SLE

308
Q

What are the complications associated with PAH?

A
  • Respiratory failure<div>- Cardiac arrhythmias</div><div>- Heart failure</div>
309
Q

What is sarcoidosis?

A

Multi-system granulomatous disorder of unknown aetiology

310
Q

What are granulomas?

A

Nodules of inflammation full of macrophages

311
Q

What is the characterstic histological changes seen in sarcoidosis?

A

”- Tissue infiltration<div>- Non-caseating granulomas</div><div>- Macrophages known as epitheliod cells</div><div>- Maintained by T cells</div><div><img></img><br></br></div>”

312
Q

Which organ system is primarily affected by symptoms in sarcoidosis?

A

Pulmonary/respiratory system (>90% of cases)

313
Q

Outline some of the extrapulmonary symptoms seen in sarcoidosis?

A
  • Erythema nodosum<div>- Lymphadenopathy</div>
314
Q

How is sarcoidosis distinguised from tuberculosis?

A
  • TB; caseating granulomas with areas of necrosis in the centre<div>- Sarcoidosis; non-caseating granulomas</div>
315
Q

Which groups are particularly at risk of sarcoidosis?

A
  • Women (2:1)<div>- Nordic/African ancestry</div>
316
Q

What is the typical presentation of sarcoidosis?

A
  • Black female<div>- Dry cough</div><div>- SOB</div><div>- Nodules on shins (eryhtema nodosum)</div>
317
Q

How is sarcoidosis thought to arise?

A
  • Exact aetiology is unknown<div>- Thought to occur due to abnormal immune response to unknown antigen(s)</div><div>- Environmental components; occuptational exposures (Alu or Ber)</div><div>- Infectious components; mycobacterium, cultibacterium</div>
318
Q

What is meant by the bimodal distribution of sarcoidosis presentation?

A
  • Two spikes in incidence<div>- Young adulthood</div><div>- Around 60 years</div>
319
Q

Which organ systems can commonly be affected by sarcoidosis

A
  • <b>Pulmonary</b>; lymphadenopathy, fibrosis, nodules<div>- <b>Hepatic</b>; nodules, cirrhosis, cholestasis</div><div>- <b>Ophthalmic</b>; uveitis, conjunctivitis, opti neuritis</div><div>- <b>Cardiac</b>; bundle branch block, heart block</div><div>- <b>Renal</b>; kidney stones, nephrocalcinosis, interstitial nephritis</div><div>- <b>Neurological</b>; nodules, pituitary involvement (DI), encephalopathy, facial nerve palsy</div><div>- <b>Skin</b>; erythema nodosum, lupus pernio</div>
320
Q

What is Lofgren’s Syndrome?

A

Specific triad of symptoms/signs seen in some sarcoidosis patients<div>- <b>Bilateral hilar lymphadenopathy</b> seen on CXR</div><div>- <b>Polyarthralgia</b></div><div>- <b>Erythema nodosum</b></div>

321
Q

What is lupus pernio?

A

“<div>- Violaceous nodules or plaques that can occur on the cheeks, nose, chin and ears</div><div>- Pathognomonic (characteristic) for sarcoidosis</div><img></img>”

322
Q

What is erythema nodosum?

A

“<div>- Erythematous, tender nodules found on the shins</div><img></img>”

323
Q

Outline some of the differential diagnoses for erythema nodosum?

A

“<b><u>SPOTTED;</u></b><div>- <b><u>S</u>arcoidosis</b></div><div>- <b><u>P</u>regnancy</b></div><div>- <b><u>O</u>ral contraceptive</b></div><div>- <b><u>T</u>uberculosis</b></div><div>- <b><u>T</u>hroat infections;</b><i>Streptococcus</i></div><div>- <b><u>E</u>verything else</b>; IBD, Non-Hodgkin Lymphoma</div><div>- <b><u>D</u>rugs</b>; sulfonamides</div>”

324
Q

Outline the differential diagnoses for sarcoidosis?

A
  • TB<div>- Lymphoma</div><div>- Hypersensitivity pneumonitis</div><div>- HIV</div><div>- Toxoplasmosis</div><div>- Histoplasmosis</div>
325
Q

Which investigation is most important to perform when a diagnosis of sarcoidosis is being considered?

A

CXR

326
Q

What is the characteristic X-Ray finding for a patient with sarcoidosis?

A

“<b>Bilateral hilar lymphadenopathy</b><div><img></img><br></br></div><div><img></img><br></br></div>”

327
Q

What are the main differentials for bihilar lymphadenopathy?

A
  • Cancer<div>- Lymphoma</div><div>- Tuberculosis</div>
328
Q

How can sarcoidosis be classified depending on chest X ray changes?

A
  • <b>Stage 0</b>; normal CXR<div>- <b>Stage I</b>; bilateral hilar lymphadenopathy</div><div>-<b> Stage II</b>; bilateral hilar lymphadenopathy AND infiltrates</div><div>- <b>Stage III</b>; infiltrates alone</div><div>- <b>Stage IV</b>; pulmonary fibrosis</div>
329
Q

What is meant by Heerfordt’s syndrome?

A

Sarcoid-associated condition characterised by;<div>- Fever</div><div>- Parotid swelling</div><div>- Uveitis; inflammation of the middle layer of the eye</div><div> o +/- Facial palsy</div>

330
Q

What routine tests are used to investigate sarcoidosis?

A

”- <b>Bloods</b>; FBCs, U&Es, <b>Ca2+</b>, LFTs<div>- <b>Electrical</b>; ECGs</div><div>- <b>Imaging</b>; CXR</div><div>- <b>Special</b>; <b>Serum ACE Level</b></div>”

331
Q

Why is it important to measure Ca2+levels in patients suspected of having sarcoidosis?

A

Within non-caseating granulomas seen in sarcoidosis there is an increased production of <b>activated vitamin D</b> (calcitriol) which can lead to hypercalcaemia

332
Q

Why are serum ACE levels measured when investigating sarcoidosis?

A

Activated macrophages within the granulomas produce ACE hence the leves are raised in these patients

333
Q

How do we further investigate pulmonary sarcoidosis?

A
  • <b>Lung function tests</b>; spirometry, diffusing capacity for carbon monoxide (DLCO) and carbon monoxide transfer coefficient (KCO)<div>- <b>Imaging</b>; high resolution CT thorax</div><div>- <b>Bronchoscopy and biopsy</b>; endobronchial biopsy, transbronchial biopsy, endobronchial ultrasound (EBUS) plus lymph node sampling</div>
334
Q

What kind of pattern may be seen in the spirometry for a patient with sarcoidosis?

A
  • <b>Restrictive</b> lung disease pattern<div>- Although an obstructive picture can be seen</div>
335
Q

What treatment is the first-line in patients with newly-diagnosed sarcoidosis?

A

No treatment in patients with no or mild symptoms as the condition can resolve spontaneously

336
Q

What are the four main treatment options in patients whose sarcoidosis symptoms persist or progress?

A
  • Monitoring<div>- Steriods</div><div>- Immunsuppression</div><div>- Transplant</div>
337
Q

Outline some of the pharmacological treatments for sarcoidosis?

A
  • <b>Oral steriods</b>; prednisolone (20-40mg, OD)<div>- <b>Bisphosphonates</b>; alendronic acid or zolendronic acid</div><div>-<b> Immunosuppressants</b>; methotrexate/azathioprine</div>
338
Q

What are the requirements for pharmacological management of sarcoidosis?

A
  • When potential danger of a fatal outcome or permanent disability<div>- Where there is unacceptable loss of quality of life</div><div>- Deteriorating lung function</div><div>- Severe progression of symptoms/disease</div><div>- Hypercalcaemia</div>
339
Q

Outline the prognosis of sarcoidosis?

A
  • 60% of sarcoidosis resolves within 6 months<div>- Small numbers of patients progress to develop pulmonary fibrosis and PAH</div><div>- Death can occur when cardiac sarcoidosis causes arrhythmias</div>
340
Q

What are the side effects of steriods?

A

“<b><u>CUSHINGOID;</u></b><div>- <b><u>C</u>ataracts</b></div><div>- <b><u>U</u>lcers</b>; GI</div><div>- <b><u>S</u>kin</b>; thinning, striae and bruising</div><div>- <b><u>H</u>ypertension</b> and hirsutism</div><div>- <b><u>I</u>mmunosuppression</b>; susceptibility to infection</div><div>- <b><u>N</u>ecrosis</b>; avascular necrosis of femoral head</div><div>- <b><u>G</u>aining</b>weight</div><div>- <b><u>O</u>steoporosis</b>; consider bisphosphonates or Ca2+ suppliments</div><div>- <b><u>I</u>nsomina</b> and mood changes</div><div>- <b><u>D</u>iabetes</b></div>”

341
Q

What is important to consider when withdrawing steroid treatment?

A
  • Sudden withdrawal of steriods can lead to life-threatening adrenal insuficiency<div>- This cultminates in cardiovascular collapse</div><div>- Instead steriod doses need to be tapered down</div>
342
Q

What is the different between secdonary adrenal insufficiency and steriod withdrawal?

A

<div>Both can occur as a result of stopping steriod therapy</div>

  • <b>Secondary adrenal insufficiency</b>; depends on dose and duration and can be extremely severe and even life-threatening<div>- <b>Steriod withdrawal</b>; can occur at any dose/regimen</div>
343
Q

What is obstructive sleep apnoea?

A

Obstructive sleep apnoea occurs when there is a collapse of the pharyngeal airway during sleep

344
Q

What are the characterstics of obstructive sleep apnoea?

A

Apnoeic episodes during sleep where the patient will stop breathing periodically for up to a few minutes

345
Q

Oultine the risk factors for obstructive sleep apnoea?

A
  • Middle age<div>- Male</div><div>- Obesity</div><div>- Alcohol</div><div>- Smoking</div>
346
Q

What are the features that are important to ask about when taking a history of a patient with suspected sleep apnoea?

A
  • Snoring<div>- Apnoeic episodes</div><div>- Morning headaches</div><div>- Waking up un-refreshed</div><div>- Daytime sleepiness</div><div>- Concentration problems</div><div>- Reduces SpO2 during sleep</div>
347
Q

Outline some of the complications that can arise in servereobstructive sleep apnoea?

A
  • Hypertension<div>- Heart failure</div><div>- MI</div><div>- Stroke</div>
348
Q

What scale can be used to assess the symptoms of sleepiness in a patient with obstructive sleep apnoea?

A

“<b><u>Epworth Sleepiness Scale;</u></b><div><img></img></div><div><b><u>Scoring;</u></b></div><div>- 0-5;lower than normal daytime sleepiness</div><div>- 6-10;normal daytime sleepiness</div><div>- 11-12;mild excessive daytime symptoms</div><div>- 13-15;moderate excessive daytime symptoms</div><div>- 16-24;severe excessive daytime symptoms</div>”

349
Q

Outline the management options for obstructive sleep apnoea?

A
  • Referral to ENT specialist or sleep clinics<div>- Correct reversible risk factors</div><div>- CPAP</div><div>- Surgery; uvulopalatopharyngoplasty (UPPP)</div>
350
Q

Which antibiotic can be used prophylatically in patients with COPD who are suffering from repeat IE-COPD?

A

Azithromycin; make sure to perform ECG prior to starting due to potential QTc prolongation