Resp fifth yr Flashcards

1
Q

What is pneumothorax?

A

occurs when air gets into the pleural space separating the lung from the chest wall. It can occur spontaneously or secondary to trauma, medical interventions (“iatrogenic”) or lung pathology.

Tension, primary, secondary

The typical patientis a young, tall, thin young man presenting with sudden breathlessness and pleuritic chest pain, possibly whilst playing sports.

RF’s
pre-existing lung disease: COPD, asthma, cystic fibrosis, lung cancer, Pneumocystis pneumonia
connective tissue disease: Marfan’s syndrome, rheumatoid arthritis
ventilation, including non-invasive ventilation
catamenial pneumothorax is the cause of 3-6% of spontaneous pneumothoraces occurring in menstruating women. It is thought to be caused by endometriosis within the thorax

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2
Q

Ix for pneumothorax?

A

Erect CXR - Measuring the size of the pneumothorax involves measuring horizontally from the lung edge to the inside of the chest wall at the level of the hilum.

CT thorax can detect a small pneumothorax that is too small to see on a chest xray or be used to accurately assess the size of the pneumothorax

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3
Q

Management of pneumothorax?

A

if no SOB and there is a < 2cm rim of air on the chest xray then no treatment required as it will spontaneously resolve. Follow up in 2-4 weeks is recommended.

If SOB and/or there is a > 2cm rim of air on the chest xray then it will require aspiration and reassessment.
If aspiration fails twice it will require a chest drain.

Unstable patients or bilateral or secondary pneumothoraces generally require a chest drain.

Persistent air leak or recurrent pneumothoraces - video-assisted thoracoscopic surgery (VATS) should be considered to allow for mechanical/chemical pleurodesis +/- bullectomy.

Stop smoking, don’t fly for 2 weeks, no scuba diving for life

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4
Q

What is tension pneumothorax?

A

It is caused by trauma to chest wall that creates a one-way valve that lets air in but not out of the pleural space. Means with each breath more air drawn in.

This is dangerous as it creates pressure inside the thorax that will push the mediastinum across, kink the big vessels in the mediastinum and cause cardiorespiratory arrest.

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5
Q

Signs of tension pneumothorax?

A

Tracheal deviation away from side of pneumothorax
Reduced air entry to affected side
Increased resonant to percussion on affected side
Tachycardia
Hypotension

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6
Q

Management of tension pneumothorax?

A

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

If a tension pneumothorax is suspected do not wait for any investigations. Once the pressure is relieved with a cannula then a chest drain is required for definitive management.

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7
Q

What is the triangle of safety for inserting chest drain?

A

The 5th intercostal space (or the inferior nipple line)
The mid axillary line (or the lateral edge of the latissimus dorsi)
The anterior axillary line (or the lateral edge of the pectoris major)

The needle is inserted just above the rib to avoid the neurovascular bundle that runs just below the rib. Once the chest drain is inserted obtain a chest xray to check the positioning.

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8
Q

Features of pneumothorax?

A

dyspnoea
chest pain: often pleuritic
sweating
tachypnoea
tachycardia

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9
Q

What is sarcoidosis?

A

granulomatous inflammatory condition. Granulomas are nodules of inflammation full of macrophages. Unknown aetiology.

It is usually associated with chest symptoms but also has multiple extra-pulmonary manifestations such as erythema nodosum and lymphadenopathy.

two spikes in incidence, in young adulthood and again around age 60. Women are affected more often and it occurs more frequently in black people compared with other ethnic groups.

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10
Q

Features of sarcoidosis?

A

Lungs - mediastinal lymphadenopathy, pulmonary fibrosis, pulmonary nodules
Skin - erythema nodosum, Lupus pernio, granulomas in scar tissue
Eyes - uveitis, conjunctivitis, optic neuritis
Systemic - fever, fatigue, WL
Liver - nodules, cirrhosis, cholestasis
Heart - bundle branch block, heart block, myocardial muscle involvement
Kidney - stones, nephritis
CNS - nodules, DI, encephalopathy
PNS - facial nerve palsy, mononeuritis multiplex
Bones - arthralgia, arthritis, myopathy

Mikulicz syndrome* there is enlargement of the parotid and lacrimal glands due to sarcoidosis, tuberculosis or lymphoma

Heerfordt’s syndrome (uveoparotid fever) there is parotid enlargement, fever and uveitis secondary to sarcoidosis

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11
Q

What is Lofgren’s syndrome?

A

A specific presentation of sarcoidosis. It is characteristic by a triad of:

Erythema nodosum
Bilateral hilar lymphadenopathy
Polyarthralgia (joint pain in multiple joints)

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12
Q

Ix for sarcoidosis?

A

Bloods - Raised serum ACE. This is often used as a screening test., Hypercalcaemia (rasied calcium) is a key finding. Raised serum soluble interleukin-2 receptor. Raised CRP. Raised immunoglobulins

CXR - hilar lymphadenopathy - stage 0-4

High-resolution CT thorax - hilar lymphadenopathy and pulmonary nodules

MRI can show CNS involvement

PET scan can show active inflammation in affected areas

Histology - via bronchoscopy with ultrasound guided biopsy of mediastinal lymph nodes - shows characteristic non-caseating granulomas with epithelioid cells.

Tests for other organ involvement:
U&Es for kidney involvement
Urine dipstick or urine albumin-creatinine ratio to look for proteinuria indicating nephritis
LFTs for liver involvement
Ophthalmology review for eye involvement
ECG and echocardiogram for heart involvement
Ultrasound abdomen for liver and kidney involvement

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13
Q

Treatment of sarcoidosis?

A

No treatment is considered as first line in patients with no or mild symptoms as the condition often resolves spontaneously. (60% of all patients resolve in 6m)

Oral steroids are usually first line where treatment is required and are given for between 6 and 24 months. Patients should be given bisphosphonates to protect against osteoporosis whilst on such long term steroids.

Second line options are methotrexate or azathioprine

Lung transplant is rarely required in severe pulmonary disease (pulmonary fibrosis and hypertension)

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14
Q

Causes and features of OSA?

A

caused by collapse of the pharyngeal airway during sleep. It is characterised by apnoea episodes during sleep where the person will stop breathing periodically for up to a few minutes

Predisposing factors:
obesity
macroglossia: acromegaly, hypothyroidism, amyloidosis
large tonsils
Marfan’s syndrome

Partner often complains of excessive snoring and may report periods of apnoea.

Consequences: daytime somnolence, compensated respiratory acidosis, hypertension, increase risk of MI and stroke

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15
Q

Ix and Tx of OSA?

A

Ix:
Epworth Sleepiness Scale - questionnaire completed by patient +/- partner
Multiple Sleep Latency Test (MSLT) - measures the time to fall asleep in a dark room (using EEG criteria)
sleep studies (polysomnography) - pulse oximetry, EEG, respiratory airflow etc.

Tx:
weight loss
continuous positive airway pressure (CPAP) is first line for moderate or severe OSAHS
intra-oral devices (e.g. mandibular advancement) may be used if CPAP is not tolerated or for patients with mild OSAHS where there is no daytime sleepiness
the DVLA should be informed if OSAHS is causing excessive daytime sleepiness
surgery - if severe - uvulopalatopharyngoplasty (UPPP).

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16
Q

What is bronchiectasis?

A

a permanent dilatation of the airways secondary to chronic infection or inflammation.

Causes - post-infective: tuberculosis, measles, pertussis, pneumonia, cystic fibrosis, bronchial obstruction e.g. lung cancer/foreign body, immune deficiency: selective IgA, hypogammaglobulinaemia, allergic bronchopulmonary aspergillosis (ABPA), ciliary dyskinetic syndromes: Kartagener’s syndrome, Young’s syndrome, yellow nail syndrome

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17
Q

Features of bronchiectasis?

A

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

O/E
abnormal chest auscultation - coarse crackles, wheeze
clubbing may be present

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18
Q

Management of bronchiectasis?

A

After assessing for treatable causes (e.g. immune deficiency) management is as follows:

physical training (e.g. inspiratory muscle training) - has a good evidence base for patients with non-cystic fibrosis bronchiectasis

postural drainage

antibiotics for exacerbations + long-term rotating antibiotics in severe cases

bronchodilators in selected cases

immunisations

surgery in selected cases (e.g. Localised disease)

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19
Q

Most common organisms in bronchiectasis?

A

Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae

20
Q

Summary of ARDS?

A

Caused by increased permeability of alveolar capillaries leading to fluid accumulation in the alveoli (i.e., non-cariogenic pulmonary oedema).

Mortality around 40%

Causes = infection (sepsis, pneumonia), massive blood transfusion, trauma, smoke inhalation, acute pancreatitis, covid, cardio-pulmonary bypass

Features - acute onset, severe, dyspnoea, tachypnoea, bilateral lung crackles, low O2 sats

Ix - CXR and ABG

Criteria - American European consensus conference - acute onset, pulmonary oedema (bilateral infiltrates on CXR), non-cariogenic, pO2.FiO2 <40kPa

Tx - managed by ITU, oxygenation/ventilation to treat the hypoxaemia, general organ support e.g. vasopressors as needed, treatment of the underlying cause e.g. antibiotics for sepsis, certain strategies such as prone positioning and muscle relaxation have been shown to improve outcome in ARDS

21
Q

What is pneumonia?

A

Infection of lung tissue - causes inflammation of lung tissue and sputum filling the airways and alveoli.

Seen as consolidation on CXR

22
Q

Classification of pneumonia?

A

Community acquired pneumonia - outside hospital

Hospital acquired pneumonia - develops more than 48h after hospital admission

Aspiration pneumonia

23
Q

Presentation of pneumonia?

A

Shortness of breath
Cough productive of sputum
Fever
Haemoptysis (coughing up blood)
Pleuritic chest pain (sharp chest pain worse on inspiration)
Delirium (acute confusion associated with infection)
Sepsis

Tachypnoea
Tachycardia
Hypoxia
Hypotension
Fever
Confusion

Bronchial breath sounds - equally loud on inspiration and expiration - caused by consolidation of lung tissue around airway
Focal coarse crackles - air passing through sputum in airways
Dullness to percussion - due to lung tissue collapse and/or consolidation

24
Q

How to assess severity of pneumonia?

A

CRB-65 out of hospital and CURB-65 in hospital

C – Confusion (new disorientation in person, place or time)
U – Urea > 7
R – Respiratory rate ≥ 30
B – Blood pressure < 90 systolic or ≤ 60 diastolic.
65 – Age ≥ 65

The CURB 65 score predicts mortality (score 1 = under 5%, score 3 = 15%, score 4/5 = over 25%). The scoring system is there to help guide whether to admit the patient to hospital:

Score 0/1: Consider treatment at home
Score ≥ 2: Consider hospital admission
Score ≥ 3: Consider intensive care assessment

25
Q

Causes of pneumonia?

A

Strep pneumonia (pneumococcus) - 80% of cases, most common cause in children - rapid onset, high fever, pleuritic, herpes labialis

H. influenza - common in COPD

Moraxella catarrhalis - immunocompromised patients, pt’s with COPD

Pseudomonas aeruginosa - CF, bronchiectasis

Staph. aureus - CF

Klebsiella - in alcoholics

Idiopathic interstitial pneumonia - group of non-infective causes of pneumonia - e.g., - cryptogenic organising pneumonia, complication of RA or amiodarone Tx

26
Q

Definition of atypical pneumonia?

A

pneumonia caused by an organism that cannot be cultured in the normal way or detected using a gram stain.

They don’t respond to penicillins and can be treated with macrolides (e.g. clarithomycin), fluoroquinolones (e.g. levofloxacin) or tetracyclines (e.g. doxycycline).

27
Q

Causes of atypical pneumonia?

A

Legionella - infected water supplies or air conditioning units, can cause hyponatraemia by causing an SIADH

Mycoplasma pneumonia - milder pneumonia, erythema multiforme rash (target lesions), neurological Sx in young patients - bilateral consolidation on CXR - Dx mycoplasma serology, positive cold agglutination test

Chlamydophilia pneumonia - presentation might be a school aged child with a mild to moderate chronic pneumonia and wheeze

Coxiella burnetti - Q fever - linked to exposure to animals and their bodily fluids

Chlamydia psittaci - typically contracted from contact with infected birds

28
Q

Summary of fungal pneumonia?

A

Pneumocystis jiroveci (PCP) pneumonia occurs in patients that are immunocompromised

poorly controlled/new HIV with low CD4 count

dry cough w/o sputum, SOBOE and night sweats

CXR - bilateral infiltrates

Exercise induced desaturation

extra pulmonary manifestations - hepatosplenomegaly, lymphadenopathy, choroid lesions

Tx - co-trimoxazole

Patients with low CD4 counts are prescribed prophylactic oral co-trimoxazole to protect against PCP.

29
Q

Ix for pneumonia?

A

CRB 0 or 1 in community - don’t need Ix

in hospital - CXR, FBC, U&Es, CRP

Moderate/severe cases - sputum cultures, blood cultures, legionella and pneumococcal urinary antigens. ABG

Patients that are immunocompromised may not show an inflammatory response and may not have raised inflammatory markers.

repeat CXR 6 weeks after to ensure no underlying secondary abnormalities

30
Q

Tx of pneumonia?

A

Follow local trust guidelines - antibiotic resistance

moderate/severe - IV antibiotics, then switched to oral if improvement clinically or by inflammatory markers

Mild CAP: 5 day course of oral antibiotics (amoxicillin or macrolide)
Moderate to severe CAP: 7-10 day course of dual antibiotics (amoxicillin and macrolide)

supportive care - O2, IV fluids

children - amoxicillin first-line, macrolide added if no response, macrolide if mycoplasma or chlamydia suspected

31
Q

Complications of pneumonia?

A

Sepsis
Pleural effusion
Empyema
Lung abscess
Death

32
Q

RFs for 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

33
Q

Use of CRP in general practice for pneumonia?

A

CRP < 20 mg/L - do not routinely offer antibiotic therapy
CRP 20 - 100 mg/L - consider a delayed antibiotic prescription
CRP > 100 mg/L - offer antibiotic therapy

34
Q

Summary of aspiration pneumonia?

A

Foreign materials gaining entry to bronchial tree. Depending on the acidity of the aspirate a chemical pneumonitis can develop, as well as bacterial pathogens adding to the inflammation.

The right middle and lower lung lobes are the most common sites affected, due to the larger calibre and more vertical orientation of the right main bronchus.

RFs - poor dental hygiene, swallowing difficulties, prolonged hospitalisation or surgical procedures, impaired consciousness, impaired mucociliary clearance

35
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

36
Q

Tx for mycoplasma pneumonia?

A

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

37
Q

Cause of upper zone pulmonary fibrosis?

A

FASSTEN CaR

Farmers lung - hypersensitivity pneumonitis
Ankylosing spondylitis
Sarcoidosis
Silicosis
TB
Eosinophilic granuloma (Langerhans cell histiocytosis)
Neurofibromatosis

Coal worker’s pneumoconiosis
A -
Radiation-induced pulmonary fibrosis

38
Q

Causes of lower zone pulmonary fibrosis?

A

BADRASH

Bronchiolitis obliterans with organising pneumonia (BOOP)
Asbestosis
Drugs - nitrofurantoin, hydralazine, INH, amiodarone,bleomycin, methotrexate
Rheumatologic disease - SLE
Aspiration
Scleroderma
Hamman Rich (interstitial pulmonary fibrosis) and IPF

39
Q

Summary of idiopathic pulmonary fibrosis?

A

the term IPF is reserved when no underlying cause exists.

IPF is typically seen in patients aged 50-70 years and is twice as common in men.

Features
progressive exertional dyspnoea over more than 3 months
bibasal fine end-inspiratory crepitations on auscultation
dry cough
clubbing

Dx
spirometry - restrictive picture (FEV1 normal/decreased, FVC decreased, FEV1/FVC increased)
impaired gas exchange - reduced 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

Tx
pulmonary rehabilitation
There is some evidence that pirfenidone (an antifibrotic agent) may be useful in selected patients (see NICE guidelines)
Nintedanib is a monoclonal antibody targeting tyrosine kinase
many patients will require supplementary oxygen and eventually a lung transplant

Prognosis - poor, average life expectancy is around 3-4 years

40
Q

Summary of interstitial lung disease?

A

an umbrella term to describe conditions that affect the lung parenchyma (the lung tissue) causing inflammation and fibrosis.

Fibrosis involves the replacement of the normal elastic and functional lung tissue with scar tissue that is stiff and does not function effectively.

41
Q

Management of interstitial lung disease?

A

Supportive and prevent further progression

Remove or treat the underlying cause
Home oxygen where they are hypoxic at rest
Stop smoking
Physiotherapy and pulmonary rehabilitation
Pneumococcal and flu vaccine
Advanced care planning and palliative care where appropriate
Lung transplant is an option but the risks and benefits need careful consideration

42
Q

Causes of drug induced pulmonary fibrosis?

A

Amiodarone
Cyclophosphamide
Methotrexate
Nitrofurantoin

43
Q

Causes of secondary pulmonary fibrosis?

A

Alpha-1 antitripsin deficiency
Rheumatoid arthritis
Systemic lupus erythematosus (SLE)
Systemic sclerosis

44
Q

Summary of hypersensitivity pneumonitis?

A

AKA Extrinsic Allergic Alveolitis

type III hypersensitivity reaction to an environmental allergen that causes parenchymal inflammation and destruction in people that are sensitive to that allergen

Bronchoalveolar lavage involves collecting cells from the airways during bronchoscopy by washing the airways with fluid then collecting that fluid for testing. This shows raised lymphocytes and mast cells in hypersensitivity pneumonitis.

Tx - remove allergen, give O2, steroids

Examples
Bird-fanciers lung is a reaction to bird droppings
Farmers lung is a reaction to mouldy spores in hay
Mushroom workers’ lung is a reaction to specific mushroom antigens
Malt workers lung is a reaction to mould on barley

45
Q

Summary of cryptogenic organising pneumonia?

A

previously known as bronchiolitis obliterans organising pneumonia

involves a focal area of inflammation of the lung tissue

idiopathic or triggered by infection, inflammatory disorders, medications, radiation or environmental toxins or allergens.

Presentation is very similar to infectious pneumonia with shortness of breath, cough, fever and lethargy. It also presents on similarly to pneumonia on a chest xray with a focal consolidation.

Dx - delayed due to similarities to infective pneumonia

Lung biopsy - definitive investigation

Tx - systemic corticosteroids

46
Q

Summary of asbestosis?

A

lung fibrosis related to the inhalation of asbestos

Asbestos is fibrogenic, meaning it causes lung fibrosis. It is also oncogenic, meaning it causes cancer.

Lung fibrosis
Pleural thickening and pleural plaques
Adenocarcinoma
Mesothelioma

Suffers are eligible for compensation if they develop asbestos related health conditions (except isolated pleural plaques).

All patients that die with known exposure to asbestos need to be referred to the coroners.