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Medicine block (Y3) > Week 3: Respiratory medicine (4) (common conditions con) > Flashcards

Week 3: Respiratory medicine (4) (common conditions con) Flashcards

1
Q

Pleural cavity

A
  • Potential space between the visceral and parietal pleura- two lays which surround the lungs- tiny bit of fluid

outer pleura –> parietal (attached to chest wall)

inner pleura –> visceral (covers lungs)

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2
Q

pleural diseases

A
  • Pneumothorax’s= air in pleural cavity
  • Pleural effusion= fluid in pleural cavity
  • Empyema= infected fluid in pleural cavity
  • Pleural tumours= benign vs malignant
  • Pleural plaques= discrete fibrous areas
  • Pleural thickening= scarring/calcification caused by
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3
Q

pneumothoraxs can be split into

A
  1. Spontaneous
    1. Primary (no lung disease)
    2. Secondary (lung disease
  2. Traumatic
  3. TENSION: emergency (haemodynamic instability
  4. Iatrogenic (e.g. post central line or pacemaker insertion)
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4
Q

risk factors of pneumothorax

A
  • Pre-existing lung disease
  • Being tall and slim
  • Smoking/cannabis
  • Diving
  • Trauma/chest procedure
  • Other conditions e..g marfans
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5
Q

management of primary pneumo

A
  • If symptomatic and rim of air >2cm on CXR give O2 and aspirate. If unsuccessful consider re-aspiration or intercostal drain. Remove drain after full re-expansion / cessation of air leak.
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6
Q

management of secondary pneumo

A

as above but lower threshold for ICD  If persistent air leak >5 days (bronchopleural fistula) refer to thoracic surgeons

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7
Q

discharge advice after pneumothorax

A

no flying or diving until resolved

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8
Q

simple pneumothorax

A
  • Tiny rim of air within pleural cavity that doesn’t impair haemodynamic stasis
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9
Q

tension pneumothorax

A
  • Causes haemodynamic instability
    • Hypotensive and tachycardic
  • Caused by the one-way flow of air
    • More and more air accumulating in pleural cavity
  • Life threatening- quick intervention
  • Causes e.g. trauma to the chest
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10
Q

primary vs secondary pneumo

A

Primary

  • No underlying lung pathology
  • Risk factors
    • Male young
    • Family history of pneumothorax
    • Smoking (x9 risk)

Secondary

  • Underlying lung pathology
    • COPD
    • Asthma
    • Bronchiectasis – inc CF
    • Lung cancer
    • Infections: TB, pneumonia
    • Marfans syndrome, Ehlers Danlos syndrome
    • RA
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11
Q

Spontaneous vs iatrogenic vs traumatic pneumo

A

Spontaneous

  • Disruption of the subpleural blebs/bulla (air filled sac)

Iatrogenic

  • Insertion of central/pacing wires
    • Esp internal jugular vein

Trauma

  • Severe chest wall injury- stab wound or gunshot wound  allows air to enter the pleural space
  • Rib fractures  puncture the visceral pleura
    • May not be easily visible
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12
Q

presentation of tension pneumothorax

A

Symptoms

  • Chest pain
    • Pleuritic in nature
    • Sudden onset
    • Sharp pain
    • +/- SOB
    • History of trauma/liung disease
  • Respiratory distress
  • Cyanosis
  • Tachycardia
  • Marked hypoxemia

Signs

  • Low BP
  • Tachycardic
  • Cyanotic
  • Coma
  • Trachea deviation
    • Away from the affected side
  • Chest movement
    • Reduced on affected side
  • Auscultation
    • Reduced/ absent breath signs
  • Will not have time to do percussion

(which would be hyper resonant on affected side)

or vocal/tactile resonance (which would be reduced

on affected side)

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13
Q

treatment if you suspect tension

A

if you suspect tension- do not wait to x-ray

Emergency needle decompression

  • First site
    • 2nd intercostal space, mid-clavicular line
    • Just lateral to the nipple
  • If first site doesn’t work
    • 5th ICS
    • Anterior axillary line, lateral to the nipple
  • Remember to go over the rib to avoid the nerve, artery and vein bundle
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14
Q

symptoms of simple pneumothorax

A
  • Symptoms
    • Chest pain
      • Pleuritic in nature- sharp stabbing
      • Sudden onset
      • Sharp pain
    • +/- SOB
    • History of trauma/lung disease
  • Signs
    • Trachea deviation – usually normal, can push the trachea to the other side
    • Chest movement reduced on affected side- collapsed lung
    • Percussion
      • Hyper resonant or resonant on affected side
    • Auscultation
      • Reduced or absent breath signs on affected side
    • Vocal/tactile resonance
      • Reduced on affected side
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15
Q

radiological finding of simple pneumo

A
  • Left lung
  • Absent lung markings
  • Collapsed lung borders seen
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16
Q

management of simple pneumo

A
  • Conservative treatment
    • Small pneumothorax
    • Pt goes home
    • Comes back to see if resolved
  • Pleural aspiration
    • Needle in pleural cavity to drain air out
    • 2.5l maximum
  • Chest drain insertion
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17
Q

Chest drain insertion

A
  • Under ultrasound guidance
  • Safe triangle
    • Superior: base of the axilla
    • Inferior: 6th rib/5th intercostal space
    • Anterior: lateral edge of pectoralis major muscle
    • Posterior: lateral edge of latissimus dorsi muscle
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18
Q

pathophysiology of pleural effusion

A

In normal pleural cavity there is tightly controlled production and absorption of pleural fluid.

  • Excess fluid in the pleural cavity
    • Imbalance between rate of production and absorption
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19
Q

simple effusion

A

when there is fluid in the pleural fluid- can be transudate or exudate

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20
Q

haemothorax

A

when the fluid is blood e.g. trauma

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21
Q

chylothorax

A

when the fluid is lymph e.g. leak from lymphatic duct

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22
Q

empyema

A

when the fluid is pus

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23
Q

examination for pleural effusion

A
  • CXR
  • ECG
  • Bloods: FBC, U&E’s, LFT’s, CRP, Bone profile, LDH, clotting
  • ECHO (if suspect heart failure)
  • Staging CT(with contrast) if suspect exudative cause
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24
Q

presenting symptoms and signs of pleural effusion

A
  • SOB (gradual onset)
  • Pleuritic chest pain – irritation of pleural lining to the fluid e.g. blood or lymph
  • Features of clinical disease
    • Congestive cardiac failure – pulmonary oedema
    • Lung malignancy
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25
Q

signs of pleural effusion

A
  • Tracheal deviation
    • Away from the affected side
  • Chest movement
    • Reduced on affected side
  • Percussion notes
    • Stony dull on affected side
  • Breath sounds
    • (Vesicular) reduced/ absent on affected side
  • Vocal resonance
    • Reduced on affected side
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26
Q

radiological findings of pleural effusion

A

Criteria for PE

  • Meniscus showing fluid in the pleural cavity (right base)
    • Beneath the yellow line= fluid
  • Loss of costophrenic angle
  • Loss of left heart border
27
Q

PE and tracheal deviation

A

If no tracheal deviation then pathology may be a mixture of atelectasis and effusion (pull + push = no deviation)

  • Will need to do a bedside US to determine if fluid or collapse
28
Q

Pleural effusion diagnosis

A

Ultrasound guided pleural aspiration

  • Biochemistry (protein, pH, LDH)
  • Cytology
  • Microbiology (including AAFB)

N.B. Never insert a chest drain unless the diagnosis is well established (e.g. known metastatic lung cancer) otherwise draining all fluid off may hinder the opportunity to obtain pleural biopsies. Only indication for urgent chest drain insertion for a new effusion would be an underlying empyema (pH of pleural fluid <7.2 or visible pus on aspirate).

Consider Thoracoscopy or CT Pleural Biopsy

29
Q

Causes of Transudate effusions (pleural protein <30 g/L)

A

Common:

  • Heart failure
  • Cirrhosis
  • Hypoalbuminaemia (nephrotic syndrome or peritoneal dialysis)

Less common:

  • Hypothyroidism, mitral stenosis, pulmonary embolism

Rare:

  • Constrictive pericarditis, superior vena cava obstruction, Meig’s syndrome
30
Q

Causes of Exudate effusions (pleural protein >30 g/L)

A

Common:

  • Malignancy
  • Infections – parapneumonic, TB, HIV (kaposi’s)

Less common:

  • Inflammatory (rheumatoid arthritis, pancreatitis, benign asbestos effusion, Dressler’s, pulmonary infarction/pulmonary embolus), Lymphatic disorders, Connective tissue disease

Rare:

  • Yellow nail syndrome, fungal infections, drugs
31
Q

Interstitial library disease (ILD)

A

Umbrella term describing a number of conditions that affect the lung parenchyma in a diffuse manner including:

  • Usual Interstitial Pneumonia (UIP)
  • Non-specific Interstitial Pneumonia (NSIP)
  • Extrinsic Allergic Alveolitis
  • Sarcoidosis
  • Several other conditions
  • Important to take a comprehensive occupational / environmental history – inhalation can lead to conditions such as silicosis (dust), asbestosis (asbestos) or pneumoconioisis (coal workers)
32
Q

diagnosis of ILD

A
  • Typically restrictive lung diseases on PFT’s (above 70%)
  • Harder to breath in than out
  • Reduced DLCO due to thickening of the lung parenchhyme due to fibrosis
33
Q

pathophysiology of ILD

A
  • Lung compliance reduced
    • Lungs are stiff and hard to expand
  • Elastic recoil of lungs is increase, the resting lung volume is smaller than normal, but rate of airflow not impaired
  • Restrictive type of ventilatory defect on spirometry
34
Q

clinical symptoms of ILD

A
  • Dry cough
  • Dyspnoea (short of breath) on exertion progressing to at rest
  • Fatigue
  • Typically gradual, insidious progression Sx
35
Q

clinical signs of ILD

A
  • Decreased lung excursion on palpation
  • Bi-basal end inspiratory lung crackles
  • Finger clubbing small pleural effusions
36
Q

Usual interstitial pneumonia (UIP)

A

Commonest type of pulmonary fibrosis  usually idiopathic

Signs and symptoms

  • SoB on activity
  • Dry cough
  • Reduced appetite
  • Clubbing
  • Reduced chest expectation

Examination

  • Auscultation
    • Fine inspiratory creptiations (VELCRO)- usually best heard in basal/ axillary areas
  • Cardiovascular- features of pulmonary hypertension
37
Q

Extrinsic Allergic Alveolitis

A

Also known as Hypersensitivity Pneumonitis

Background

Inhalation of organic antigen to which the individual has been sensitised

Clinical presentation

  • ACUTE – short period from exposure, 4-8 hrs. Usually reversible: spontaneously settle 1-3 days. Can recur.
  • CHRONIC – chronic exposure (months – years). Less reversible.

Common Drug causes:

  • Amiodarone
  • Bleomycin
  • Methotrexate
  • Nitrofurantoin
  • Penicillamine
38
Q

ILD Treatment Principles

A

Earlier treatment is started the better the outcomes

  • Depends on underlying pathology
    • Occupational exposure – remove
    • Environmental exposure – remove (e.g. pet birds)
    • Drug associated – avoid
    • Stop smoking
    • MDT approach – maybe suitable for specialist medications such as Pirfenidone to slow progression
    • Treatment of infective exacerbations
    • Oxygen if respiratory failure
    • Palliative care
    • Transplantation
39
Q

sarcoidosis

A
  • Multisystem inflammatory condition of unknown cause
  • Non-caseating granulomas (Histology important)
  • Immunological response
  • Commonly involves Resp system BUT can affect nearly all organs
  • 50% get spontaneous remission, others get progressive disease
40
Q

investigations for sarcoidosis

A
  • PFTs: (obstructive until) fibrosis
  • CXR: 4 stages
  • Bloods: renal function, ACE, Calcium
  • Urinary Calcium
  • Cardiac involvement: ECG, 24 tape, ECHO, cardiac MRI
  • CT/MRI head: headaches – Neuro sarcoid
41
Q

Lung cancer

A
  • Lung Cancer is the biggest cause of cancer related death worldwide and in the UK
  • 48,000 new cases / year in the UK
  • 35,000 deaths / year in the UK
  • Number of cases in women continue to rise
  • 5 year survival approximately 16%
  • 72% of LC in the UK caused by smoking
42
Q

Lung Cancer Clinical Features / Presentations

A

Usually present late- higher risk of metastasis- poor outocmes

  • general: weight loss, chronic cough, SoB
  • Asymptomatic, incidental finding
  • Any respiratory symptom/systemic deterioration
  • Superior Vena Cava Obstruction
  • Horner’s syndrome
  • Metastatic disease – liver, adrenals (Addison’s), bone, pleural, CNS
  • Paraneoplastic – clubbing, hypercalcaemia, anaemia, SIADH, Cushing’s syndrome, Lambert-Eaton myasthenic syndrome
  • Increased risk of thrombo-embolic disease
43
Q

signs of lung cancer

A
  • Clubbing
  • Enlarged lymph nodes
  • Dysponea
  • cachexia
44
Q

RF for lung cancer

A
  • Large number of smoking pack years
  • Airflow obstruction
  • Increasing age
  • Family history of lung cancer
  • Exposure to other carcinogens, e.g. asbestos
45
Q

Investigations for lung cancer

A

MDT approach vital (Physicians, Oncologists, Surgeons, Radiologists, Pathologists, Palliative Care Team, Specialist Nurses, Primary Care)

  1. Bloods – FBC, U&E, Calcium, LFT’s, INR
  2. CXR
  3. Staging CT – Spiral CT Thorax and Upper Abdo – helps to stratify TNM stage
46
Q

Histology options for lung cancer

*

A
  • US guided neck node FNA for cytology if lymphadenopathy
  • Bronchoscopy – endobronchial, transbronchial, endobronchial ultrasound (if mediastinal lymphadenopathy)
  • CT Biopsy
  • Thoracoscopy if pleural effusion present
47
Q

PET Scan - lung cancer

A
  • MDT Decision if patient is a surgical candidate and initial CT suggestive of low stage
  • Helps to detect small metastases not seen on staging CT
48
Q

TNM staging

A
49
Q

Histological Classification

A

Classified primarily into two groups which account for about 95% of cases

  1. Small cell (oat cell) lung cancer (SCLC)
  2. Non-small cell lung cancer (NSCLC)

Includes squamous cell, adenocarcinoma- NON SMOKERS, and large cell carcinoma, bronchoalveolar cancer

Others -, bronchial gland ca, carcinoid tumour

50
Q

Small Cell LC Treatment & Prognosis

A
  • Rapid growth rate and almost always too extensive for surgery at time of diagnosis
  • Mainstay of treatment is chemotherapy
    • Also palliative radiotherapy
  • Untreated – median survival is 8-16 weeks
  • Combination chemotherapy – median survival 7- 15 months
51
Q

Lung Cancer Treatment Summary

A
  • Curative surgery for stages I & II – assuming fit for surgery
  • Surgery & adjuvant chemotherapy clinical trial for stage IIIa – assuming fit for surgery & chemo
  • Chemotherapy – consider in patients with stage III/IV disease and PS 0-2
  • Radiotherapy – curative (CHART = continuous hyperfractionated accelerated radiotherapy) for people not fit for surgery OR palliative
  • Palliative Care
  • Do nothing / watch & wait
52
Q

LC Metastasis commonly to:

A
  • Liver
  • Bone
  • Brain
  • Adrenal gland
  • Pleura
53
Q

Paraneoplastic syndromes associated with lung cancer

A

Small cell lung cancer

  • Ectopic ACTH
  • SIADH
    • hyponatraemia

Squamous cell carcinoma

  • Hypercalcaemia (PTH secreting hormones)
    • Stones moans and groans)
54
Q

Obstructive sleep apnoea

A
  • Upper airway obstruction during sleep
  • Clinical definition = upper airway narrowing, provoked by sleep, causing sufficient sleep fragmentation to result in significant daytime symptoms, usually excessive sleepiness
55
Q

RF of OSA

A
  • Male
  • High BMI
  • Undersized or set back mandible
56
Q

Pathophysiology of OSA

A
  • Upper airway patency depends on dilator muscle activity. All muscles relax during sleep (including pharyngeal dilators).
  • Some narrowing of the upper airway is normal
  • Excessive narrowing can be due to either an already small pharyngeal size during awake state which undergoes a normal degree of muscle relaxation during sleep causing critical narrowing OR excessive narrowing occurring with relaxation during sleep
57
Q

Causes of small pharyngeal size

A
  • Fatty infiltration of pharyngeal tissues and external pressure from increased neck fat and/or muscle bulk
  • Large tonsils
  • Craniofacial abnormalities
  • Extra submucosal tissue, e.g. myxoedema
58
Q

Causes of excessive narrowing of the airway during sleep

A
  • Obesity may enhance residual muscle dilator action
  • Neuromuscular disease with pharyngeal involvement may lead to greater loss of dilator muscle tone, e.g. stroke, MND, myotonic dystrophy
  • Muscle relaxants – sedatives, alcohol
  • Increasing age
59
Q

Clinical Effects of sleep apnoea

A
  • Severe OSA leads to repetitive upper airway collapse, with arousal required to re-activate the pharyngeal dilators. i.e. you have to wake uo
  • There may be associated hypoxia and hypercapnia which are corrected during the inter-apnoeic hyperventilatory period.
  • Chronic hypoxia can cause pulmonary hypertension e.g. cor pulmonale
  • Recurrent arousals lead to highly fragmented and unrefreshing sleep – snoring and apnoea attacks often witnessed by partner
  • Excessive daytime sleepiness results (Epworth Sleepiness Scale score >9)
  • With every arousal there is a rise in BP, often over 50 mmHg. It is not clear if this damages the CVS. There is also a rise in daytime BP.
  • Nocturia
  • Less common - Nocturnal sweating, reduced libido, oesophageal reflux
60
Q

Epworth Sleepiness Scale

A

used in sleep apnea diagnosis

Points for following:0=would never doze, 1=slight chance, 2=moderate chance, 3=high chance

  • Sitting & reading
  • Watching TV
  • Sitting in a public place, e.g. theatre
  • Passenger in a car for an hour
  • Lying down to rest in the afternoon  Sitting & talking
  • Sitting quietly after lunch without alcohol  In a car, while stopped in traffic
61
Q

Diagnosis – Sleep Study – Types

A
  • Overnight oximetry alone
  • Limited sleep study – oximetry, snoring, body

movement, heart rate, oronasal flow, chest/abdominal movements, leg movements – usual study of choice

  • Full polysomnography – limited study plus EEG, EMG
62
Q

sleep apnoea management

A

Treatment is given based on symptoms/quality of life – NOT on severity seen on sleep study - Also consider livelihood, e.g. driving as occupation

SIMPLE APPROACHES:

Weight loss, sleep decubitus rather than supine, avoid/reduce evening alcohol intake

FOR SNORERS & MILD OSA:

  • Mandibular advancement devices, consider pharyngeal surgery as last resort

FOR SIGNIFICANT OSA:

  • Nasal CPAP, consider gastroplasty/bypass, and rarely tracheostomy

FOR SEVERE OSA & CO2 RETENTION:

  • May require a period of NIV (non invasive ventilation) prior to CPAP if acidotic, but compensated CO2 may reverse with CPAP alone
63
Q

Sleep apnoea and driving

A
  • Do not drive while sleepy- stop and have a nap
  • Should notify DVLA on diagnosis
  • Doctors can advise to stop driving altogther
64
Q

CPAP

A
  1. Usually given via nasal mask, but can use mouth/nose masks
  2. Upper airways splinted open with approximately 10cm H2O pressure – this prevents airways collapse, sleep fragmentation, and ultimately daytime somnelence
  3. Also opens collapsed alveoli and improves V/Q matching

Medicine block (Y3) (38 decks)

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