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Junior Medicine > Respiratory Conditions > Flashcards

Respiratory Conditions Flashcards

1
Q

What are the characteristics of asthma?

A
  • chronic inflammation of the airways
  • Causes reversible airway obstruction either spontaneously or with treatment
  • There is increased airway narrowing to a variety of stimuli
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2
Q

What are the differentials for wheeze?

A
  • Acute asthma exacerbation
  • Bronchitis (viral or bacterial)
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3
Q

Describe the pathophysiology of asthma

A
  • Airway epithelial damage - shedding and subepithelial fibrosis with basement membrane thickening
  • An inflammatory reaction characterised by eosinophils, T-lymphocytes (Th2) and mast celss
  • Inflammatory mediators: histamine, leukotrienes and prostaglanins
  • Cytokines amplify inflammatory response
  • Increased number of mucus secreting goblet cells with smooth muscle hyperplasia and hypertrophy
  • Mucus plugging in fatal and severe asthma
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4
Q

What is the criteria for safe discharge after an asthma exacerbation?

A
  • PEFR >75%
  • Stop regular nebulised for 24 hours prior to discharge
  • Inpatient asthma nurse review to assess inhaler technique and adherance
  • Provide PEFR meter and written asthma action plan
  • At least 5 days of oral prednisolone
  • GP to follow up within 2 working days
  • Respiratory clinic follow up within 4 weeks
  • For severe or worse, consider psychosocial factors
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5
Q

What is eospinophilic asthma?

A

Some asthma patients have eosinophilic inflammation which typically responds to steroids

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6
Q

Apart from asthma, what are some other causes of eosinophilia?

A
  • Airway inflammation (COPD)
  • Hayfever/ allergy
  • Allergic bronchopulmonary aspergillosis
  • Drugs
  • Churg-Strauss / Vasculitis
  • Eosinophilic Pneumonia
  • Parasites
  • Lymphoma
  • SLE
  • Hyperoeosinphilic syndrome
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7
Q

What are some of the triggers for asthma?

A
  • Smoking
  • URTI (mainly viral)
  • Allergens (polle, dust mite, pets)
  • Exercise
  • Cold air
  • Occupational irritants
  • Pollution
  • Drugs - beta blockers (including eye drops!), aspirin
  • Food and drink: dairy, alcohol, orange juice
  • Stress
  • If very severe : consider causes as heroin, pre-menstrual, psychosocial
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8
Q

What is the NICE definition of COPD?

A

Airflow obstruction that is usually progressive, not fully reversible and does not change markedly over several months

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9
Q

What is the pathophysiology behind COPD?

A

Umbrella term encompasses emphysema and chronic bronchitis

There is:

  • Mucus gland hyperplasia
  • Loss of cilial function
  • Alveolar wall destruction causing enlargement of air spaces distal to terminal bronchiole
  • Chronic inflammation and fibrosis of small airways
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10
Q

What are the main causes of COPD?

A
  • Smoking
  • alpha - 1 antitrypsin deficiency
  • Industrial exposure e.g. soot
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11
Q

How is COPD managed as an outpatient?

A

COPD care bundle

  • SMOKING CESSATION
  • Pulmonary rehabilitation
  • Bronchodilators
  • Antimuscarinics
  • Steroids
  • Mucolytics
  • Diet
  • LTOT if appropriate
  • Lung volume reduction if appropriate
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12
Q

What is the benefit of LTOT in COPD patients?

A
  • Extended hypoxia can cause renal and cardiac damage
  • Continuous o2 for at least 16 hours per day has a survival benefit
  • only offered if pO2 is persistantly <7.3kPa or below 8kPa with Cor Pulmonale
  • Patient must be non-smoker and not retain high CO2 levels
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13
Q

How should patients who have had pneumonia be followed up?

A
  • HIV test
  • Immunoglobins
  • Penumococcal IgG serotying
  • Haemophilus influenza b IgG
  • Follow up in clinic in 6 weeks with repeat CXR to ensure resolution
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14
Q

What are some of the causes of non-resolving pneumonia?

A

CHAOS

  • Complication - lung abscess, empyema
  • Host - immunocompromised
  • Antibiotics - inadeqaute dose, poor oral absorption
  • Organism - resistant or unexpected organism not covered by empirical abx
  • Second diagnosis - PE, cancer, organising pneumonia
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15
Q

What are some of the clinical features of TB?

A
  • Fever
  • Night sweats (drenching)
  • Weight loss over weeks-months
  • Malaise
  • Respiratory TB: cough +/- purulent sputum, haemoptysis, may have pleural effusion
  • Non respiratory TB: skin (eythema nodosum), lymphadenopathy, bone/joints, CNS (meningitis), GU, Miliary (disseminated), Cardiac (pericardiacl effusion)
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16
Q

What are some of the differentials of haemoptysis?

A
  • Infection
    • Pneumonia
    • TB
    • Bronchiectasis/ CF
    • Cavitating lung lesion (often fungal)
  • Malignancy
    • ​lung cancer or metastasis
  • Haemorrhage
    • bronchial artery erosion
    • vasculitis
    • coagulopathy
  • Others: PE
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17
Q

Describe the basics of anti-TB therapy

A

RIPE is standard regimen

Rifampicin, Isoniazid, Pyrazinamide, Ethambutol

All Taken for the first 2 months then only Rifampicin for next 4 months (minimum 6 months total)

  • weight is important - dose is weight dependent
  • Need to check baseline LFTs and monitor closely
  • Check visual acuity before giving ethambutol
  • Compliance is crucial - directly observed therapy is sometimes used
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18
Q

What are some of the major side effects of TB treatment?

A
  • Rifampicin: Hepatitis, rashes, febrile reaction, orange/ red urine or tears, many drug interactions
  • Isoniazid: Hepatitis, rashes, peripheral neuropathy, psychosis
  • Pyrazinamide: Hepatitis, vomiting, rashes, arthralgia
  • Ethambutol: Retrobulbar neuritis
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19
Q

What is bronchiectasis?

A

Chronic dilatation of one or more bronchi

Bronchi experience poor mucus clearance and therefore prone to recurrent bacteral infections

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20
Q

What is the gold standard investigation for bronchiectasis? What is a classic finding?

A

High resolution CT

Signet ring sign (bronchi are wider than their corresponding arteries)

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21
Q

What are some of the causes of bronchiectasis?

A
  • Post infective: whooping cough, TB
  • Immune deficiency: Hypogammaglobinaemia
  • Genetic / Mucociliary clearance deficits: CF, primary cilliary dyskinesia, Young’s sydrome, Kartagener syndrome
  • Obstruction: foreign body, tumour, extrinsic lymph node
  • Toxic insult: gastric aspiration, inhalation of toxic chemicals/ gasses
  • Allergic bronchopulmonary aspergillosis
  • Secondary immune deficiency: HIV, malignancy
  • RA
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22
Q

What common organisms are seen in bronchiectasis?

A
  • Haemophilus influenxae
  • Pseudomonas aeruginosa
  • Moraxella catarrhalis
  • funghi - aspergillus, candida
  • non-tb mycobacteria
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23
Q

How is bronchiectasis managed?

A
  • Treat the underlying cause
  • Chest physio
  • Abx according to sputum culture
  • Supportive measures
    • flu vaccine
    • bronchodilators
  • Pulmonary rehab if MRC dyspnoea score >3
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24
Q

Describe the MRC dyspnoea scale

A
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25
Q

What is cystic fibrosis?

A

Autosomal recessive disease leading to mutations in CFTR channel causing multisystemic disease commonly affective the respiratory and GI systems

It is characterised by thickened secretions

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26
Q

How is a diagnosis of CF made?

A
  • 1 or more characteristic phenotypic features
  • Hx of CF in sibling
    • newborn screen
  • Increased sweat chloride concentration >60mmol/L
    • identification of 2 CF mutations on genotyping
    • abnormal nasal epithethelial ion transport
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27
Q

How can CF present?

A
  • Meconium ileus
    • 15-20% newborn CF patients as the bowel is blocked by sticky secretions
    • signs of intestinal obstruction soon after birth: vomiting, abdominal distension, delay in passing meconium
  • Intestinal malabsorption
    • Evident in infancy due to severe deficiency of pancreatic enzymes
  • Recurrent chest infections
  • Newborn screening
28
Q

What are some of the complications of CF?

A
  • Respiratory infections
  • Low body weight
  • Distal intestinal obstruction syndrome
  • CF related diabetes
29
Q

What lifestyle advice do you give to CF patients?

A
  • No smoking
  • Avoid other patients who have CF
  • Avoid friends/ relatives with colds/ infections
  • Avoid jacuzzis (pseudomonas)
  • Clean and dry nebulisers thoroughly
  • Avoid stables, compost or rotting vegetation = aspergillus risk
  • Get annual influenza immunisation
  • Take sodium chloride tablets in hot weather / after vigorous exercise
30
Q

What is the pleural cavity?

A

A potential space between 2 pleural spaces creased by the outer parietal pleura and the inner visceral pleura

31
Q

What is pneumothorax?

A

Air in the pleural cavity

32
Q

What is a pleural effusion?

A

Fluid in the pleural cavity

33
Q

What is am empyema?

A

Infected fluid in the pleural cavity

34
Q

What are pleural plaques?

A

Discrete fibrous areas on the pleura

35
Q

What are the types of pneumothorax?

A
  1. Spontaneous
    1. Primary (no lung disease)
    2. Secondary (lung disease)
  2. Traumatic
  3. Tension (emergency)
  4. Iatrogenic (post central line or pacemaker insertion)
36
Q

Give some risk factors for developing a pneumothorax?

A
  • Pre-existing lung disease
  • Tall
  • Smoking/ cannabis
  • Diving
  • Trauma/ Chest procedure
  • Associated with other conditions e.g, Marfan’s
37
Q

How should pneumothoraxs be managed?

A
  • Aspirate if symptomatic and rim of air >2cm on CXR
  • Give O2
  • If aspitation unsucussful consider re-aspiration or intercostal drain
  • If peristent air leak >5 days refer to thoracic surgeons
38
Q

What is a tension pneumothorax?

A
39
Q

What initial investigations are done if suspecting pleural effusion?

A
  • History and examination
  • CXR
  • ECG
  • Bloods: FBC, U&E, LFTs, CRP, Bone profile, LDH, clotting
  • ECHO is suspecting HF
  • Staging- CT with contrast if suspecting exudate cause
40
Q

How is a diagnosis of pleural effusion made?

A

Ultrasound guided pleural aspiration

Send aspirate for biochemisty (protein, pH, LDH), cytology, microbiology

41
Q

Which criteria is used to determine whether a pleural effusion is transudate or exudate?

A

LIGHT’s criteria

42
Q

Give some of the causes of transudate pleural effusions (pleural protein <30 g/L)

A

Common

  • HF
  • Cirrhosis
  • Hypoalbuminaemia (nephrotic syndrome or peritoneal dialysis)

Less common

  • Hypothyroidism
  • Mitral stenosis
  • PE
  • RARE: constrictive pericarditis, SVC obstruction
43
Q

Give some of the causes of exudate pleural effusions

A

Common:

  • Malignancy
  • Infections - parapneumonic, TB, HIV

Less common:

  • Inflammatory: (RA, pancreatitis, benign asbestos effusion)
  • Lymphatic disorders
  • Connective tissue disorders

Rare:

  • Yellow nail syndrome, fungal infections, drugs
44
Q

How are pleural effusions managed?

A
  • Treat the underlying cause (if known)
    • diagnostic tap is not always required
  • If effusion perists, therapeutic aspitation/ draininge is required
45
Q

What is interstitial lung disase?

A

A collection of conditions that affect the lung parenchyma

includes: usual interstitial pneumonia, non-specific intersistial pneumonia, extrinsic allergic alveolitis, sarcoidosis

46
Q

Give some of the classical findings of usual interstitial pneumonia (commonest form of pulmonary fibrosis)

A
  • Finger clubbing
  • Reduced chest expansion
  • Auscultation: fine inspiritory crepitations best hear at basal/ axillar areas
  • Cardiovascular: features of pulmonary hypertension
47
Q

What is extrinsic allergic alveolitis?

A

Also known as hypersensitivity pneumonia

Inhalation of an organis antigen to which the individual has been sensitised

Acute: short period from exposure (4-8hours) usually reversible

Chronic: chronic exposure over months - years. less revsersible

48
Q

What is sarcoidosis?

A

A multisystem inflammatory condition of unknown cause

  • causes non-caseating granulomas
  • Commonly involves respiratory system but can affect all organs
  • 50% get spontaneous remission, 50% get progressive disease
49
Q

What investigations should be done if suspecting sarcoidosis?

A
  • Pulmonary function tests
  • CXR
  • Bloods: renal function, Calcium
  • Urinary calcium
  • Cardiac: ECG, 24hr tape, ECHO, cardiac MRI
  • CT/MRI head if headaches- neuro sarcoid
50
Q

Give some risk factors for lung cancer

A
  • Smoking - large number of pack years
  • Airflow obstruction
  • increasing age
  • FHx of lung cancer
  • Exposure to other carcinogens (asbestos)
51
Q

Give some of the clinical features/ presentations of lung cancer

A
  • Asymptomatic (incidental finding)
  • Respiratory problems/ systemic deterioration
  • Superior Vena Cava Obstruction
  • Horner’s syndrome
  • Metastatic disease, liver, adrenals, bone, pleura, CNS
  • Clubbing
  • Hypercalcaemia
  • Anaemia
52
Q

What investigations should be done if suspecting lung cancer?

A
  • Bloods: FBC, U&E, Ca2+, LFTs, INR
  • CXR
  • Staging CT
  • Histology: USS guided neck node biopsy, CT biopsy, bronchoscopy, thoracoscopy (if pleural effusion present)
  • PET scan
53
Q

What are the 2 main histological groups of lung cancer?

A
  1. Small cell lung cancer
  2. Non-small cell lung cancer
    1. includes squamous cell, adenocarcinoma, large cell carcinoma, bronchoalveolar
54
Q

Summaries the treatmen options for lung cancer

A
  • Stage I and II can have curative surgery
  • Surgery & adjuvant chemotherapy in clinical trial for stage 3a
  • Chemotherapy if patients stage 3/4
  • Radiotherapy can be curative or palliative
  • Palliative care
55
Q

What is obstructive sleep apnoea?

A

Upper airway narrowing provoked by sleep can cause sufficient sleep fragmentation and result in significant daytime symtpoms and exessive sleepiness

56
Q

What are some of the risk factors for obstructive sleep apnoea?

A
  • Male
  • Obesity
  • Undersized/ set back mandible
57
Q

Describe the pathophysiology behind obstructive sleep apnoea

A
  • For the upper airway to stay patent it depends on dilator muscle - all muscles relax during sleep
  • Some narrowing of the upperairway is normal
  • excessive narrowing is due to already small pharyngeal size or excessive relaxation during sleep
58
Q

What can cause small pharyngeal size leading to OSA?

A
  • Fatty infiltration of pharyngeal tissues
  • External pressure from increase neck fat/ muscle bulk
  • Large tonsils
  • Craniofacial abnormalities
  • Extra submucosal tissue e.g. myxoedema
59
Q

What are some of the causes of excessive airway narrowing during sleep?

A
  • Obesity - enchances residual muscle dilator action
  • Neuromuscular disease
  • Muscle relaxants - sedatives, alcohol
  • Increasing age
60
Q

What are some of the effects of OSA?

A
  • Repeated upper airway collapse causes associated hypoxia and hypercapnia
  • Unrefreshed sleep
  • Snoring and apnoea witnessed by partner
  • Excessive daytime sleepiness
  • Rise in BP
  • Nocturia
  • Nocturnal sweating
  • Reduced Libido
61
Q

Which criteria is used to assess daytime sleepiness in OSA?

A

Epworth Sleepiness Scale

62
Q

How is OSA diagnosed?

A
  • Overnight oximetry
  • Limited sleep study
  • Full polysomnography
63
Q

How is OSA managed?

A

Treatment given based on QoL, not the sleepines score

Conservative:

  • Weight loss
  • Sleep on the side rather than supine
  • Avoid evening alcohol

For snorers:

  • Mandibular advancement devices
  • Pharyngeal surgery a last resort

For significant OSA:

  • Nasal CPAP
  • Gastric bypass
  • Tracheostomy (rare!)
64
Q

What advice should you give patients with OSA about driving?

A
  • Do not drive whilst sleepy - stop and have a nap
  • Patient should notify DVLA on diagnosis
  • Advise HGV drivers to stop all together
65
Q

What is the difference between CPAP and NIV

A

CPAP = continuous positive airway pressure

  • not a form of ventilatory support
  • supplies constant pressure in inspiration and expiration

NIV= non invasive ventilatory support

  • does provide ventilatory support
  • set at 2 levels (bilevel) of pressure

Junior Medicine (6 decks)

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