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Medicine > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What type of histology is lung cancer most commonly?

A
  • Adenocarcinoma (40%)
  • Squamous cell carcinoma (20%)
  • Small cell lung cancer (20%)
  • Large cell carcinoma (10%)
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2
Q

Signs and symptoms of lung cancer?

A

SOB, cough, haemoptysis, finger clubbing, recurrent pneumonia, weight loss, lymphadenopathy

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3
Q

What is the pathophysiology of small cell lung cancer?

A

Neurosecretory granules that release hormones-> paraneoplastic syndromes

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4
Q

Investigations for lung cancer?

A
  • CXR-> hilar enlargement, opacity, pleural effusions, collapse
  • PET-CT
  • Bronchoscopy + endobronchial US
  • Histology-> bronchoscopy or skin
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5
Q

What might lung cancer show on a CXR?

A

Hilar enlargement, peripheral opacity, pleural effusion, collapse

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6
Q

Treatment for lung cancer (non-SCLC)?

A
  • Surgery-> lobectomy etc
  • Radiotherapy
  • Chemo-> adjuvant or palliative
  • Endobronchial treatment (palliative to relieve obstruction)
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7
Q

Treatment for lung cancer (SCLC)?

A

Chemo + radiotherapy

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8
Q

What are some of the extrapulmonary and paraneoplastic syndromes that can present in lung cancer?

A
  • Recurrent laryngeal palsy
  • Phrenic nerve palsy
  • Horner’s syndrome
  • SVC obstruction
  • Cushing’s
  • SIADH
  • Hypercalcaemia
  • Limbic encephalitis
  • Lambert-Eaton myasthenic syndrome
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9
Q

How might SVC obstruction (complication of lung cancer) present?

A

Facial swelling, SOB, distended veins in neck/chest, Pemberton’s sign (hands above head causes facial swelling)

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10
Q

How might Horner’s syndrome present and what can cause it?

A
  • Ptosis + anhidrosis + miosis

- Due to Pancoast’s tumour of pulmonary apex pressing on sympathetic ganglion

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11
Q

What is Lambert-Eaton myasthetic syndrome?

A
  • In SCLC-> antibodies produced against tumour
  • Target calcium channels on presynaptic terminals
  • Symptoms include autonomic symptoms, proximal weakness, dysphagia etc
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12
Q

What is a mesothelioma?

A
  • Mesothelial cells of pleura-> malignancy
  • Linked with asbestos exposure
  • Palliative chemo + poor prognosis
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13
Q

What is pneumonia?

A

Infection of the lung tissue causing inflammation + sputum production

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14
Q

When does hospital acquired pneumonia occur?

A

48 hours after admission

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15
Q

Signs + symptoms of pneumonia?

A
  • SOB, cough, fever, haemoptysis, pleuritic chest pain, delirium, sepsis
  • Bronchial breathing
  • Focal coarse crackles
  • Dullness to percussion
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16
Q

What is the CURB65 score and what are its components?

A
  • Determines severity of community acquired pneumonia

- Confusion, urea >7, RR >30, BP <90/<60, age 65

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17
Q

What should be done for a patient with a CURB65 score of 0 or 1?

A

Treat at home

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18
Q

What should be done for a patient with a CURB65 score of 2?

A

Consider admission to hospital

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19
Q

What should be done for a patient with a CURB65 score of 3?

A

Consider ICU assessment

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20
Q

What organisms typically cause pneumonia?

A
  • Strep pneumoniae (50%)
  • H.influenzae (20%)
  • Other-> moraxella catarrhalis, pseudomonas aeruginosa, s.aureus
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21
Q

What organisms can cause atypical pneumonia?

A
  • Can’t be cultured normally or detected by gram stain

- Leigonnaire’s disease, mycoplasma pneumoniae, chlamydophilia, coxiella burnetti, chlamydia psittaci

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22
Q

What is fungal pneumonia and who does it usually present in?

A

Pneumocystis jiroveci-> in HIV patients with low CD4 cell count

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23
Q

What is the treatment for fungal pneumonia?

A

Co-trimoxazole

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24
Q

What is the treatment for atypical pneumonias?

A
  • Macrolides (eg clarithromycin), fluoroquinolones (levofloxacin), tetracyclines (eg doxycyclines)
  • NOT penicillins
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25
Q

Investigations for pneumonia?

A
  • Bloods-> RBC, U+E, CRP (can guide treatment)
  • CXR
  • Sputum and blood culture
  • Urinary antigen sample (legionella + pneumococcal)
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26
Q

What is the treatment of mild community acquired pneumonia?

A
  • Amoxicillin oral for 5 days

- 2nd line-> clarithromycin or doxycycline

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27
Q

What is the treatment for moderate to severe community acquired pneumonia?

A
  • Oral amoxicillin, clarithromycin or doxycycline for 7-10 days
  • IV co-amoxiclav + clarithromycin or erythromycin for 5 days then review
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28
Q

Complications of pneumonia?

A

Sepsis, effusion, empyema, abscess, death

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29
Q

What is FEV1 and when is it reduced?

A
  • Forced expiratory volume in 1 second

- Reduced in obstruction (ability of air to flow out of lungs)

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30
Q

What is FVC and when is it reduced?

A
  • Forced vital capacity (ie total air can inhale in full inhalation)
  • Reduced in restrictive disease
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31
Q

What spirometry results would suggest obstructive disease?

A

FEV1 less that 75% of FVC ie FEV1:FVC ratio <75%

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32
Q

What spirometry results would suggest restrictive disease?

A

FEV1 and FVC equally reduced and FEV1:FVC ratio >75%

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33
Q

What are causes of obstructive lung disease?

A

Asthma (reversible) and COPD (non-reversible)

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34
Q

What are causes of restrictive lung disease?

A

Interstitial lung disease, neuro (eg MND), scoliosis, obesity

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35
Q

What is peak flow and how is it used?

A
  • Measures peak expiratory flow rate

- Record as percentage of predicted based on sex/height/age

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36
Q

What is the pathophysiology behind asthma?

A
  • Chronic inflammation causing episodic bronchoconstrcition due to hypersensitivity
  • Smooth muscles contract + reduced diameter causes obstruction
  • Reversible obstruction that responds to bronchodilators
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37
Q

Presentation of chronic asthma?

A
  • Episodic dry cough + wheeze + SOB
  • Diurnal variation (worse at night)
  • Atopy and food allergies
  • Bilateral polyphonic wheeze on exam
  • Triggered by infection, exercise, animals, cold/damp, dust, stress
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38
Q

Investigations for chronic asthma?

A
  • Peak flow diary
  • Fractional exhaled NO spirometry + bronchodilator (for reversibility)
  • Direct bronchial challenge with histamine
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39
Q

NICE guideline ladder for chronic asthma treatment?

A
  • Step 1-> add SABA
  • Step 2-> add low dose ICS
  • Step 3-> add oral LRTA
  • Step 4-> add LABA
  • Step 5-> consider change to MART regime
  • Step 6-> increase ICS to moderate dose
  • Step 7-> consider increase to ICS high dose or oral theophylline or inhaled LAMA
  • Step 8-> refer to specialist
  • Additional-> self-management programme, yearly review, flu jab etc
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40
Q

What are the clinical signs of moderate acute asthma?

A
  • PEFR 50-75% predicted
  • Resp rate >25
  • HR >110
  • Unable to complete full sentences
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41
Q

What are the clinical signs of severe acute asthma?

A
  • PEFR 33-50% predicted
  • Resp rate >25
  • HR >110
  • Unable to complete full sentences
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42
Q

What are the clinical signs of life threatening acute asthma?

A
  • PEFR <33%
  • Sats <92%
  • Tired
  • No wheeze (no air entry, silent chest)
  • Haemodynamic instability (shock)
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43
Q

Treatment options for acute asthma?

A
  • Salbutamol nebs (5mg back to back)
  • Ipratropium bromide nebs
  • Steroids (oral pred or IV hydrocortisone 5 days)
  • O2 if needed (94-98%)
  • Aminophylline infusion
  • IV salbutamol
  • IV magnesium sulphate
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44
Q

Monitoring requirements in acute asthma?

A
  • RR, respiratory effort, peak flow, sats, chest auscultation
  • ABG-> may be respiratory alkalosis then normal pCO2 + hypoxia (concerning) then respiratory acidosis (concerning)
  • May need K+ and HR monitoring when using salbutamol (hyper + tachy)
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45
Q

Long-term management when a patient has had an acute asthma attack?

A
  • Discharge with asthma action plan
  • Consider rescue pack ie steroids can initiate when needed
  • Refer to specialist when 2+ attacks in 12 months
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46
Q

What is chronic obstructive pulmonary disease?

A
  • Non-reversible deterioration of air flow through lungs usually due to damage from smoking
  • Damage causes obstruction-> hard to ventilate-> prone to infection and exacerbations
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47
Q

Presentation of COPD?

A
  • Smoker + chronic SOB, cough, sputum production, wheeze, recurrent respiratory infections
  • Not usually any clubbing or haemoptysis-> consider alternative
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48
Q

Differentials for COPD?

A

Asthma, fibrosis, lung cancer, HF

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49
Q

What is the MRC dyspnoea scale and what are the different stages?

A

Assesses the disability caused by dyspnoea (SOB)

  • Stage 1-> SOB on strenuous exercise
  • Stage 2-> SOB when walking up hill
  • Stage 3-> SOB when walking flat
  • Stage 4-> have to stop when walk 100 meters on flat surface due to SOB
  • Stage 5-> can’t leave house due to SOB
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50
Q

Investigations for COPD?

A
  • FBC (eg polycythaemia in chronic hypoxia) + U&Es
  • CXR
  • Sputum culture (chronic pseudomonas)
  • Spirometry-> obstructive picture ie when FEV1 less than 70% of FVC (FEV1/FVC <0.7)
  • Transfer factor for CO ie TLCO (decreased)
  • Serum alpha-1 antitrypsin deficiency (worse disease outcomes)
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51
Q

Long term management of COPD (with asthmatic/steroid-responsive features)?

A
  • Step 1-> SABA or SAMA
  • Step 2-> add LABA + ICS
  • Step 3-> LABA + LAMA + ICS
  • Other options (severe)-> oral theophylline, mucolytic therapy (eg carbocysteine), prophylactic antibiotics (azithromycin)
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52
Q

Long term management of COPD (without asthmatic/steroid responsive features)?

A
  • Step 1-> SABA or SAMA
  • Step 2-> add LABA + LAMA
  • Step 3-> LABA + LAMA + ICS
  • Other options (severe)-> oral theophylline, mucolytic therapy (eg carbocysteine), prophylactic antibiotics (azithromycin)
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53
Q

When is long term oxygen therapy contraindicated in COPD?

A

-Current smoker (fire hazard)

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54
Q

What is the pathophysiology behind respiratory acidosis?

A
  • Raised CO2 makes blood acidotic due to breakdown to carbonic acid (H2CO3)-> cause low pH
  • Chronically compensated by raising bicarb but takes a long time (so not good in acute) and may be chronically high (eg COPD)
55
Q

Why does COPD exacerbation result in respitatory acidosis?

A

Chronic CO2 retention-> kidneys produce bicarbonate to balance acid + normalise pH-> can’t keep up during acute exacerbation

56
Q

What will you see on a blood gad result for type 1 respiratory failure?

A

Low pO2 + normal pCO2

57
Q

What will you see on a blood gad result for type 1 respiratory failure?

A

Low pO2 + raised pCO2

58
Q

What is the target range for oxygen saturations when managing a patient with COPD and why?

A
  • Usually 88-92% unless proved to not retain CO2 (eg bicarb normal)
  • Chronic CO2 retention-> respiratory drive not determined by this and is instead by hypoxia-> correcting hypoxia may reduce respiratory drive
59
Q

Treatment for acute exacerbation of COPD?

A
  • Salbutamol nebs
  • Ipratropium nebs
  • Steroids-> prednisolone (oral 30mg for 7-14 days) or hydrocortisone
  • Antibiotics if indicated
  • Chest physio
  • IV aminophylline
  • NIV
  • Intubation + ventilation
60
Q

What is BiPAP (bilevel positive airway pressure)?

A

Cycle of high and low pressure ventilation to correspond to inspiration and expiration

61
Q

When is BiPAP (bilevel positive airway pressure) used?

A

Type 2 respiratory failure refractory to treatments

62
Q

What is an important thing to rule out before using BiPAP (bilevel positive airway pressure)?

A

Pneumothorax

63
Q

What is CPAP (continuous positive airway pressure)?

A

Air is continuously given to the lungs to keep airway expanded and allow air to travel in and out

64
Q

What are the indications for CPAP (continuous positive airway pressure)?

A

Obstructive sleep apnoea, congestive HF, pulmonary oedema

65
Q

What is interstitial lung disease?

A

An umbrella term for conditions affecting the lung parenchyma (tissue) causing inflammation and fibrosis

66
Q

What is fibrosis?

A

When elastic functional tissue is replaced with stiff scar tissue

67
Q

Investigations for interstitial lung disease (general)?

A
  • Clinical diagnosis
  • High resolution CT-> ‘ground glass’ appearance
  • Lung biopsy + histology
68
Q

Management of interstitial lung disease (general)?

A
  • Treat underlying causes
  • Home oxygen
  • Smoking cessation
  • Chest physio
  • Pulmonary rehab
  • PCV + flu vaccines
  • Lung transplant
69
Q

What is idiopathic pulmonary fibrosis?

A

Progressive lung fibrosis with no clear cause

70
Q

How might idiopathic pulmonary fibrosis present?

A
  • SOB and dry cough for over 3 months
  • Usually over 50s
  • Bibasal fine inspiratory crackles
  • Finger clubbing
71
Q

Treatment options for idiopathic pulmonary fibrosis?

A
  • Pirfenidone-> antifibrotic + anti-inflammatory

- Nitedanib-> monoclonal antibody

72
Q

What drugs can cause pulmonary fibrosis?

A

Amiodarone, methotrexate, nitrofurantoin, cyclophosphamide

73
Q

What conditions can cause secondary pulmonary fibrosis?

A

RA, SLE, systemic sclerosis, A1AT deficiency

74
Q

What is hypersensitivity pneumonitis (ie extrinsic allergic alveolitis)?

A

A type III hypersensitivity reaction to an environmental allergen causing parenchymal inflammation and destruction

75
Q

What are some examples of hypersensitivity pneumonitis (ie extrinsic allergic alveolitis)?

A

Bird fancier’s lung, farmer’s lung, mushroom worker’s lung

76
Q

Investigation of choice for hypersensitivity pneumonitis (ie extrinsic allergic alveolitis)?

A

Bronchoalveolar lavage + bronchoscopy-> wash with fluid + collect for testing (will see raised lymphocytes and mast cells)

77
Q

Treatment of hypersensitivity pneumonitis (ie extrinsic allergic alveolitis)?

A
  • Remove allergen
  • Oxygen
  • Steroids
78
Q

What is asbestosis?

A
  • Lung disease due to asbestos exposure

- Fibrogenic + carcinogenic

79
Q

What is the pathophysiology behind asbestosis?

A

Fibrogenic + oncogenic-> pleural thickening + plaques-> fibrosis, adenocarcinomas and mesothelioma

80
Q

What is important to do when a patient dies of asbestosis?

A

Refer to the coroner

81
Q

What is a pleural effusion?

A

Collection of fluid in the pleural cavity

82
Q

What are the two types of pleural effusion?

A
  • Exudative-> high protein count (>3g/dL)

- Transudative-> lower protein (<3g/dL)

83
Q

What are the causes of exudative pleural effusion?

A
  • Inflammatory-> protein leaks out of tissues into pleural space
  • Lung cancer, pneumonia, RA, TB
84
Q

What are the causes of transudative pleural effusion?

A
  • Fluid in pleural space

- CCF, hypoallbuminaemia, hypothyroidism, Meig’s syndrome (right effusion + ovarian malignancy)

85
Q

What is Meig’s syndrome?

A

Right sided pleural effusion + ovarian malignancy

86
Q

How might a pleural effusion present?

A

SOB, dull to percussion, reduced breath sounds, tracheal deviation (away from)

87
Q

What findings may be present on CXR in a pleural effusion?

A
  • Blunting of costophrenic angles
  • Fluid in lung fissures
  • Meniscus-> curve up where meets chest wall + mediastinum
  • Tracheal + mediastinal deviation (when large)
88
Q

Investigations for pleural effusion?

A
  • CXR

- Fluid sample via aspiration or drain-> protein count, pH, glucose, LDH, microbiology

89
Q

Treatment for pleural effusion?

A
  • Conservative if small
  • Pleural aspiration-> needle in + relieve pressure
  • Chest drain-> can prevent recurring
90
Q

What is an empyema?

A

Effusion caused by infection

91
Q

When might you suspect an empyema

A

Pneumonia that’s improving but new/ongoing fever

92
Q

Investigation for empyema?

A
  • CXR

- Aspirate-> pus, acidic pH, low glucose, high LDH

93
Q

Treatment for empyema?

A

Chest drain + antibiotics

94
Q

What is a pneumothorax?

A

Air in the pleural space-> separates lung from chest wall

95
Q

What can cause a pneumothorax?

A
  • Spontaneous
  • Trauma
  • Iatrogenic (lung biopsy, mechanical ventilation)
  • Pathology-> infection, asthma, COPD
96
Q

How does pneumothorax present?

A
  • Often a tall, young, thin man
  • Sudden SOB + pleuritic chest pain
  • Often after playing sports
97
Q

Investigation for pneumothorax?

A
  • CXR-> gold standard + measure from lung edge to chest wall at hilum level (horizontal)
  • CT thorax-> for small PTX
98
Q

CXR findings for pneumothorax?

A
  • Area between lung tissue + chest wall where no lung markings
  • Often a line demarcating PTX
99
Q

Management of pneumothorax (when <2cm on CXR)?

A
  • None needed

- 2-4 week follow up

100
Q

Management of pneumothorax (when >2cm air on CXR + SOB)?

A
  • Aspiration and reassessment

- Chest drain if aspiration fails twice

101
Q

When is a chest drain indicates when treating a pneumothorax?

A
  • Aspiration fails twice
  • Bilateral
  • Secondary PTX
  • Unstable patient
102
Q

Where is a chest drain inserted in pneumothorax treatment?

A
  • Triangle of safety-> 5th IC space (inferior nipple line) + mid axillary (lat dorsi edge) + anterior axillary line (pec major edge)
  • Insert needle above rib-> avoid NV bundle
  • Always check position with CXR
103
Q

What is a tension pneumothorax?

A

When a 1-way valve is created into the pleural space due to trauma

104
Q

Why can a tension pneumothorax cause cardio-respiratory arrest?

A

Air trapped during inspiration + can’t get out when expire-> pressure in thorax-> pushed mediastinum across + kink big vessels-> CR arrest

105
Q

What are the clinical signs of tension pneumothorax?

A

Tracheal deviation (away), reduced air entry, increases resonance to percussion, tachycardia, hypotension

106
Q

Treatment for tension pneumothorax?

A
  • Immediately insert large bore cannula into 2nd IC space + mid clavicular line
  • Chest drain after
107
Q

What usually causes a pulmonary embolism?

A

Thrombus from DVT (usually) travels through venous system + to right heart + pulmonary arteries-> block blood flow to lung tissue-> puts strain on right heart

108
Q

What are the risk factors for developing a PE/DVT?

A

Immobility, recent surgery, long haul flights, pregnancy, oestrogen (OCP/HRT), malignancy, polycythaemia, SLE, thrombophilia

109
Q

What is used for prophylaxis of PE/DVT?

A

LMWH eg enoxaparin

110
Q

What are the contraindications for using LMWH as PE/DVT prophylaxis?

A

Active bleeding, recent stroke, warfarin/DOAC therapy

111
Q

What are the contraindications to anti-embolic compression stockings for PE/DVT prophylaxis?

A

Peripheral arterial disease

112
Q

Presentation of PE?

A

Symptoms-> SOB, cough, haemoptysis, pleuritic chest pain

Signs-> tachycardia, high RR, low fever, hypotension, signs of DVT

113
Q

Investigations for PE?

A
  • Well’s score-> CTPA if likely + D-dimer if unlikely
  • D-dimer-> CTPA if positive
  • CTPA-> IV contrast + chest CT
  • VQ scan-> when CTPA unsuitable (eg renal impairment) + will be perfusion deficit (blocked by clot)
  • ABG-> respiratory alkalosis (due to high RR so blow off CO2)
114
Q

How does a ventilation-perfusion (V/Q) scan work?

A

Radioactive isotopes inhaled (V) + contrast with isotopes injected (Q)-> compare images

115
Q

Management of PE?

A
  • Apixaban or rivaroxaban first line
  • Continue for 3 months (reversible cause), 3-6 months (unclear cause or recurrent) or 6 months + review (active cancer)
  • Use LMWH + bridge to warfarin long-term if DOACs unsuitable
  • Thrombolysis if massive + haemodynamic instability
116
Q

When is thrombolysis used in PE and what does it involve?

A
  • When massive PE with haemodynamic compromise present-> large risk of bleeding
  • IV cannula + inject fibrinolytic meds-> eg strektokinase or alteplase
  • Can also use catheter-directed (ie onto thrombus) but risk of artery damage
117
Q

What is pulmonary hypertension?

A

Increased resistance + pressure of blood in pulmonary arteries-> right heart strain-> back pressure into systemic venous system

118
Q

What are the five groups of causes of pulmonary hypertension?

A

1-> primary or due to connective tissue disease (SLE etc)
2-> left HF (eg MI) or systemic hypertension
3-> chronic lung disease (eg COPD)
4-> pulmonary vascular disease (eg PE)
5-> Misc-> sarcoidosis, glycogen storage disease, haem disorders

119
Q

Signs and symptoms of pulmonary HTN?

A

SOB, syncope, tachycardia, raised JVP, hepatomegaly, peripheral oedema

120
Q

Investigations for pulmonary HTN?

A
  • CXR-> dilated arteries + RV hypertrophy
  • ECG-> right axis deviation, large R waves on V1-3 (right side) + large S waves on V4-6 (left side), RBBB
  • Raised BNP
  • Echo-> can estimate pressures
121
Q

Management of pulmonary HTN?

A

Primary-> epoprostenol, macitentan, sildenafil
Secondary-> treat the underlying cause
Supportive-> when resp failure arrhythmias, HF

122
Q

What is sarcoidosis?

A

Granulomatous nodules of inflammation full of macrophages throughout body (usually lungs)

123
Q

What is the typical presentation of sarcoidosis?

A

20-40 year old black lady with a dry cough, SOB and shin nodules

124
Q

What organs can sarcoidosis affect and how might this present?

A
  • Lungs-> nodules, pulmonary fibrosis, mediastinal lymphadenopathy
  • Systemic-> fever, fatigue, weight loss
  • Liver-> nodules, cirrhosis, cholestasis
  • Eyes-> uveitis, conjunctivitis, optic neuritis
  • Erythema nodosum-> tender red nodules on shins
  • Lupus pernio-> raised purple lesions on cheeks + nose
  • Granulomas
  • Heart, kidneys, PNS, bones
125
Q

What is Lofgren’s syndrome and how does it present?

A

Specific presentation of sarcoidosis presenting with triad of-> erythema nodosum + bilateral hilar lymphadenopathy + polyarthralgia

126
Q

Investigations for sarcoidosis?

A
  • Histology (gold standard)-> via bronchoscopy + detect granulomas
  • Bloods-> high serum ACE, hypercalcaemia, high CRP etc
  • CXR-> hilar lymphadenopathy
  • Other imaging-> high resolution CT thorax, brain MRI, PET-scan
  • U+Es, urine dip, LFTs, ECG etc-> depends on other organ involvement
127
Q

Treatment options for sarcoidosis?

A
  • Mild-moderate-> none
  • Need treatment-> oral steroids for 6-24 months + bisphosphonates
  • Can also use MTX, azathioprine etc
  • Lung transplant
128
Q

What is the prognosis for sarcoidosis?

A
  • Often spontaneously resolves in 6 months

- May result in fibrosis + HTN + death

129
Q

What is obstructive sleep apnoea?

A

When a patient stops breathing for a few minutes during sleep due to collapse of pharyngeal airway

130
Q

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

A

Middle aged, male, obese, alcohol, smoking

131
Q

How might obstructive sleep apnoea present?

A
  • Often reported by partner-> apnoea + snoring

- Morning headache, wake up unrefreshed, daytime sleepiness

132
Q

What are the complications of obstructive sleep apnoea (ie what can it put you at risk of)?

A

HTN, HF, MI, stroke

133
Q

What are the management options for obstructive sleep apnoea?

A
  • Referral to ENT or sleep clinic-> urgent if HGV driver etc
  • Sleep studies-> monitor sats, HR, RR, breathing
  • Correct risk factors
  • CPAP machine
  • Uvulopalatopharyngoplasty

Medicine (13 decks)

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