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Y3 Medicine > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What 6 symptoms must you ask about in a resp history?

A
  • cough
  • dyspnoea
  • chest pain
  • wheeze
  • sputum
  • haemoptysis
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2
Q

Describe each of the 5 levels of the MRC dyspnoea score

A
  1. not troubled by breathlessness except on strenuous exercise
  2. SoB when hurrying or going up hill
  3. walks slower than contemporaries on level ground or has to stop for breath when walking at own pace
  4. Stops after walking about 100m or after a few mins on level ground
  5. too breathless to leave house, or when changing
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3
Q

Describe the 5 levels of the WHO performance status

A
  1. fine
  2. restricted in strenuous activity but can carry out light work
  3. self care fine but unable to carry out any work activities, active for 50% waking hours
  4. only limited self care, confined to bed or chair for > 50% waking hours
  5. completely disabled, cannot self care
  6. dead
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4
Q

Describe the difference between restrictive and obstructive spirometry

A

restrictive: normal FEV1/ FVC but reduced FCV
obstructive: FEV1/ FVC< 80%, FVC normal

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5
Q

Give 3 examples of obstructive lung diseases

A

Asthma (reversible), COPD (non reversible), bronchiectasis

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6
Q

Give 3 examples of restrictive lung diseases

A

interstitial lung disease, scoliosis, marked obesity, neuromuscular causes

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7
Q

What are the 4 causes of low PaO2?

A
  • hypoventilation
  • diffusion impairment
  • pulmonary shunt
  • v/q mismatch
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8
Q

What is the alveolar- arterial gradient useful for?

A

Determining if there is a lung pathology causing ABG abnromalities- if the gradient between the alveoli and artery is >4kPa there is lung pathology, if <4kPa pathology is not todo with lungs- drugs, encephalopathy etc

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9
Q

How is the alveolar- arterial gradient calculated?

A

PAO2 (alveolar partial pressure of O2)= 20 (Air PO2) - PaCO2 (same as pCO2)/0.8

PAO2- PaO2 (arterial O2)= A-a gradient (should be <2kPa)

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10
Q

Describe how anaphylaxis presents

A
  • rapid onset pruitis, angiodema, urticaria, hoarseness, stridor/ wheeze, chest tightness and bronchospasms
  • within minuites of exposure to source (drugs, food, sting, bite)
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11
Q

Describe the management of anaphylaxis (inc drug doses) with hypotension (7)

A
  • remove trigger and maintain airway (may need to call anaesthetist)
  • give 15L O2
  • IM adrenaline 0.5mg every 5 mins
  • IV hydrocortisone 200mg
  • IV chlorphenamine 10mg
  • lie flat and give 500ml 0.9% saline over 15 mins -> give more after if necessary
  • NEB salbutamol 5mg if bronchospasm
  • NEB adrenaline if laryngeal odema
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12
Q

Define a mild and moderate asthma attack

A

Mild: PEFR >75% no features of severe asthma
Moderate: PEFR 50-75% no features of severe asthma

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13
Q

Define a severe asthma attack

A

Severe is one of: PERF 33-50%, cannot complete a sentence in one breath, RR>25, HR>110

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14
Q

Define a life threatening and near fatal asthma attack

A

Life threatening: PERF <33%, sats <92% or ABG pO2< 8kPa, cyanosis, poor respiratory effort, silent chest, exhaustion, confusion, hypotension or arrhythmias
Near Fatal: Raised pCO2

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15
Q

Describe how you manage a severe asthma attack inc drug doses (5)

A

ABCDE

  • Oxygen: aim forsats 94-98%, ABG if <92%
  • 5mg back to back salbutamol nebs (every 15 mins if moderate)
  • 40mg oral pred/ IV hydrocortisone if PO not possible
  • Ipratropirum bromide 0.5mg neb
  • IV theophyline/ aminophylline if refractory or life threatening
  • ITU/ anaesthetist assesment and urgent CXR if life threatening
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16
Q

Describe how you would determine between an infective and non infective exacerbation of COPD

A

If infective: change in sputum colour/ volume, fever, raised WCC/ CRP

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17
Q

Describe the management of an infective exacerbation of COPD (5)

A

ABCDE

  • Oxygen via a fixed performance face mask due to risk of CO2 retention, aim for 88-92% until ABG
  • Salbutamol (5mg) and ipratropium bromide (0.5mg) nebs
  • 30mg pred STAT and OD for 7 days
  • Abx (amoxicillin 500mg or doxy)
  • CXR
  • Consider IV aminophylline if refractory
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18
Q

What would you do if someone with an infective exacerbation of COPD went into T2 resp failure with a pH of 7.25- 7.35?

A

NIV-> if pH drops further consider ITU referral

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19
Q

How do you determine if someone with COPD is a CO2 retainer?

A

Do an ABG:

  • if retainer bicarb will be raised, this means you aim for 88-92% sats
  • pCO2 may be raised and pH low due to acute illness but bicarb will not adjust quickly
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20
Q

Give the CURB-65 criteria

A

Confusion (MMT2 or more points worse than baseline)
Urea >7.0
Resp rate > 29
Blood pressure <90mmHg systolic or <60mmHg diastolic
Age >65

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21
Q

what is the difference between LRTI and pneumonia

A

pneumonia has CXR changes

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22
Q

Which Abx would be used for CURB 1, 2 and >3 community acquired pneumonia?

A

1: PO amoxicillin 500mg TDS for 5 days or PO doxy 200mg OD 5 days
2: Amoxicillin (same regime) AND doxy (same regime) –> if allergic just doxy
3 or more: legionella urine antigen test + Co-Amoxiclav IV 1.2g tds and Doxycycline oral 200mg od for 5 days. Meropenem IV in place of co- amox if allergic

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23
Q

Which antibiotic is used for HAP?

A

Co- amox oral if mild, IV is severe.

If allergic doxy PO for mild and meropenem IV if severe

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24
Q

Define massive haemoptysis

A

> 240mls in 24 hrs or >100 mls/ day over consecutive days

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25
Q

How do you manage massive haemoptysis (6)

A

ABCDE

  • line pt on side of suspected lesion
  • oral tranexamic acid for 5 days or IV
  • Stop NSAIDs, aspirin, anticoagulants
  • Abx if evidence of infection
  • consider vit K
  • CT aortogram- interventional radiologist may be able to undertake bronchial artery embolisation
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26
Q

How will a tension pneumothorax present?

A

Hypotension, tachycardia, tracheal deviation, sudden onset pain and SOB, high RR, resp failure, hyperresonance and no breath sounds unilaterally

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27
Q

How is tension pneumothorax treated?

A

Large bore IV cannula into 2nd ICS MCL and then chest drain into affected side

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28
Q

How can PE present?

A
  • pleurtic chest pain
  • SOB
  • haemoptysis
  • low cardiac output
  • rarely a cough
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29
Q

Give 6 risk factors for PE?

A
  • surgery
  • pregnancy
  • fractures
  • varicose veins
  • malignancy
  • reduced mobility
  • previous proven VTE
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30
Q

How are PE managed?

A

ABCDE

  • Oxygen
  • fluid resus if hypotensive
  • thrombolysis if massive PE confirmed by echo or CT or cardiac arrest imminent and outweighs bleeding risk
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31
Q

What ECG changes may be caused by PE?

A

Right heart strain:
ST depression and T inversion in V1-4, II, III and aVF.
Most common change seen is sinus tachy.

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32
Q

Give 6 absolute contraindications of thrombolysis

A
  • Haemorhagic or ischaemic stroke in last 6 months
  • CNS neoplasia
  • recent trauma or surgery
  • GI bleed< 1 month ago
  • bleeding disorder
  • aortic dissection
  • warfarin, pregnancy, liver disease and infective endocarditis are relative contraindications
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33
Q

give 5 complications of thrombolysis

A
  • bleeding
  • hypotension
  • intracranial haemorrhage/ stoke
  • reperfusion arrhythmias
  • systemic embolisation of thrombus
  • allergic reactions
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34
Q

Other than asthma what can cause a wheeze?

A

Bronchitis most common, pulmonary odema, COPD exacerbation, foreign body, allergic reaction, PE less common

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35
Q

State the criteria for safe asthma discharge after exacerbation? (7)

A
  • PEFR >75%
  • Nebs stopped for 24 hrs
  • inpatient asthma nurse r/v for inhaler technique
  • PEFR meter given and asthma action plan in place
  • 5 days oral pred given
  • GP follow up within 2 working days
  • resp clinic follow up within 4 weeks
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36
Q

Give 5 differentials for eosinophillia

A
  • airway inflammation due to asthma or COPD
  • hayfever/ allergies
  • drugs
  • vasculitis
  • eosinophillic pneumonia
  • parasites
  • lymphoma
  • SLE
  • allergic bronchopulmonary aspergillosis
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37
Q

Give 5 potential asthma triggers

A

smoking, upper resp infections (mainly viral), allergens (pollen, house dust mite, pets), exercise and cold air, pouultion, drugs (aspirin and B blockers in particular), stress

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38
Q

Give 3 features of good asthma control

A
  • no day or nightime symptoms
  • no need for rescue meds
  • no attacks
  • no limitations of physical activity
  • normal lung function
  • no side effects
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39
Q

Give the 4 pathophysiological features of COPD

A
  • mucous gland hyperplasia
  • loss of cillary function
  • emphysema
  • chronic inflammation w/ fibrosis
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40
Q

State treatment options available for COPD management as an out pt

A
  • ’ COPD care bundle’
  • smoking cessation
  • pulmonary rehab
  • bronchodilators
  • antimuscarinics
  • steroids
  • mucolytics (carbocysteine)
  • LTOT if appropriate
  • lung volume reduction surgery if appropriate
41
Q

Why is LTOT used?

A

extended periods of hypoxia can cause renal and cardiac damage

42
Q

When is LTOT indicated?

A

When the pt has a pO2 consistently below 7.3kPa or 8 with cor pulmonale, they dont smoke and they dont retain very much CO2

43
Q

How long does the pt need to be on oxygen for per day for it to have a benefit

A

16hrs

44
Q

Why does pulmonary rehab work?

A

Pt with COPD tend not to exercise because it makes them breathless, this leads to reconditioning which makes them breathless more easily and so a negative cycle develops. Pulmonary rehab aims to break this cycle with a 6-12 week programme of supervised and unsupervised exercise, nutritional advice and disease education.

45
Q

What extra tests should be done for a high CURB 65 score?

A

serology and urine legionella antigen test to look for atypical causes

46
Q

How should pneumonia be followed up?

A

CXR in 6 weeks, HIV test, immunoglobulins, pneumococcal IgG serotypes, H. influenzae b IgG

47
Q

What could cause a non resolving pneumonia? (CHOAS)

A
  • Complication (empyema, abscess)
  • Host immunocompromised
  • Antibiotic (wrong type, dose or administration)
  • Organism resistant or atypical
  • Second diagnosis (PE< cancer, organising pneumonia)
48
Q

How does TB present?

A
  • usually with fever and nocturnal sweats (drenching)
  • weight loss over weeks- months
  • malaise
  • resp tb: cough, sputum, haemoptysis
  • non resp: skin (erythema nodusum), lymphadenopathy, joint pain, abdo, meningitis, milllary tb, pericaridal effusion .
49
Q

Give 5 differentials for haemoptysis

A
  • infections: pneumonia, TB, bronchiectasis, CF, cavitating lung lesion (usually fungal)
  • malignancy (primary or mets)
  • haemorrhage: bronchial artery erosion, vasculitis, coagulopathy
  • PE
50
Q

Give 3 risk factors for TB

A
  • Known history of TB contact
  • Born in a country with high TB incidence
  • Foreign travel to country with high TB incidence
  • Evidence of immunosurpression
  • poverty, overcrowding, poor nutrition etc
51
Q

How should suspected TB be investigated?

A
  • 3x sputum samples for alcohol and acid fact bacilli & TB culture
  • CXR
  • if no sputum production consider bronchoscopy/ bronchial lavage
  • FBC, LFT, U&E, HIV testing, vit D levels
  • CT chest if CXR or clinical features atypical
  • MRI brain/ spine if millary tb suspected + Lumbar puncture
52
Q

How should TB be managed?

A
  • In a side room with infection control measures
  • Start Abx if unclear between pneumonia and TB
  • Notify TB specialist nurses and public health
  • Rifampicin and isoniazid for 6 months
  • pyrazinamide and ethambutol for 2 months
  • treatment is often started before sputum cultures return as they can take 6-8 weeks
53
Q

What 3 things must be checked before starting TB treatment and monitored during and why?

A
  • Bodyweight- anti TB meds doses are weight dependant
  • LFTs for baseline as anti TB meds are hepatotoxic
  • Visual acuity- ethambuol can cause retrobulbar nephritis
54
Q

What is given along side isoniazid as prophylaxis against peripheral neuropathy?

A

pyridoxine

55
Q

What is the gold standard test for diagnosis of bronchiectasis?

A

High resolution CT- signet ring sign

56
Q

Give 5 causes for bronchiectasis

A
  • Post infective (whooping cough, TB)
  • Immuno deficiency (hypogamaglobulinaemia)
  • genetic/ mucocillary clearance defects (CF, youngs syndrome, primary cillary dyskineasia)
  • obstruction (foreign body, tumour)
  • toxic insult (gastic aspiration, toxic chemical/ gas inhalation)
  • secondary immune deficiency (HIV, malignancy)
  • RA, IBD
57
Q

Give 3 common organisms which can cause bronchiectasis?

A
  • haemophilus influenza
  • pseudomonas aeruginosa - moraxella catarrhalis
  • Non TB mycobacteria
  • candida and aspergillus
58
Q

How is bronchiectasis managed?

A
  • treat cause
  • physiotherapy for mucus clearance
  • Abx according to sputum cultures/ sensitivities for acute exacerbations and often chronic surpressive therapy
  • flu vaccine
  • bronchodilators and mucolytics if required
  • pulmonary rehab is MRC score >2
59
Q

What is the inheritance pattern of CF?

A

auto recessive mutation of CFTR gene

60
Q

Describe the criteria for CF diagnosis

A

1 or more characteristic features or a history of CF in a sibling or a positive new born screening test AND increase sweat chloride concentration, two CF mutations on genotyping or demonstration of abnormal nasal epithelial ion transport

61
Q

Which 4 ways can CF present?

A
  • +ve new born screening test
  • recurrent chest infections
  • meconium ileus (billious vomiting abdo distension and delay in passing muconium shortly after birth
  • intestinal malabsorbtion–> main cause if severe deficiency of pancreatic enzymes
62
Q

Give 5 features of CF

A
  • chronic sinusitis
  • nasal polyps
  • recurrent LRTIs
  • salty sweat
  • bronciectasis
  • liver disease, portal hypertension and gall stones
  • pancreatic insuffiency and diabetes
  • steatorrhoea
  • distal intestinal obstruction
  • infertility (males >females)
  • osteoporosis
  • clubbing
  • arthropathies
  • ronchi or coarse crackles
63
Q

What are the 4 main complications of CF?

A
  1. Respiratory infections (may need prophylactic abx)
  2. Low body weight (may need NG or PEG feeding, high kcal diet and supplements)
  3. distal intestinal obstruction syndrome
  4. CF related diabetes
64
Q

What is distal intestinal obstruction syndrome?

A

Faecal obstruction in ileocaecum due to thick dehydrated faeces. Caused by pancreatic insufficiency, also salt deficiency/ hot weather. presents with RIF mass and pain, constipation.

65
Q

What lifestyle advice should be given to those with CF?

A
  • dont smoke
  • avoid others with CF
  • avoid friends/ relatives with infections and colds
  • avoid hot tubs due to pseudomonas risk
  • clean and dry nebulisers thoroughly
  • avoid stables, compost or rotting veg due to aspergillius fumigatus inflation risk
  • Get your flu jabs
  • sodium chloride tablets in hot weather/ vigorous exercise
66
Q

Give 3 risk factors for pneumothorax

A
  1. preexisting lung disease
  2. height
  3. smoking/ cannabis
  4. diving
  5. trauma
  6. CT syndromes eg marfans
67
Q

What are the 4 types of pneumothorax?

A
  1. spontaneous (primary or secondary)
  2. traumatic
  3. tension
  4. iatrogenic (central lines or pacemakers)
68
Q

How are pneumothorax managed?

A

Primary: if symptomatic and rim of air >2cm on CXR give O2 and aspirate. If unsuccessful reaspirate of put in intercostal chest drain (5th ICS, upper boarder of rib, Mid axillary line).
Secondary: if >2 cm or breathless do chest drain, if size 1-2 cm aspirate if not admit and watch.
If persistent air leak for >5 days refer to thoracic surgeons.

69
Q

How should a pleural effusion be investigated?

A
  • CXR
  • ECG
  • FBC, U&E, LFT, CRP, bone profile, LDH, clotting
  • Echo if suspect heart failure
  • staging CT with contract if suspect exudative cause
  • US guided aspiration with biochemistry, cytology and microbiology (inc AAFB)
70
Q

What is the only indication for an urgent chest drain insertion for a pleural effusion?

A

Underlying empyema- pH of pleural fluid <7.2 or visible pus on aspirate

71
Q

Give 4 causes of a transudative effusion (<30g/L protein)?

A
  • heart failure
  • cirrhosis
  • hypoalbuminaemia (nephrotic syndrome or peritoneal dialysis)
  • hypothyroidism, mitral stenosis or PE are less common causes
72
Q

Give 3 causes of exudative effusion

A
  • malignancy
  • infections (parapneumonic, TB, HIV)
  • RA, pancreatitis, lymphatic disorders, dresslers, pulmonary infarction and PE are less common causes
73
Q

What criteria can be used to determine if a pleural fluid is exudate or transudate if the protein conc is between 25 and 35 g/L?

A 
Lights critera:
Exudate if:
- protein >0.5
- LDH >0.6
- pleural fluid LDH> 2/3 of upper limit of normal
74
Q

Give 3 types of interstitial lung disease

A
  • usual interstitial pneumonia (UIP) (most common)
  • non specific interstitial pneumonia (NSIP)
  • extrinsic allergic alveolitis
  • sarcoidosis
75
Q

What specific bloods should be done for all new diagnosis of ILD

A

ANA, ENA, Rh F, ANCA, Anti GBM, ACE, Ig G to precipitins

76
Q

Describe how UIP normally presents?

A
  • clubbing, reduced chest expansion
  • fine inspiratory crepitations
  • slow onset breathlessness on exertion, dry cough, age >45
77
Q

Describe how extrinsic allergic alveolitis can present? (2)

A

acute: 4-8 hrs after exposure to an organic antigen, usually settles in 1-3 days
chronic: chronic exposure over months/ years to an anitgen, less reversible

78
Q

What is sarcoidosis?

A

A multisystem inflammatory condition of unknown cause commonly affecting the resp system (causing ILD) but can affect nearly all organs. Causes non-caseating granulomas (histology important). 50% get spontaneous remission.

79
Q

How should sarcoidosis be investigated?

A
  • PFTs (obstructive pattern until fibrosis occurs)
  • CXR
  • Bloods: renal function, ACE, Calcium
  • urinary calcium
  • cardiac involvement: ECG, echo, MRI
  • CT/ MRI head if headaches (neuro sarcoid)
80
Q

What are the principles to ILD treatment?

A
  • remove exposures eg pets/ birds
  • avoid drugs which couldve caused it
  • pirfenidone (downregulates growthfactors and procollagen I and II so decreases lung fibrosis)
  • stop smoking
  • ? n- acetylcysteine, immunosurpression sometimes
  • transplantation
  • treat infections which are often atypical
  • oxygen
  • MDT and palliative care
81
Q

How can lung cancer present?

A
  • persistant cough and other resp symptoms
  • incidental finding
  • SVC obstruction
  • clubbing
  • horners syndrome
  • mets to liver, adrenals (addisons), bone, pleura (pleural effusion)
  • SIADH
  • hypercalcaemia (hyperparthyroid)
  • cushings syndrome (ACTHrp)
  • constitutional symptoms
82
Q

Give 4 risk factors for lung cancer

A
  • smoking a lot
  • airflow obstruction
  • age
  • fhx lung cancer
  • exposure to carcinogens eg asbestos
83
Q

What are the histology options of lung cancer investigations?

A
  • US guided neck node fine needle aspiration if lymphadenopathy
  • bronchoscopy
  • CT biopsy
  • thoracoscopy if pleural effusion present
84
Q

When is a PET scan used during investigation of lung cancer?

A

If a pt is a surgical candidate and initial CT suggestive of low stage as it helps to detect

85
Q

What stages of lung cancer have potential for curative surgery?

A

I and II

Surgery and neoadjuvant chemo for IIa

86
Q

What is mainstay of treatment for Small cell LC?

A

Chemotherapy and palliative radiotherapy- rapid growing so rarely a surgical candidate

87
Q

What is the clinical definition for Obstructive sleep apnoea?

A

Upper airway narrowing, provoked by sleep, causing sufficient sleep fragmentation to result in significant daytime symptoms such as sleepiness

88
Q

Why does obstructive sleep apnoea occur?

A

Airway patency depends on dilatory muscle activity which relax during sleep. Some narrowing is normal but in pts with a lot of neck fat, small mandible, large tonsils, neuromuscular disease, sedatives or old age narrowing is such that it cuts off airway and causes them to wake momentarily to reactivate their pharyngeal dilators.

89
Q

How may sleep apnoea present?

A
  • daytime sleepiness
  • sleep attacks
  • high BP- with every wakening their BP rises (bad for CVS) and there is also an increase in day time BP
  • nocturia
  • usually males with large neck sizes and smaller/ set back mandible
90
Q

How can sleepiness be quantified?

A

Epworth sleepiness scale

91
Q

How can sleep be studied?

A
  • overnight oximetry
  • limited sleep study- oximetry, snoring, body movement, heart rate, oronasal flow, chest/ abdomen and leg movements
  • full polysomnography- limited sleep study plus EEG and EMG
92
Q

How is obstructive sleep apnoea treated?

A
  • weight loss, reduce alcohol intake
  • mandibular advancement devices, pharyngeal surgery last resort for snores
  • Nasal CPAP, consider gastroplasty/ bypass if significant OSA
  • Severe OSA and CO2 retention may require period of NIV prior to CPAP if acidotic but compensated CO2 retention may be reversed with CPAP alone
93
Q

What driving advice should be given to those with OSA diagnosis?

A

Do not drive while sleepy- stop and have a nap. They also need to notify the DVLA. the dr can advice drivers to stop altogether eg HGV drivers.

94
Q

When should you step up chronic asthma control? (4)

A
  • using salbutamol >2 times a week
  • symptoms >2 times per week
  • waking >1 time per week
  • exacerbation needing oral steroids in last 2 yrs
95
Q

Describe the stepwise management for asthma as per the BTS 2016 guidelines

A
  • for infrequent short lived wheeze give SABA
  • then step up to low dose ICS (200-400)
  • then add LABA to low dose ICS (combo inhaler)
  • If this doesnt do anything then stop LABA and increase ICS dose (upto 200)
  • If LABA helps a bit but need more, increase ICS to 800
  • Next add a leukotriene receptor antagonist (monteleukast), theophylline or LAMA (tiotropium)
  • Then consider increasing ICS or (if already done) adding a 4th drug and refer for specialist care
  • The next step is daily oral steroids
96
Q

Give 4 complications of pneumonia

A 
Abscess 
Empyema 
Respiratory failure 
Acute respiratory distress syndrome
Septic shock 
Pleural effusion 
AF
97
Q

Give 4 paraneoplastic syndromes caused by lung cancer and state which type of cancer usually causes each syndrome

A 
Cushings- acth release from small cell
Siadh - ADH from small cell
Acromegaly- gh or ghrh from small cell 
Hypercalcaemia- pthrp from squamous cell or osteolytic mets
Svc obstruction- any
Horners syndrome- any apical
VTE- any
Anaemia of chronic disease- any
98
Q

How does sarcoidosis cause hypercalcaemia?

A

Causes increased macrophage synthesis of 1,25 dihydroxy vitamin d, high increase ca absorption, mobilisation and reabsorbtion

99
Q

Other than humoral hypercalcaemia of malignancy (pthrp from squamous cell or renal carcinomas), what other 3 ways can cancer cause hypercalcaemia?

A

1) ectopic pth secretion, by various differnt cancer types
2) osteolytic bone mets causing calcium mobilisation from bone into blood
3) lymphocyte synthesis of 1,25 dihydroxy vit d from lymphomas

Y3 Medicine (9 decks)

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