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Medicine > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Typical causative organisms of CAP

A 
Streptococcus pneumoniae (commonest), Haemophilus influenzae (common in COPD), Moraxella catarrhalis
Atypical: Mycoplasma pnuemoniae (dry cough), Staphylococcus aureus
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2
Q

Causative organisms of HAP

A

Gram neg enterobacteria
Staph aureus
Pseudomonas
Klebsiella

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3
Q

Investigations for pneumonia

A 
Oxygen saturation
ABG is sats are low
BP
Bloods - FBC, U+E, LFT, CRP
CXR
Sputum for microscopy and cultures
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4
Q

CAP severity scoring system

A 
CURB-65
Confusion (AMT =<8)
Urea >7
Resp rate >=30
BP <90 systolic (and/or diastolic 60)
Age >= 65
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5
Q

Management (acute and follow up) of CAP depending on severity

A

CURB65: 0-1 oral abx at home, 2 requires hospital therapy for IV abx, >=3 consider ITU

Abx, oxygen, IV fluids, VTE prophylaxis, analgesia
Follow up at 6 weeks (+/- CXR)

Abx guidelines: amoxicillin (doxycycline or erythromycin if pen allergic), co-amoxiclav if severe

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6
Q

Antibiotics for HAP

A

Co-amoxiclav

Tazocin if severe

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7
Q

Complications of pneumonia

A

Pleural effusion, empyema, lung abscess, resp failure, sepsis, brain abscess, pericarditis

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8
Q

Pneumonia in immunocomp patients

A

Pneumocystis jirovecii
Dry cough, exertional dyspnoea, reduced sats, fever, bilateral creps
Ix: induced sputum MCS, bronchoalveolar lavage
Mx: high dose co-trimoxazole, +/- steroids

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9
Q

What is bronchiectasis

A

Chronic inflamm of bronchi and bronchioles leading to permanent dilatation and thinning of the airways

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10
Q

Main organisms causing bronchiectasis

A

Haemophilus influenzae, Strep pneumonia, Staph aureus, Pseudomonas aeruginosa

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11
Q

Causes of bronchiectasis

A

Congenital: cystic fibrosis, primary ciliary dyskinesia, Kartageners
Post-infection: measles, pertussis, bronchiolitis, pneumonia, TB, HIV
Other: bronchial obstruction, allergic bronchopulmonary aspergillosis, RA, UC, idiopathic

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12
Q

Clinical features of bronchiectasis

A

Symptoms: persistent cough, copious purulent sputum, intermittent haemoptysis
Signs: clubbing, coarse inspiratory creps, wheeze (asthma, COPD, ABPA)

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13
Q

Complications of bronchiectasis

A

Pneumonia, pleural effusion, pneumothorax, haemoptysis, cerebral abscess, amyloidosis

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14
Q

Investigations for bronchiectasis

A

Sputum culture
CXR (cystic shadows, thickened bronchial walls (tramline and ring shadows)
HRCT chest (signet ring)
Spirometry (obstructive)
Bronchoscopy
Other tests - serum immunoglobulins, CF sweat test

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15
Q

Management of bronchiectasis

A

Chest physiotherapy
Flutter valve devices may air sputum removal
Mucolytics
Antibiotics in acute settings (ciprofloxacin if pseudomonas)
Salbutamol nebs (if asthma, COPD, CF, ABPA)
Prednisolone
Surgery if localised disease

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16
Q

Clinical features of cystic fibrosis (neonates –> children and young adults)

A

Failure to thrive, meconium ileus, rectal prolapse
Resp - bronchiectasis, recurrent chest infections, pneumothorax, haemoptysis, resp failure, cor pulmonale (finger clubbing, cyanosis, bilateral coarse crackles)
GI - DM, steatorrhoea, gallstones
Other - male infertility, osteoporosis, arthritis, vasculitis, nasal polyps

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17
Q

Management of cystic fibrosis

A

Antibiotics, postural drainage/ chest physiotherapy, pancreatic supplements (creon), high fat diet, bronchodilators, heart/lung transplant
Ivacaftor and lumacaftor target the CFTR protein

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18
Q

Subtypes of non-small cell lung cancer and their typical features

A

NSCLC is more common than SCLC
Squamous cell lung cancer - central, PTHrP (hypercalcaemia), finger clubbing, HPOA
Adenocarcinoma - peripheral, most common for non-smokers (although majority of cases are smokers), gynaecomastia, HPOA.
Large cell lung carcinoma - peripheral, poor prognosis, poor differentiation, may secrete beta-HCG

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19
Q

Features of small cell lung cancer

A

Central, arise from APUD cells, associated with ADH (hyponatraemia) and ACTH secretion (Cushings), Lambert-Eaton syndrome
The ACTH can cause bilateral adrenal hyperplasia and hypokalaemic alkalosis due to cortisol

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20
Q

Features of lung cancer

A

Persistent cough, haemoptysis, dyspnoea, chest pain, weight loss, anorexia

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21
Q

Complications of lung cancer

A

Superior vena cava obstruction, hoarseness (recurrent laryngeal nerve palsy), Horners (pancoast tumour), rib erosion, pericarditis, AF, mets to brain, bone, liver, adrenals

Lambert eaton, hypercalcaemia (PTHrP), Cushings (ACTH secretion), hyponatraemia (ADH secretion)

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22
Q

Investigations for lung cancer

A 
CXR (usually the first investigation)
CT (investigation of choice)
Bronchoscopy (allows for biopsy)
PET scan (usually for NSCLC)
Bloods (raised platelets)
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23
Q

referral criteria for lung cancer

A

2-week-wait referral if: CXR suggests lung cancer, or aged 40+ with unexplained haemoptysis

offer 2-week-wait if: 40+ with 2+ unexplained symptoms (or 1+ and a smoker): cough, fatigue, dyspnoea, chest pain, weight loss, anorexia

Consider 2-week-wait if: 40+ with persistent or recurrent chest infections, or finger clubbing, or lymphadenopathy, or chest signs suggestive of lung cancer, or thrombocytosis

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24
Q

Management for NSCLC

A

Only 20% eligible for surgery

Curative or palliative radiotherapy

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25
Q

Contraindications for surgery in lung cancer

A

Assess general health, stage 3b/4 (mets), FEV1 <1.5L, malignant pleural effusion, tumour near hilum, vocal cord paralysis, SVCO

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26
Q

Malignant mesothelioma cause, mx, prognosis

A

Cause - asbestos
Mx - palliative chemo
Prognosis is poor (<2y)

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27
Q

Allergic bronchopulmonary aspergillosis (ABPA)

  • what is it
  • who does it affect
A

type 1 and 3 hypersensitivity reaction to Aspergillus fumigatus
Asthmatics and CF patients at risk

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28
Q

Allergic bronchopulmonary aspergillosis (ABPA) symptoms

A

Bronchoconstriction then permanent damage, causing bronchiectasis -> wheeze, cough, purulent sputum, dyspnoea

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29
Q

Allergic bronchopulmonary aspergillosis (ABPA) investigations

A

CXR (transient segmental collapse, consolidation, bronchiectasis)
Aspergillus in sputum
Eosinophilia
Serum IgE (raised)

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30
Q

Allergic bronchopulmonary aspergillosis (ABPA) management

A

Prednisolone
Itraconazole
Bronchodilators

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31
Q

Important questions to ask in asthma history

A

Symptoms
Precipitants - cold, exercise, emotion, allergens, pollution, NSAIDs, beta blockers
Diurnal variation
Exercise tolerance (quantify)
Disturbed sleep (quantify as nights/week)
Acid reflux?
Other atopic disease - eczema, hayfever, allergy, family history
Home - pets, carpet, feather pillow/duvet, floor cushions?
Job
Days/week off school/work

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32
Q

Investigations for asthma

A

Spirometry (measures vol and speed of air) - obstructive
FEV1 significantly reduced, FVC normal, FEV1% <70%
reversible obstruction following bronchodilators

Fractional exhaled nitric oxide (FeNO) - rises in inflam cells, so levels will be high in asthma

Consider CXR if old and hx of smoking

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33
Q

Chronic asthma management in children >5

A

SABA (salbutamol)

  • > Low dose ICS (budesonide)
  • > Oral LTRA (montelukast)
  • > Stop LTRA and start LABA (salmeterol)
  • > MART (ICS+LABA)
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34
Q

Side effects of asthma drugs

A

SABA and LABA - tremor
ICS - oral candidiasis, stunted growth
LTRA - GI discomfort, sleep/movement disorders

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35
Q

Asthma management in adults

A

SABA
+ICS
+LTRA
+LABA (dont stop LTRA)

SABA + LTRA + MART (ICS + LABA)

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36
Q

Acute asthma management in children

A

Mild-mod: salbutamol via spacer give 1 puff every 30-60 sec up to 10 puffs, if symptoms not controlled then refer to hospital

Prednisolone should be given to all children with an asthma exacerbation (3-5 days)

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37
Q

Acute asthma severities

A

Moderate - PEFR 50-75% of best/predicted, normal speech, RR <25, Pulse <110, sats >92

Severe - PEFR 33-50%, cant complete sentences, RR>25, pulse>110, sats <92

Life-threatening - PEFR<33%, silent chest, cyanosis, feeble resp effort (normal pCO2), bradycardia, dysrhythmia, hypotension, exhaustion, confusion, coma

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38
Q

Treatment of acute asthma (severe or life threatening)

A 
O2 (maintain 94-98%)
5mg salbutamol nebs
40-50mg oral prednisolone 
500 micrograms ipratropium bromide nebs
Consider 2g magnesium sulfate IV
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39
Q

Follow up for acute severe asthma

A

GP should be notified within 24hours of discharge and should review the patient within 48 hours
Check inhaler technique
Review treatment
Resp specialist should follow up all patients admitted with a severe asthma attack for at least one year

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40
Q

COPD includes which two lung conditions

A 
Chronic bronchitis (chronic cough and sputum production)
Emphysema (enlarged alveoli with destruction of alveolar walls)
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41
Q

Pink puffers vs. blue bloaters

A

Pink puffer - increased alveolar ventilation, near normal pO2 and normal/low pCO2, breathless but not cyanosed. May develop type 1 resp failure

Blue bloater - reduced alveolar ventilation, low pO2 and high pCO2, cyanosed but not breathless and may go on to develop cor pulmonale. Rely on hypoxic drive to maintain resp effort (88-92%) type 2 resp failure.

42
Q

Investigations for COPD

A

Spirometry (obstructive, irreversible)
ABG (low pO2 +/- hypercapnia)
CXR (hyperinflation, flat hemidiaphragm, large central pulmonary arteries, reduced peripheral vascular markings)
CT (bronchial wall thickening, air space enlargement)
ECG (right atrial and ventricular hypertrophy if cor pulmonale)

43
Q

Management of chronic COPD

A

Stop smoking, exercise, diet advice

If asthmatic features of features of steroid responsiveness:

  1. SABA or SAMA
  2. LABA + ICS (if already on SAMA discontinue and switch to SABA)
  3. LABA + ICS + LAMA

If no asthmatic features or no features of steroid responsiveness:

  1. SABA or SAMA
  2. LABA + LAMA (if already taking SAMA, discontinue and switch to SABA)

Flu and pneumococcal vaccinations
Long term oxygen therapy (+ NIV if hypercapnic)
Consider surgery

44
Q

what is type 1 resp failure and what are some examples

A

pO2<8kPa with normal/low paCO2
Ventilation/perfusion mismatch, hypoventilation, abnormal diffusion, or right to left cardiac shunts

V/Q mismatch: pneumonia, pulm oedema, PE, asthma, emphysema, pulm fibrosis, ARDS

45
Q

what is type 2 resp failure and what are some examples

A

pO2 <8kPa with paCO2 >6kPa
Alveolar hyperventilation +/- V/Q mismatch
Examples: asthma, COPD, pneumonia, end-stage pulm fibrosis, OSA, sedation, cervical cord lesion, MG, GBS, kyphoscoliosis

46
Q

Management of type 1 resp failure

A

Treat underlying cause
Oxygen (24-60%) via face mask
Assisted ventilation if pO2 <8kPa despite 60% O2

47
Q

Management of type 2 resp failure

A

Treat underlying cause
Controlled O2: start at 24% via venturi
Recheck ABG after 20 min - if pCO2 is steady or lower then increase O2 conc to 28%, if pCO2 has increased by >1.5kPa consider assisted ventilation (non-invasive positive pressure ventilation), if this fails consider intubation and ventilation

48
Q

Symptoms of PE

A

Acute breathlessness, pleuritic chest pain, haemoptysis, dizziness, syncope

49
Q

Signs of PE

A

Pyrexia, cyanosis, tachypnoea, tachycardia, hypotension, raised JVP, pleural rub, pleural effusion, check for DVT

50
Q

Investigations for PE

A

D-Dimer +/- CTPA or V/Q scan

FBC, U+E, baseline clotting
ABG
CXR
ECG (normal, or tachycardia, RBBB, inverted T in V1-V4, S1Q3T3)

51
Q

Criteria for suspecting PE

A 
Well's Score-
Clinical signs and symptoms of DVT (=3)
Tachycardia (=1.5)
Recently bed ridden or major surgery (=1.5)
Previous DVT or PE (=1.5)
Haemoptysis (=1)
Cancer (=1)
Alternative diagnosis less likely than PE (=1)

Score <4 = unlikely
Score >4 = likely

52
Q

How to investigate PE based on Well’s score

A

<4 (unlikely) -> D-Dimer
If D-dimer +ve then do CTPA or empirical LMWH
If D-dimer -ve then consider other diagnoses

> 4 (likely) -> immediate CTPA or treat empirically with LMWH fi there will be a delay in CTPA

53
Q

PE treatment

A

If haemodynamically unstable -> thrombolyse for massive PE (alteplase)

If haemo stable - LMWH (unfractionated if renal impairment) for 5 days then start DOAC or warfarin (with warfarin stop LMWH when INR 2-3)

54
Q

Pneumothorax causes

A

Spontaneous in young thin men
asthma, COPD, TB, pneumonia, lung abscess, cancer, CF, lung fibrosis, sarcoidosis, connective tissue disorders, trauma, iatrogenic

55
Q

Symptoms of pneumothorax

A

May be asymptomatic

Sudden onset dyspnoea, pleuritic chest pain

56
Q

Signs of pneumothorax

A

Unilateral: Reduced expansion, hyper-resonance to percussion, diminished breath sounds
Tension pneumothorax - trachea deviated away from affected side

57
Q

Investigations for pneumothorax

A

CXR (dont bother if tension pneumothorax - delays treatment)

ABG

58
Q

Types of pneumothorax

A

Primary - spontaneous, no other lung conditions (young thin male)
Secondary - lung comorbidities
Tension - air drawn into pleural space with each inspiration and no route for escape during expiration (one way valve). EMERGENCY.

59
Q

Management for non-tension pneumothorax

A

Primary: SOB or >2cm on CXR -> aspiration (chest drain if unsuccessful)

Primary: <2cm and no SOB -> O/P review in 2-4 weeks

Secondary: SOB or >2cm on CXR -> chest drain

Secondary: <2cm and no SOB -> aspiration if >1cm (chest drain if unsuccessful), if <1cm then admit and observe for 24h with O2

60
Q

Management of tension pneumothorax

A

Needle decompression and chest tube insertion.

Insert a large bore (14-16G) needle with a syringe, partially filled with 0.9% saline, into the 2nd intercostal space midclavicular line on the affected side. Withdraw plunger to allow air to to bubble through saline in syringe.
Then insert a chest tube. (5th intercostal mid axillary line)

61
Q

Pleural effusion transudate vs exudate causes

A

Transudate (<25g/L protein) - cardiac failure, constrictive pericarditis, fluid overload, cirrhosis, nephrotic

Exudate (>35g/L protein) - infection (pneumonia, TB), inflammation (RA, SLE), malignancy

62
Q

Pleural effusion signs

A

Decreased expansion, stony dull percussion, diminished breath sounds on affected side
Reduced vocal resonance
There may be tracheal deviation in large effusions

63
Q

Pleural effusion investigations

A 
CXR
Ultrasound
Contrast CT
Diagnostic aspiration
Pleural biopsy
64
Q

Management of pleural effusion

A

Recurrent aspiration
Pleurodesis
Indwelling pleural catheter
Drugs to alleviate symptoms

65
Q

What is obstructive sleep apnoea syndrome?

A

Intermittent closure/collapse of the pharyngeal airway causing apnoeic episode during sleep. terminated by partial arousal from sleep

66
Q

Clinical features of obstructive sleep apnoea

A 
Obese, middle aged man
Snoring
Tiredness
Poor sleep quality
Morning headache
Decreased libido
Nocturia
Reduced cognitive performance
67
Q

Investigations for obstructive sleep apnoea

A

Epworth sleepiness scale

Diagnostic sleep studies

68
Q

Management for obstructive sleep apnoea

A

Weight loss
CPAP
Intra-oral devices (mandibular advancement) if CPAP is not tolerated
Inform DVLA if excessive daytime sleepiness

69
Q

What is cor pulmonale and what are some causes

A

Right heart failure due to chronic pulmonary artery hypertension
Causes - chronic lung disease, pulmonary vascular disorders, neuromuscular and skeletal diseases

70
Q

Clinical features of cor pulmonale

A

Dyspnoea, fatigue, syncope

Signs: cyanosis, tachycardia, raised JVP, RV heave, loud P2, pansystolic murmur (tricuspid regurg), hepatomegaly, oedema

71
Q

Sarcoidosis population group

A

More common in african-caribbean women aged 20-40

72
Q

Acute sarcoidosis clinical features

A

Fever, erythema nodosum, polyarthralgia, bilateral hilar lymphadenopathy

73
Q

Pulmonary features of sarcoidosis

A

Bilateral hilar lymphadenopathy, fibrosis

Dry cough, progressive dyspnoea, reduced exercise tolerance, chest pain

74
Q

Non-pulmonary features of sarcoidosis

A

lymphadenopathy, hepatomegaly, splenomegaly, uveitis, conjunctivitis, dry eyes, glaucoma, bells palsy, erythema nodosum, arrhythmias, hypercalcaemia, renal stones

75
Q

Investigations for sarcoidosis

A

Tissue biopsy is diagnostic and shows non-caseating granulomata
Bloods - raised ESR, lymphopenia, deranged LFTs, raised serum ACE, hypercalcaemia, raised immunoglobulins
24hr urine - high calcium
CXR
ECG - arrhythmias, BBB
Lung function tests - restrictive
bronchoalveolar lavage
ultrasound
bone x-rays - punched out lesions in terminal phalanges
CT/MRI

76
Q

CXR sarcoidosis staging

A 
0- normal
1- BHL
2- BHL + peripheral pulm infiltrates
3- diffuse pulm infiltrates alone
4- progressive pulmonary fibrosis, honey comb, pleural involvement
77
Q

Management of sarcoidosis

A

BHL alone requires no treatment, most recovers spontaenously.
Acute sarcoidosis - bed rest, NSAIDs
Consider corticosteroids or immunosuppression.

78
Q

Clinical features of interstitial lung disease

A

Dyspnoea on exertion, non-productive paroxysmal cough, abnormal breath sounds, abnormal CXR or HRCT, restrictive pulmonary spirometry

79
Q

Examples of interstitial lung disease associated with a known cause

A 
Occupational (asbestosis, siliocosis, cotton workers lung, coal workers pneumonconiosis)
Drugs (bleomycin, nitrofurantoin, etc)
Hypersensitivity pneumonitis (aka. EAA)
Infection (TB, fungi, viral)
GORD
80
Q

Examples of interstitial lung disease associated with systemic disorders

A

Sarcoidosis, RA, SLE, Sjögrens, UC, autoimmune thyroid

81
Q

Idiopathic examples of interstitial lung disease

A

Idiopathic pulmonary fibrosis
Cryptogenic organising pneumonia
Non-specific interstitial pneumonitis

82
Q

What is extrinsic allergic alveolitis (EAA)?

A

In sensitised inderviduals, repetitive inhalation of allergens provokes a hypersensitivity reaction (acute or chronic phases)

83
Q

Causes of extrinsic allergic alveolitis

A

Bird-fanciers and pigeon-fanciers lung
Farmers and mushroom-workers lung
Malt workers lung

84
Q

Clinical features of EAA (acute and chronic)

A

Acute (4-6h post exposure): fever, rigors, myalgia, dry cough, dyspnoea, fine bibasal crackles

Chronic: finger clubbing, increasing dyspnoea, weight loss, exertional dyspnoea, type 1 resp failure, cor pulmonale

85
Q

Acute phase investigations for EAA

A

FBC (netrophilia), high ESR, ABG, serum antibodies
CXR (upper zone consolidation)
Lung function tests (reversible restriction)

86
Q

Chronic phase investigations for EAA

A 
Bloods, serum antibodies
CXR (upper zone fibrosis, honeycomb)
CT chest (nodules, ground glass)
Lung function tests (restrictive)
Bronchoalveolar lavage (increased lymphocytes and mast cells)
87
Q

Management of EAA

A

Acute: remove allergen, give O2, oral prednisolone
Chronic: avoid allergen, wear face mask or positive pressure helmet, long term steroids, compensation

88
Q

Idiopathic pulmonary fibrosis population group

A

typically seen in patients aged 50-70 years, twice as common in men
Commonest type of interstitial lung disease

89
Q

Features of idiopathic pulmonary fibrosis

A

Progressive exertional dyspnoea

Bibasal fine end-inspiratory crepitations, dry cough, clubbing

90
Q

Diagnosing idiopathic pulmonary fibrosis

A

High resolution CT chest diagnostic investigation of choice (honeycombing, traction bronchiectasis, ground glass)
Spirometry - restrictive, FEV1 normal/decreased, FVC decreased, FEV1% increased
Impaired gas exchange - reduced transfer factor (TLCO)
CXR - bilateral interstitial shadowing (ground glass, honeycombing)
ANA positive in 30%, RhF positive in 10%

91
Q

Management and prognosis of idiopathic pulmonary fibrosis

A

Pulmonary rehabilitation
Supplementary oxygen
Lung transplant

Poor prognosis (3-4 year life expectancy)

92
Q

TB primary disease

A

non-immune host exposed to mycobacterium tuberculosis -> small lung lesion (Ghon focus develops), composed of tubercle-laden macrophages.
In immunocompetent people then initial lesion usually heals by fibrosis. Those who are immunocompromised may develop disseminated disease (miliary TB)

93
Q

TB secondary disease

A

Host becomes immunocompromised and the initial infection becomes reactivated, generally at lung apex

94
Q

Clinical features of TB

A 
Low grade fever, anorexia, weight loss, malaise, night sweats, clubbing, erythema nodosum
Cough, haemoptysis
Enlarged lymph nodes
Bone tenderness
TB meningitis
UTI symptoms
Pericarditis, pericardial effusion
95
Q

Diagnostic tests for latent TB

A

Tuberculin skin test - intradermal injection of purified protein derivative tuberculin. Size of skin induration is used to determine positivity depending on vaccination history and immune status

Interferon gamma release assays - measure amount of interferon-gamma released from T cells reacting to TB antigen. More sensitive than TST

96
Q

Diagnosing active pulmonary TB

A

CXR - fibronodular/linear opacities in upper zone usually
Sputum smear (three specimens) stained for acid-fast
Sputum culture (takes 1-3 weeks)
Nucleic acid amplification test

97
Q

Management of TB

A

ACTIVE: Rifampicin and isoniazid for 6 months. Pyrazinamide and ethambutol for the first 2 months

LATENT: 3 months of isoniazid (with pyridoxine) and rifampicin

98
Q

Side effects of TB meds

A

Rifampicin - enzyme inducer, altered liver function, orange-red urine
Isoniazid - peripheral neuropathy (give pyridoxine to prevent), hepatitis
Pyrazinamide - hepatotoxicity
Ethambutol - colour blindness, reduced visual acuity, optic neuritis

99
Q

Inhaler technique for metered dose inhalers

A 
Remove cap and shake
Breath out gently
Put mouthpiece in mouth and as you begin to breath in (slowly and deep), press cannister down and continue to inhale steadily and deeply
Hold breath for 10 seconds
Wait 30sec before next dose
100
Q

Causes of clubbing

A

Cardiac - cyanotic congenital heart disease, bacterial endocarditis, atria myxoma
Resp - lung cancer, CF, bronchiectasis, abscess, empyema, TB, asbestosis, mesothelioma, fibrosing alveolitis
Others - Crohns, cirrhosis, PBC, Graves, Whipples, coeliacs

Medicine (15 decks)

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