Respiratory Flashcards

(151 cards)

1
Q

Venous thromboembolism (VTE)

A

an umbrella term used to describe deep vein thrombosis (DVT) with or without pulmonary embolism (PE)

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2
Q

Risk factors for Venous thromboembolism (VTE)

A
↑ age
obesity
FH of VTE
pregnancy 
immobility
hospitalisation 
anaesthesia 
surgery
acute medical illness
prolonged travel
smoking
dehydration
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3
Q

Underlying conditions predisposing to Venous thromboembolism (VTE)

A
malignancy 
thrombophilia
HF
antiphospholipid syndrome 
Behcets
polycythaemia
sickle cell
nephrotic syndrome 
Homocystinuria
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4
Q

Drugs predisposing to Venous thromboembolism (VTE)

A

COCP
HRT (risk higher in oestrogen + progesterone vs only oestrogen)
tamoxifen/raloxifene
antipsychotics e.g. olanzapine

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5
Q

Prophylaxis for Venous thromboembolism (VTE)

A

mechanical:

  • compression stocking
  • intermittent pneumatic compression devices

medication:
-LMWH/UFH/fondaparinux (use UFH if CKD/↓ renal function)

presurgical intervention
-stop COPC/HRT 4 weeks before surgery

postsurgical interventions

  • early mobilisation
  • sufficent hydration
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6
Q

Deep vein thrombosis (DVT)

A

the development of a blood clot in the major vein in the leg/thigh/pelvis/abdomen

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7
Q

Pathological conditions leading to DVT

A

Virchows triad

  • vascular endothelial damage
  • venous stasis
  • hypercoaguability
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8
Q

Presentation of Deep vein thrombosis (DVT)

A

may be asymptomatic or present with PE

symptoms usually unilateral
-limb pain & tenderness, swelling of calf/thigh, pitting oedema, distension of superficial veins, ↑skin temp, erythema, heard/thickened palpable vein, discolouration (red/purple)

NB severe signs of DCT can mimic cellulitis

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9
Q

Wells score for Deep vein thrombosis (DVT)

A

Clinical feature:
-Active cancer (treatment ongoing,
within 6 months, or palliative) 1
-Paralysis, paresis or recent
plaster immobilisation of the lower extremities 1
-Recently bedridden for 3 days or more or
major surgery within 12 weeks requiring
general or regional anaesthesia 1
-Localised tenderness along the distribution
of the deep venous system 1
-Entire leg swollen 1
-Calf swelling at least 3 cm larger than
asymptomatic side 1
-Pitting oedema confined to the symptomatic leg 1
-Collateral superficial veins (non-varicose) 1
-Previously documented DVT 1
-An alternative diagnosis is at least as likely as DVT -2

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10
Q

Actions for wells score for Deep vein thrombosis (DVT)

A

IF wells score ≥2 points (DVT is likely)

  • proximal leg USS within 4h
    • if +ve = treat DVT
    • if -ve do a d-dimer
  • if USS can’t be done within 4h
    • do d-dimer +interim therapeutic anticoagulation until USS (should be within 24h)

NB if D-dimer is +ve but scan is negative then the USS should be repeated after 6-8 days

IF wells score <1 point (DVT unlikely)

  • d-dimer within 4h
    • if -ve = DVT unlikely
    • if +ve = arrange USS within 4h (if not possible then as above)
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11
Q

Investigations for Deep vein thrombosis (DVT)

A

D-dimer (↑)

Doppler USS

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12
Q

Wells score for DVT

A

≥2 points DVT is likely

<1 point DVT is unlikely

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13
Q

Pulmonary embolism (PE)

A

caused by obstruction of the pulmonary arterial tree by an embolus (usually thrombus)

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14
Q

Presentation of Pulmonary embolism (PE)

A

sudden onset, may have precipitating event that sets them off

dyspnoea, pleuritic*/retrosternal chest pain, haemoptysis, tachycardia, tachypnoea, low grade fever
dizziness, syncope, ↑JVP
obstructive shock (if massive PE)
signs of DVT (unilateral, swollen, erythematous leg/calf)

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15
Q

Wells score for Pulmonary embolism (PE)

A

Similar to DVT score

≤4 points = PE unlikely
>4 points = PE likley

NB you can also use the PE rule out criteria (PERC)
a negative PERC reduces likelihood of PE to <2%

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16
Q

Actions based on Wells score for Pulmonary embolism (PE)

A

Wells score >4 (PE likely)

  • immediate CTPA
    • if delay in CTPA = give interim anticoagulation
    • if CTPA -ve consider USS doppler of leg if DVT symptoms

Wells score ≤4 (PE unlikely)

  • arrange D-dimer
    • if +ve = immediate CTPA / if delayed give interim anticoagulation
    • if -ve = PE unlikely so consider alternative diagnosis
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17
Q

Investigations for Pulmonary embolism (PE)

A

CTPA
-preferred for definitive diagnosis of PE

ECG

  • sinus tachycardia
  • S1Q3T3 (large S wave in lead I, large Q wave & inverted T wave in lead III)

D-Dimer (↑)
-very non specific but very sensitive

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18
Q

Investigations for Pulmonary embolism (PE)

A

CTPA
-preferred for definitive diagnosis of PE

ECG

  • sinus tachycardia
  • S1Q3T3 (large S wave in lead I, large Q wave & inverted T wave in lead III)

D-Dimer (↑)
-very non specific but very sensitive

CXR

  • usually normal
  • recommended for all pts prior to CTPA*

V/Q scan
-preferred over CTPA in pts with renal impairment

Leg USS, ABG

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19
Q

Management of Pulmonary embolism (PE)

A

If haemodynamically unstable = thrombolysis
If in cardiac arrest with suspected PE give thrombolysis and continue CPR for 60-90 min

1st line:

  • DOACs e.g. apixaban/riveroxaban
  • in renal impairment use UFH/LMWH
  • in antiphospholipid syndrome use LMWH

Duration:

  • 3 months minimum if provoked
  • 6 months minimum if unprovoked
  • 3-6 months if caused by cancer

NB for unprovoked PE consider investigating the patient for underlying cancer or follow up closely

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20
Q

Asthma

A

a chronic inflammatory disease of the respiratory system characterised by bronchial hyperresponsiveness,

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21
Q

Asthma

A

a chronic inflammatory disease of the respiratory system characterised by bronchial hyperresponsiveness, episodic acute exacerbation and reversible airway obstruction (i.e. intermittent bronchospasm)

affects ~10% of children & 5-10% of adults

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22
Q

Risk factors for asthma

A
personal history of atopy (hay fever/eczema)
Family history of asthma/atopy
inner city environment 
socio-economic deprivation
obesity
prematurity
maternal smoking
low birth weight
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23
Q

Presentation of asthma

A

wheeze, chest tightness, SOB, cough

  • worse at night / early morning cough
  • presents on exercise, exposure to cold, other triggers or irritants

expiratory wheeze on auscultation

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24
Q

Investigations of asthma

A

FEV1/FVC ratio

  • <80% of predicted
  • FEV1 ↓ & FVC normal
  • obstructive picture

PEFR ± reversibility testing with salbutamol
-PEFR ↓ but reversible with SABA

fractional exhaled nitrous oxide (FeNO) (↑)

CXR
-for smokers & older people

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25
Management of asthma
All pts should have a personalised asthma action plan All pts should have a SABA e.g. salbutamol for symptomatic relief between each step ensure adequate inhaler technique and compliance consider stepping down treatment every 3 months or so if asthma is well controlled 1: SABA + low dose ICS 2: SABA + low dose ICS + trial of LTRA 3: SABA + low dose ICS + LABA ± LTRA 4: SABA + MART (ICS + LABA) ± LTRA 5: SABA + medium dose ICS in MART ± LTRA 6: expert help
26
Step 1 for asthma management
SABA + low dose ICS consider SABA only therapy if infrequent short lived wheeze & normal lung function after SABA
27
Step 3 for asthma management
SABA + low dose ICS + long acting beta agonist (LABA) ± leukotriene receptor antagonist (LTRA) LTRA only used if pt shows response to it examples of LABA include salmetarol
28
Step 4 for asthma management
SABA Low dose ICS + LABA in a MART regime ± leukotriene receptor antagonist (LTRA) MART = maintenance & deliver therapy i.e. 1 inhaler as preventer and reliever
29
Step 5 for asthma management
SABA + moderate dose ICS in MART ± leukotriene receptor antagonist (LTRA) can also consider separate ICS & LABA inhalers
30
Step 6 for asthma management
Options include - seek expert help - try high dose ICS as a separate inhaler - trial of long acting muscarinic receptor antagonist (LAMA) - trial of theophylline
31
Acute asthma exacerbation
an acute/subacute episode of progressive worsening of symptoms of asthma generally a clinical diagnosis
32
Risk factors for severe exacerbation of asthma
``` previous near fatal asthma previous admission for asthma need ≥3 medication for control non compliance/denial of illness obesity smoking/second hand smoke ≥1 severe exacerbations in last 12 months ```
33
Presentation of Acute exacerbation of asthma
``` dyspnoea/wheeze/cough -worsening -no response to salbutamol tachycardia, tachypnoea accessory muscle use hypoxia, altered mental status silent chest paradoxical breathing exhaustion ```
34
Moderate acute asthma exacerbation
``` PEFR 50-75% sats ≥92% normal speech RR <25 HR <110 ```
35
severe acute asthma exacerbation
``` PEFR 33-50% sats ≥92% can't complete sentences RR ≥25 HR ≥110 ```
36
life threatening acute asthma exacerbation
``` PEFR <33% sats <92% silent chest/cyanosis/poor respiratory effort bradycardia/dysrhythmia/hypotension altered consciousness ```
37
near fatal acute asthma exacerbation
indicated by a ↑ PCO2 / normal PCO2 or need for mechanical ventilation indicates exhaustion
38
Severity of acute asthma exacerbation
may be moderate, severe, life threatening or near fatal depends on PEFR, RR, sats, HR, ability to complete sentences and PCO2
39
Management of acute asthma exacerbation
ABCDE assessment, ABG O2 via non rebreather mask (target sats 94-98%) SABA e.g. salbutamol - via spacer or O2 driven nebuliser - 5mg - 4 puffs + 2 puffs every 2 min for up to 10 puffs - nebs can be back to back, but monitor K+ Ipratropium bromide - 500 micrograms via nebuliser - can be given with salbutamol but not back to back Steroids - 100mg hydrocortisone IV - 40-50mg prednisolone PO for minimum 5 days IV Magnesium sulphate IV amiophylline ITU support for airway management -make sure you call for help early
40
Discharge criteria post acute asthma exacerbation
stabile on discharge medications for 12-24h no use of nebulisers for >24h inhaler technique checked & recorded PEFR >75% of best/predicted if life threatening then GP follow up organised within 2 days of discharge
41
Chronic obstructive pulmonary disease (COPD)
a lung disease characterised by airway obstruction that is not fully reversible leading to persistent respiratory symptoms the airflow limitation is usually progressive & is associated with an abnormal inflammatory response in the lungs usually diagnosed in people in the 50s
42
Aetiology of Chronic obstructive pulmonary disease (COPD)
smoking*** (~90% of cases) alpha-1 anitrypsin deficiency air pollution fine dust
43
Presentation of Chronic obstructive pulmonary disease (COPD)
``` chronic productive cough dyspnoea (especially exertional) wheeze barrel chest nail clubbing peripheral oedema hyperresonant lung ```
44
Investigations of Chronic obstructive pulmonary disease (COPD)
FEV1/FVC - <70% - no reversibility CXR - hyperinflation & bullae - flat hemidiaphragm - also to exclude lung cancer FEV1 (↓) FBC (
45
Investigations of Chronic obstructive pulmonary disease (COPD)
FEV1/FVC - <70% - no reversibility CXR - hyperinflation & bullae - flat hemidiaphragm - also to exclude lung cancer FEV1 (↓) FBC (↑ haematocrit, anaemia)
46
Severity of Chronic obstructive pulmonary disease (COPD)
Mild (Stage I) - FEV1/FVC <70% - FEV1 >80% - symptoms must be present for diagnosis Moderate (Stage II) - FEV1/FVC <70% - FEV1 50-79% severe (Stage III) - FEV1/FVC <70% - FEV1 30-49% very severe (Stage IV) - FEV1/FVC <70% - FEV1 <30%
47
Management of Chronic obstructive pulmonary disease (COPD)
Smoking cessation*** pulmonary rehabilitation Step 1 - asthmatic features present = LABA + ICS + SABA - no asthmatic features = LABA (e.g. salmeterol) + LAMA (e.g. tiotropium) + SABA Step 2 - SABA (PRN) - LABA + LAMA + ICS for everyone Step 3: -trial of theophylline Oral prophylactic Abx - azithromycin (1st line) - do ECG to exclude QT prolongation & LFTs - give to pts who don't smoke, have optimised treatment but have frequent exacerbations Long term O2 therpay -if pt fits criteria
48
Features suggesting steroid responsiveness in Chronic obstructive pulmonary disease (COPD)
I.e. asthmatic features - previous history of asthma / atopy - ↑ eosinophils - substantial variation in FEV1 (≥400ml) - substantial diurnal variation in PEFR (≥20%)
49
Most important intervention in Chronic obstructive pulmonary disease (COPD) management
smoking cessation vital in any pt that still smokes
50
Acute exacerbation of Chronic obstructive pulmonary disease (COPD)
defined as an acute worsening of respiratory symptoms that results in addition therapy needs one of the most common reasons for pts to present to the hospital
51
Aetiology of Acute exacerbation of Chronic obstructive pulmonary disease (COPD)
Most commonly viral ``` haemophilus influenzae (most common) strep pneumonia (most common bacterial cause) Others: mortadella catarrhalis, staph aureus ```
52
Presentation of Acute exacerbation of Chronic obstructive pulmonary disease (COPD)
``` ↑ dyspnoea ↑ cough ↑ wheeze ↑ volume/purulence of sputum fevers, chills, sore throat ↓ exercise tolerance respiratory distress (dyspnoea, tachypnoea, confusion, cyanosis, peripheral oedema) respiratory failure ```
53
Investigations for Acute exacerbation of Chronic obstructive pulmonary disease (COPD)
ABG -↓PaO2, ↑PaCO2, pH <7.35 CXR - hyperinflation, flattened diaphragm - possible consolidation if infection sats (↓) sputum/blood cultures ECG, FBC, U&Es
54
Management of Acute exacerbation of Chronic obstructive pulmonary disease (COPD)
↑ dose & frequency of SABA via inhalers with spacers oral steroids: - 30mg prednisolone for 7-14 days - consider osteoporosis prophylaxis if requiring frequent courses Abx (PO) - if sputum purulent / clinical signs of pneumonia - amoxicillin / clarithromycin / doxycycline (all 1st line on BNF) O2 if below target sats consider NIV -for persistent hypercapnia respiratory failure consider IV theophylline -if poor response to bronchodilators
55
Small cell lung cancer (SCLC)
also known as oat cell carcinoma, is a malignant epithelial tumour arising from the cells lining the lower respiratory tract ~15% of all lung cancer rapidly growing & highly malignant, spreading early (almost always inoperable at presentation) seen generally in older adult smokers (both active & passive smoking is a risk factor)
56
Presentation of Small cell lung cancer (SCLC)
``` dyspnoea, cough, haemoptysis, chest pain weight loss, fatigue dysphagia, hoarseness, wheezing/stridor recurrent pneumonias superior vena cava syndrome ```
57
Investigations for Small cell lung cancer (SCLC)
CXR - central mass - hilar lymphadenopathy - pleural effusion CT chest/abdo/pelvis -investigation of choice bronchoscopy ± biopsy PET scan
58
Management of Small cell lung cancer (SCLC)
consider pts in early stages for surgery generally chemo + radiotherapy = management of choice if extensive disease = palliative chemo
59
Complications of Small cell lung cancer (SCLC)
Lambert-Eaton syndrome: - myasthenia like syndrome - antibody against presynaptic voltage-gated calcium channel SIADH -leading to hyponatraemia ACTH secretion -leads to bushings syndrome & adrenal hyperplasia Superior vena cava syndrome -dyspnoea, face & arm swelling, periorbital & conjunctival oedema, pulseless JVP distension
60
Referral criteria for suspected lung cancer
referral to specialist on 2 week wait - if CXR findings are suggestive of cancer - if ≥40 y/o + unexplained haemoptysis Urgent CXR (within 2 weeks) - if age ≥40yrs + ≥2 of the following unexplained symptoms - if age ≥40yrs + ≥1 symptom if they ever smoked - cough - fatigue - SOB - chest pain - weight loss - loss of appetite
61
Non-Small cell lung cancer (NSCLC)
a group of malignant epithelia tumours representing ~85% of all lung cancers most common risk factor is active & passive smoking
62
Types of Non-Small cell lung cancer (NSCLC)
Squamous (42& of NSCLC) - often central presenting as obstructive lesion of bronchus leading to infection - local spread common but metastasis occur relatively late adenocarcinoma (39% of NSCLC) - typically peripheral - most common type of cancer in non-smokers large cell lung carcinoma (8% of NSCLC) - anaplastic, poorly differentiated tumours that metastasis early - poor prognosis carcinoid tumours (7% of NSCLC) ``` Bronchoalveolar tumour (4% of NSCLC) -associated with ++ sputum ```
63
Presentation of Non-Small cell lung cancer (NSCLC)
``` persistent cough haemoptysis dyspnoea chest pain weight loss fatigue anorexia hoarseness recurrent pneumonias superior vena cava syndrome ```
64
Investigations for Non-Small cell lung cancer (NSCLC)
CT chest/abdo/pelvis -investigation of choice CXR - usually preliminary - may show mass bronchoscopy + biopsy pet scanning
65
Management of Non-Small cell lung cancer (NSCLC)
surgery (indicated in ~20% of pts) - lobar resection - lobectomy curative or palliative radio therpay generally poor responsiveness to chemo
66
Respiratory failure
the acute or chronic inability of the reparatory system to maintain adequate gas exchange leading to hypoxia ± hypercapnia
67
Types of respiratory failure
Type I respiratory failure: - hypoxic respiratory failure - PaO2 <8kPa - PaCO2 normal Type II respiratory failure: - hypercapnic respiratory failure - PaO2 <8kPa - PaCO2 >6kPa
68
Aetiology of type I respiratory failure
``` COPD pneumonia pulmonary oedema pulmonary fibrosis asthma PE cyanotic congenital heart disease ARDS bronchiectasis obesity kyphoscoliosis ```
69
Aetiology of type II respiratory failure
``` COPD severe asthma (when pt is exhausted) drug overdose/poisoning muscular disorders severe ARDS ```
70
Presentation of respiratory failure
``` tachypnoea dyspnoea cyanosis tachycardia confusion ↓GCS arrhythmias hypercapnia (hypoventilation, headache, coma, asterix) ``` NB clinical features of the underlying cause will be present
71
Investigations for respiratory failure
ABG*** CXR, FBC, TFTs, U&Es, LFTs, CK, troponin, ECG, CT-CTPA
72
Management of respiratory failure
resuscitation & ABCDE assessment treat underlying cause Hypoxia - O2 - CPAP (↑ O2) - mechanical ventilation Hypercapnia - NIV/BIPAP (↑O2, ↓CO2) - mechnaical ventilation
73
BIPAP (NIV) vs CPAP
CPAP helps ↑ O2 but doesn't affect CO2 NIV/BIPAP helps ↑O2 & ↓CO2
74
Tuberculosis (TB)
an infectious disease caused by mycobacterium tuberculosis typically affecting the lungs NB notifiable disease in the UK spreads via inhalation of infected droplets
75
Types of Tuberculosis (TB)
Primary TB latent TB/inactivated TB secondary TB -e.g. from reactivation of latent disease miliary TB -disseminated TB usually seen in immunocompromised pts
76
Risk factors for Tuberculosis (TB)
``` homelessness institutionalisation e.g. prisons alcohol/drug misuse HIV +ve immunocompromised crowded lying ethnic minority background travel to/heritage from high prevalence areas ```
77
presentation of Tuberculosis (TB)
``` cough fever haemoptysis night sweats malaise chest pain dyspnoea erythema nodosum ```
78
Investigations for Tuberculosis (TB)
CXR - upper lobe opacities ± consolidation - bilateral hilar lymphadenopathy Sputum smear - 3 samples needed - uses Ziehl-Nielsen staining Sputum culture - gold standard - helps asses drug sensitivity - take a long time to get back NAAT -can help with rapid diagnosis mantoux test - to screen for latent TB - alternative is inferno-gamma test (if mantoux test is inconclusive)
79
Management of Tuberculosis (TB)
Active TB: - 2 months of rifampicin + isoniazid + pyrazinamide + ethambutol - then 4 months of rifampicin + isoniazid Latent TB: - 3 months of rifampicin + isoniazid - alternatively 6 months of isoniazid NB isoniazid is always given with pyridoxine to prevent peripheral neuropathy
80
Side effects of Tuberculosis (TB) drugs
Rifampicin: - enzyme inducer - orange secretions - hepatitis Isoniazid: - enzyme inhibitor - agranulocytosis - hepatitis Pyrazinamide: - hyperuraemia (gout) - arthralgia - hepatitis Ethambutol: - optic neuritis - monitor visual acuity
81
Pneumonia
inflammation of the lungs with consolidation & interstitial infiltration most commonly caused by bacteria
82
Types of pneumonia
Community acquired pneumonia (CAP): -pneumonia acquired outside hospital/healthcare facilities Hospital acquired pneumonia (HAP): -pneumonia acquired >48h after admission to hospital Atypical pneumonia -caused buy atypical organisms e.g. legionella
83
Causes of pneumonia
CAP: - strep pneumoniae (most common) - H. Influenzae, staph aureus, mycoplasma pneumoniae HAP: - <5 days = strep pneumoniae - >5 days = H.influenzae ± staph aureus (also pseudomonas or MRSA) In alcoholics the usually cause is klebsiella pneumoniae NB pneumonia post H.influenzae is often caused by staph aureus
84
Risk factors for pneumonia
``` infants/young children elderly smoking alcohol misuse asthma COPD malignancy immunosuppression IVDU hospitalisation ```
85
Presentation of pneumonia
``` cough with purulent sputum fever malaise dyspnoea chest pain (pleuritic) tachycardia hypoxia bronchial breathing & crackles on auscultation dullness on percussion ```
86
Investigations for pneumonia
CXR -new consolidation FBC (↑ WCC) CRP (↑) U&Es Blood cultures
87
Scoring system for pneumonia
``` CURB65 score -C = Confusion -U = Urea >7.0 mmol/L -R = RR ≥30 -B = BP ≤90/60 =65 = age ≥65yrs ``` Score 0-1 = home based care Score ≥2 = consider hospital care Score ≥3 = intensive care assessment NB in primary care the CRB65 score can be used, i.e. leaving out the urea
88
Management of Community acquired pneumonia (CAP)
low severity: - 5 days of amoxicillin - 5 days of clarithromycin/erythromycin if penicillin allergy) moderate severity: -7 days of amoxicillin + macrolide e.g. erythromycin high severity: -co-amoxiclav, ceftriaxone, tazocin NB clarithromycin is contraindicated in pregnancy so if pregnant & allergic to penicillin then use erythromycin, otherwise clarithromycin tends to be favoured
89
Management of Hospital acquired pneumonia (HAP)
Consider broad spectrum IV Abx then tailor treatment when sensitivities available generally based on local guidelines & sensitivities
90
Aspiration pneumonia
results from the inhalation of oropharyngeal secretions or stomach contents into the lower airways leading to chemical pneumonitis, lung injury and resultant bacterial infection most commonly seen in hospitals & care homes
91
Risk factors for Aspiration pneumonia
``` impaired consciousness poor mobility NBM advanced age swallowing disorders (e.g. oesophageal strictures, dysphagia) neurological disorders (e.g. strokes, MS, Parkinsons) poly pharmacy poor dental hygiene ```
92
Aetiology of Aspiration pneumonia
Similar to normal pneumonia strep pneumoniae, staph aureus, H. influenzae, pseudomonas aeruginosa IN alcoholics its frequently Klebsiella pneumoniae
93
Presentation of Aspiration pneumonia
``` fever, headache, N&V, anorexia, myalgia cough dyspnoea pleuritic chest pain purulent sputum tachycardia ↓ breath sounds on auscultation crackles on auscultation dullness on percussion ```
94
Investigations for Aspiration pneumonia
CXR - new consolidation - or atelectasis FBC (↑WCC, neutrophilia) sputum & blood cultures
95
Management of Aspiration pneumonia
- tracheal suction if aspiration is noticed early - mechanical removal of object via bronchoscopy (e.g. in children) - Abx treatment as per pneumonia - NB if severe then IV/PO co-amoxiclav NB remember to be mindful of pts swallow with PO meds even Abx
96
Sarcoidosis
a chronic granulomatous disorder of unknown aetiology characterised by non-caseating granulomas commonly affecting the lungs, skin and eyes, its a diagnosis of exclusion NB lungs are affected in 90% of pts
97
Epidemiology of sarcoidosis
most commonly seen in young adults (20-40y/o) | more common in people of african or northern european/scandinavian origin
98
Presentation of sarcoidosis
- erythema nodosum - swinging fever - polyarthralgia (common in acute attacks) - dyspnoea, non productive cough - weight loss, night sweats, fatigue - lupus pernio (violaceous soft infiltration of skin of nose/cheeks) - anterior & posterior uveitis - lymphadenopathy NB acute attacks are more common in white populations remitting after 2yrs
99
Investigations for Sarcoidosis
CXR - bi-hilar lymphadenopathy - bilateral infiltrations FBC - anaemia - leukopenia mantoux test - negative - to exclude TB spirometry: -restrictive pattern Ca2+ (↑), ACE levels (↑) U&Es, phosphate, LFTs
100
Pleural effusion
a collection of fluid between the pleural & visceral pleural surfaces in the thorax i.e. the pleural cavity
101
Aetiology of pleural effusion
Transudates (<30g/L of protein) - HF (most common cause of transudates) - cirrhosis, hypoalbuminaemia, hypothyroidism, nephrotic syndrome, meigs syndrome (bening ovarian tumour causing ascites + pleural effusion) Exudates (>30g/L of protein) - pneumonia (most common) - malignancy (often cause large unilateral effusion) - especially breast & lung cancer - RA, SLE, PE, TB, pancreatitis, Dresslers syndorme Haemothorax - pleural effusion due to blood - usually secondary to trauma
102
Presentation of Pleural effusion
small effusions <300ml are usually asymptomatic ``` dyspnoea, pleurite chest pain, dry non productive cough dullness on percussion ↓ breath sounds ↓ chest expansion ↓ tactiel vocal remits ``` signs & symptoms of underlying cause will be present
103
Investigations for Pleural effusion
CXR - blunting of costophrenic angles - opacification of lung fields with fluid level Pleural fluid analysis - from USS guided aspiration - pH, protein, LDH, cytology, microbiology USS + aspiration CT/MRI (helps find underlying cause) NB use lights criteria if protein levels between 25-35g/L i.e. borderline of transudate & exudate
104
Management of Pleural effusion
treat underlying cause therapeutic thoracentesis (avoid taking >1.5L as it can cause fluid shift leading to pulmonary oedema) pleurodesis chest drain / long term indwelling pleural drainage
105
Criteria for pleural effusion
Lights criteria | -used if protein level 25-35g/L in pleural fluid to differentiate transudate & exudate
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Criteria for pleural effusion
Lights criteria: used if protein level 25-35g/L in pleural fluid to differentiate transudate & exudate Exudate is likely if one of the following - pleural fluid protein divided by serum protein >0.5 - pleural fluid LDH divided by serum LDH >0.6 - pleural fluid LDH >2/3 of upper limit of serum LDH
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Pneumothorax
a collection of air in the pleural cavity leading to partial or complete collapse of the lung
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Types of Pneumothorax
Primary spontaneous Pneumothorax (PSP) -usually seen in health young people Secondary spontaneous Pneumothorax (SSP) - in pts with pre-exisitng lung disease - e.g. rupture of bullae in COPD Traumatic pneumothorax -traumatic cause Tension pneumothorax - life threatening emergency - usually post trauma
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Presentation of Pneumothorax
``` dyspnoea pleuritic chest pain with sudden onset ipsilateral reduced breath sounts ipsilateral hyper resonance on percussion tachypnoea hypoxia tachycardia ```
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Investigations for Pneumothorax
CXR - visible rim on air between lung margin & chest wall - absence of lung markings consider CT or USS -usually for complex cases
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Management of Primary spontaneous Pneumothorax (PSP)
<2cm rim of air + pt not SOB - consider discharge - repeat CXR to check resolution >2cm or symptomatic pt -attempt simple aspiration If aspiration failed i.e. >2cm rim of air or still SOB -chest drain
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Management of Secondary spontaneous Pneumothorax (SSP)
pt >50y/o / rim >2.0cm / pt SOB -chest drain Rim of air = 1-2cm - trial of aspiration - if it fails = chest drain Rim of air <1cm -admit for 24h of observation ± O2
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Tension Pneumothorax
life threatening emergency usually seen post trauma presents with respiratory distress (hypoxia, cyanosis, diaphoresis, dyspnoea, tachypnoea), haemodynamic instability (hypotension, tachycardia), trachea is deviated away from affected side this is a clinical diagnosis and should be treated immediately (do not wait for imaging) treatment includes emergency needle decompression & chest drain insertion
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Obstructive sleep apnoea (OSA)
a clinical condition in which there is intermittent & repeated upper airway obstruction during sleep leading to poor sleep quality & frequent arousals - apnoeas (≥10sec pauses in breathing) - hypopnoea (≥10sec periods with breathing ↓50%) pone of the most common causes of secondary hypertension
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Risk factors for Obstructive sleep apnoea (OSA)
``` obesity*** male gender smoking excess alcohol consumption macroglossia acromegaly hypothyroidism ``` adenotonsilar hyperplasia especially in children
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Presentation of Obstructive sleep apnoea (OSA)
sleep partner complains of excessive snoring or describes apnoeas ``` daytime somnolence snoring waking headaches unrefreshing sleep sleep fragmentation irritability ```
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Investigations for Obstructive sleep apnoea (OSA)
Epworth sleepiness scale (asses for daytime sleepiness) - score >10 suggests need for investigation - score >18 / Road traffic accident or near miss = urgent referral Polysomnography -≥5 respiratory events e.g. apnoea/hypopnoea/arosals per hour associated with OSA symptoms
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Management of Obstructive sleep apnoea (OSA)
weight loss smoking cessation avoid alcohol/sedative CPAP (gold standard) - 1st line in moderate/severe OSA - acts as pneumatic splint maintaining airway patency - min 4h per night BiPAP -considered if hypoventilation or COPD Mandibular advancement splints -alternative to CPAP if mild/moderate OSA or intolerant to CPAP
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Driving and Obstructive sleep apnoea (OSA)
must inform DVLA & stop driving until adequate control is achieve i.e. ↓daytime sleepiness
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Pulmonary hypertension
a rise in mean pulmonary arterial pressure (mPAP) which can be due to a variety of use defined as ↑ mean PAP ≥25 mmHg at rest
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Idiopathic Pulmonary hypertension (PAH)
a rare disorder defined by ↑ pulmonary arterial pressure & ↑ pulmonary vascular resistance with normal pulmonary artery wedge pressure in the absence of a known cause often severe and rapidly progressing treated with high dose calcium channel blockers
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Aetiology of Pulmonary hypertension
Group 1: -idiopathic Group 2: -secondary to left heart disease, Valvular heart disease or restrictive cardiomyopathy Group 3; -secondary to chronic lung disease or environmental hypoxaemia Group 4: -due to chronic thrombotic disorders, embolic disease or both Group 5: -metabolic disorders, haematological disease & systemic illness NB generally the most common causes are severe respiratory or cardiac disease
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Presentation of Pulmonary hypertension
``` progressive dyspnoea weakness fatigue exertional dizziness/syncope loud S2 (often split) ↑ JVP symptoms of right HF ```
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Investigations for Pulmonary hypertension
Right heart catheterisation -↑ PAP ≥25 mmHg at rest CXR -prominent R heart border ECG, Echo, CT/MRI thorax
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Management of Pulmonary hypertension
treat underlying cause pulmonary vasodilators if acute deterioratio if idiopathic PH (PAH) give high dose calcium channel blockers
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Cor Pulmonale (Pulmonary heart disease)
altered structure (hypertrophy/dilation) or impaired function of the right ventricle due to pulmonary hypertension diagnosed via echo prominent signs of right sided HF will be present
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Cystic fibrosis (CF)
autosomal recessive disorder causing ↑ viscosity of secretion due to defect in the cystic fibrosis transmembrane conductance regulatory gene (CFTR) which codes cAMP-regulated chloride channels 80% of cases in UK are due to delta F508 (DF508) most common inherited condition in white populations
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Presentation of Cystic fibrosis (CF)
- meconium ileus in neonates (very indicative fo CF) - failure to thrive - recurrent chest infections (causes include staph aureus, pseudomonas, Burkholida cepacia, aspergillus) - malabsorption, steatorrhoea, pancreatitis - CF related diabetes - nasal polyps - clubbing - cholestasis, cholecystolithiasis - subfertility/infertility
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Investigations for Cystic fibrosis (CF)
Newborn screening - +ve on newborn blood spot test - day 5-7 post birth Sweat test - +ve - >60mmol/L of sweat chloride genetic testing -for CFTR gene lung function tests sinus X-ray/CT
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Genetics of Cystic Fibrosis (CF)
autosomal recessive disorder of cystic fibrosis transmembrane conductance regulatory gene (CFTR) 80% of cases in UK are due to delta F508 (DF508) gene
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Management of Cystic fibrosis (CF)
regular chest physio & postural drainage - twice a day minimum - should be taught from young age high calorie diet -with high fat intake minimise contact with other CF pts -to prevent spread of burkholdia cepacia Vitamin supplementation & pancreatic enzyme supplementation if DF508 +ve -trial lumacaftor or Ivacaftor
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Bronchiectasis
an abnormal, irreversible dilation in the bronchial tree caused by cycles of bronchial inflammation leading to mucous plugging & progressive airway destruction ~70% of cases are in older women
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Aetiology of Bronchiectasis
post-infective (most common cause) -TB, measles, pertussis, pneumonia cystic fibrosis, primary ciliary dyskinesia/Kartengers syndrome, immunodeficiency & HIV, bronchial obstruction e.g. malignancy, allergic brochopulmonary aspergillosis, COPD
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Presentation of Bronchiectasis
chronic productive cough with copious mucopurulent sputum (may be blood stained) dyspnoea chest pain clubbing On auscultation - coarse early inspiratory crackles - rhonchi (low pitch snore like noises) - wheeze
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Investigations for Bronchiectasis
CXR - baseline CXR for all pts - ~90% of pts have abnormal CXR - tram lines, fluid levels, ring shadows high resolution CT chest (HRCT) - gold standard - bronchial wall dilation - bronchial wall thickening Sputum MC&S -H.influenzae is the most commonly isolated routine bloods, serum immunoglobulins, serum electrophoresis, antibody screening, ciliary function tests, lung function tests
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Management of Bronchiectasis
Influenza & pneumococcal vaccines chest physio & postural drainage inspiratory muscle training Abx for acute exacerbation -1st line : amoxicillin/clarithromycin/doxycyline Long term Abx -if ≥3 expectations per year requiring Abx or exacerbations causing significant morbidity Bronchodilators -after assessing reversibility of airflow obstructions surgery -if localised disease
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Asbestosis
a type of pneumoconiosis
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Asbestosis
a type of pneumoconiosis caused by inhalation of asbestos fibres occurring primarily as a result of occupational exposure severity is related to length of exposure, with a 20-30 year latent period presents with gradual onset dyspnoea/SOB, ↓ exercise tolerance ± wheezing/productive cough, with fine bilateral inspiratory crackles, clubbing, cor pulmonale Investigated with CXR (lower zone linear interstitial fibrosis & pleural thickening), pulmonary function tests (restrictive patterns), HRCT no specific management available
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Causes of upper zone lung fibrosis
Acronym for causes of upper zone fibrosis: ``` CHARTS C - Coal worker's pneumoconiosis H - Histiocytosis/ hypersensitivity pneumonitis A - Ankylosing spondylitis R - Radiation T - Tuberculosis S - Silicosis/sarcoidosis ```
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Mesothelioma
an aggressive neoplasm arising from mesothelial cells lining the pleural cavity associated with asbestos exposure, more commonly seen in men aged >75yrs often locally advanced but rarely metastasises presents with dyspnoea, chest wall pain, weight loss, clubbing, painless pleural effusion investigated with CXR (unilateral pleural effusion, irregular pleural thickening), CT, thoracoscopy management includes radiotherapy, chemo and surgery prognosis is poor, with median survival <12 months
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Occupational asthma
pts with asthma may preset with concerns that chemical at their work are worsening their symptoms OR on history taking symptoms appear better at weekends / on holidays /away from work
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Occupational asthma
pts with asthma may preset with concerns that chemical at their work are worsening their symptoms OR on history taking symptoms appear better at weekends / on holidays /away from work most commonly associated with isocyanates investigated with serial PEFR at work & away from work treated by respiratory specialist
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Silicosis
common occupational lung disease caused by inhalation of crystalline silica dusts commonly seen in mining, slate works, foundries and potteries presents with chronic cough, sputum, exertional dyspnoea, fatigue, weight loss investigated with CXR (egg-shell calcification of hilar lymph nodes, bilateral diffuse ground glass opacities), spirometry (restrictive pattern) no definitive treatment NB Caplan syndrome - pneumoconiosis + RA
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Coal workers pneumoconiosis (Black lung disease)
occupational lung disease caused by long term exposure to coal dust particles, severity linked to extent of exposure may present with simple pneumoconiosis (often asymptomatic, often incidentally found) may progress to progressive massive fibrosis (PMF) which presents as SOB on exertion & cough + black sputum Investigated with CXR (upper zone fibrosis), spirometry (mixed obstructive / restrictive picture) managed with irritant avoidance & supportive care
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Interstitial lung disease (ILD)
a heterogenous group of disorders characterised by inflammation & progressive scarring (fibrosis) of the lung
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Aetiology of Interstitial lung disease (ILD)
Idiopathic pulmonary fibrosis (IPF) ``` hypersensitivity pneumonitis (extrinsic allergic alveolitis) -Pigeon breeders lung, farmers lung, bird fanciers lung ``` pneumoconiosis -asbestosis, coal workers lung, silicosis radiation pneumonitis Medication - amiodarone, bleomycin, methotrexate - nitrofurantoin, sulfalazine, cabergoline ``` cocaine sarcoidosis vasculitis sarcoidosis TB ```
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Medications causing Interstitial lung disease (ILD)
- amiodarone - bleomycin - methotrexate - nitrofurantoin - sulfalazine - cabergoline - bromocriptine
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Presentation of Interstitial lung disease (ILD)
``` progressive dyspnoea -exertional dyspnoea → dyspnoea at rest persistent non productive cough fatigue clubbing bibasal inspiratory crackles/rales cyanosis ```
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Investigations for Interstitial lung disease (ILD)
CXR - reticular opacities - ground glass opacities CT/HRCT - honey combing - traction bronchiectasis Spirometry - Restrictive pattern i.e. ↓FEV1 & ↓FVC - normal/↑ FEV1/FVC bronchoalveolar lavage & biopsy
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Management of Interstitial lung disease (ILD)
smoking cessation supportive therapy - O2 - pulmonary rehab - vaccination e.g. influenza/pneumococcal lung transplant -end stage ILD For Idiopathic pulmonary fibrosis (IPF) -antifibrotic agents e.g. pirfenidone
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Idiopathic pulmonary fibrosis (IPF)
no underlying cause found usually seen in men aged 50-75yrs consider treating with antifibrotic agents e.g. pirfenidone