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Year 3 > Respiratory > Flashcards

Respiratory Flashcards

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
Q

Management of asthma

A

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

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26
Q

Step 1 for asthma management

A

SABA + low dose ICS

consider SABA only therapy if infrequent short lived wheeze & normal lung function after SABA

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27
Q

Step 3 for asthma management

A

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

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28
Q

Step 4 for asthma management

A

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

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29
Q

Step 5 for asthma management

A

SABA + moderate dose ICS in MART ± leukotriene receptor antagonist (LTRA)

can also consider separate ICS & LABA inhalers

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30
Q

Step 6 for asthma management

A

Options include

  • seek expert help
  • try high dose ICS as a separate inhaler
  • trial of long acting muscarinic receptor antagonist (LAMA)
  • trial of theophylline
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31
Q

Acute asthma exacerbation

A

an acute/subacute episode of progressive worsening of symptoms of asthma

generally a clinical diagnosis

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32
Q

Risk factors for severe exacerbation of asthma

A 
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
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33
Q

Presentation of Acute exacerbation of asthma

A 
dyspnoea/wheeze/cough 
-worsening 
-no response to salbutamol 
tachycardia, tachypnoea
accessory muscle use
hypoxia, altered mental status 
silent chest
paradoxical breathing 
exhaustion
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34
Q

Moderate acute asthma exacerbation

A 
PEFR 50-75%
sats ≥92%
normal speech
RR <25
HR <110
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35
Q

severe acute asthma exacerbation

A 
PEFR 33-50%
sats ≥92%
can't complete sentences
RR ≥25
HR ≥110
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36
Q

life threatening acute asthma exacerbation

A 
PEFR <33%
sats <92%
silent chest/cyanosis/poor respiratory effort
bradycardia/dysrhythmia/hypotension
altered consciousness
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37
Q

near fatal acute asthma exacerbation

A

indicated by a ↑ PCO2 / normal PCO2 or need for mechanical ventilation

indicates exhaustion

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38
Q

Severity of acute asthma exacerbation

A

may be moderate, severe, life threatening or near fatal

depends on PEFR, RR, sats, HR, ability to complete sentences and PCO2

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39
Q

Management of acute asthma exacerbation

A

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

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40
Q

Discharge criteria post acute asthma exacerbation

A

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

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41
Q

Chronic obstructive pulmonary disease (COPD)

A

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

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42
Q

Aetiology of Chronic obstructive pulmonary disease (COPD)

A

smoking*** (~90% of cases)

alpha-1 anitrypsin deficiency
air pollution
fine dust

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43
Q

Presentation of Chronic obstructive pulmonary disease (COPD)

A 
chronic productive cough
dyspnoea (especially exertional)
wheeze
barrel chest
nail clubbing 
peripheral oedema 
hyperresonant lung
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44
Q

Investigations of Chronic obstructive pulmonary disease (COPD)

A

FEV1/FVC

  • <70%
  • no reversibility

CXR

  • hyperinflation & bullae
  • flat hemidiaphragm
  • also to exclude lung cancer

FEV1 (↓)
FBC (

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45
Q

Investigations of Chronic obstructive pulmonary disease (COPD)

A

FEV1/FVC

  • <70%
  • no reversibility

CXR

  • hyperinflation & bullae
  • flat hemidiaphragm
  • also to exclude lung cancer

FEV1 (↓)
FBC (↑ haematocrit, anaemia)

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46
Q

Severity of Chronic obstructive pulmonary disease (COPD)

A

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%
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47
Q

Management of Chronic obstructive pulmonary disease (COPD)

A

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

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48
Q

Features suggesting steroid responsiveness in Chronic obstructive pulmonary disease (COPD)

A

I.e. asthmatic features

  • previous history of asthma / atopy
  • ↑ eosinophils
  • substantial variation in FEV1 (≥400ml)
  • substantial diurnal variation in PEFR (≥20%)
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49
Q

Most important intervention in Chronic obstructive pulmonary disease (COPD) management

A

smoking cessation

vital in any pt that still smokes

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50
Q

Acute exacerbation of Chronic obstructive pulmonary disease (COPD)

A

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

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51
Q

Aetiology of Acute exacerbation of Chronic obstructive pulmonary disease (COPD)

A

Most commonly viral

haemophilus influenzae (most common)
strep pneumonia (most common bacterial cause)
Others: mortadella catarrhalis, staph aureus
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52
Q

Presentation of Acute exacerbation of Chronic obstructive pulmonary disease (COPD)

A 
↑ dyspnoea
↑ cough
↑ wheeze
↑ volume/purulence of sputum 
fevers, chills, sore throat 
↓ exercise tolerance 
respiratory distress (dyspnoea, tachypnoea, confusion, cyanosis, peripheral oedema)
respiratory failure
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53
Q

Investigations for Acute exacerbation of Chronic obstructive pulmonary disease (COPD)

A

ABG
-↓PaO2, ↑PaCO2, pH <7.35

CXR

  • hyperinflation, flattened diaphragm
  • possible consolidation if infection

sats (↓)
sputum/blood cultures
ECG, FBC, U&Es

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54
Q

Management of Acute exacerbation of Chronic obstructive pulmonary disease (COPD)

A

↑ 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

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55
Q

Small cell lung cancer (SCLC)

A

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)

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56
Q

Presentation of Small cell lung cancer (SCLC)

A 
dyspnoea, cough, haemoptysis, chest pain
weight loss, fatigue 
dysphagia, hoarseness, wheezing/stridor
recurrent pneumonias 
superior vena cava syndrome
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57
Q

Investigations for Small cell lung cancer (SCLC)

A

CXR

  • central mass
  • hilar lymphadenopathy
  • pleural effusion

CT chest/abdo/pelvis
-investigation of choice

bronchoscopy ± biopsy
PET scan

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58
Q

Management of Small cell lung cancer (SCLC)

A

consider pts in early stages for surgery

generally chemo + radiotherapy = management of choice

if extensive disease = palliative chemo

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59
Q

Complications of Small cell lung cancer (SCLC)

A

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

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60
Q

Referral criteria for suspected lung cancer

A

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
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61
Q

Non-Small cell lung cancer (NSCLC)

A

a group of malignant epithelia tumours representing ~85% of all lung cancers

most common risk factor is active & passive smoking

62
Q

Types of Non-Small cell lung cancer (NSCLC)

A

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
Q

Presentation of Non-Small cell lung cancer (NSCLC)

A 
persistent cough
haemoptysis
dyspnoea 
chest pain
weight loss
fatigue
anorexia
hoarseness 
recurrent pneumonias
superior vena cava syndrome
64
Q

Investigations for Non-Small cell lung cancer (NSCLC)

A

CT chest/abdo/pelvis
-investigation of choice

CXR

  • usually preliminary
  • may show mass

bronchoscopy + biopsy
pet scanning

65
Q

Management of Non-Small cell lung cancer (NSCLC)

A

surgery (indicated in ~20% of pts)

  • lobar resection
  • lobectomy

curative or palliative radio therpay

generally poor responsiveness to chemo

66
Q

Respiratory failure

A

the acute or chronic inability of the reparatory system to maintain adequate gas exchange leading to hypoxia ± hypercapnia

67
Q

Types of respiratory failure

A

Type I respiratory failure:

  • hypoxic respiratory failure
  • PaO2 <8kPa
  • PaCO2 normal

Type II respiratory failure:

  • hypercapnic respiratory failure
  • PaO2 <8kPa
  • PaCO2 >6kPa
68
Q

Aetiology of type I respiratory failure

A 
COPD
pneumonia
pulmonary oedema 
pulmonary fibrosis 
asthma
PE
cyanotic congenital heart disease
ARDS
bronchiectasis 
obesity
kyphoscoliosis
69
Q

Aetiology of type II respiratory failure

A 
COPD
severe asthma (when pt is exhausted)
drug overdose/poisoning 
muscular disorders 
severe ARDS
70
Q

Presentation of respiratory failure

A 
tachypnoea
dyspnoea
cyanosis 
tachycardia
confusion 
↓GCS
arrhythmias 
hypercapnia (hypoventilation, headache, coma, asterix)

NB clinical features of the underlying cause will be present

71
Q

Investigations for respiratory failure

A

ABG***

CXR, FBC, TFTs, U&Es, LFTs, CK, troponin, ECG, CT-CTPA

72
Q

Management of respiratory failure

A

resuscitation & ABCDE assessment
treat underlying cause

Hypoxia

  • O2
  • CPAP (↑ O2)
  • mechanical ventilation

Hypercapnia

  • NIV/BIPAP (↑O2, ↓CO2)
  • mechnaical ventilation
73
Q

BIPAP (NIV) vs CPAP

A

CPAP helps ↑ O2 but doesn’t affect CO2

NIV/BIPAP helps ↑O2 & ↓CO2

74
Q

Tuberculosis (TB)

A

an infectious disease caused by mycobacterium tuberculosis typically affecting the lungs

NB notifiable disease in the UK

spreads via inhalation of infected droplets

75
Q

Types of Tuberculosis (TB)

A

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
Q

Risk factors for Tuberculosis (TB)

A 
homelessness
institutionalisation e.g. prisons 
alcohol/drug misuse 
HIV +ve
immunocompromised 
crowded lying 
ethnic minority background 
travel to/heritage from high prevalence areas
77
Q

presentation of Tuberculosis (TB)

A 
cough
fever
haemoptysis 
night sweats
malaise
chest pain
dyspnoea 
erythema nodosum
78
Q

Investigations for Tuberculosis (TB)

A

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
Q

Management of Tuberculosis (TB)

A

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
Q

Side effects of Tuberculosis (TB) drugs

A

Rifampicin:

  • enzyme inducer
  • orange secretions
  • hepatitis

Isoniazid:

  • enzyme inhibitor
  • agranulocytosis
  • hepatitis

Pyrazinamide:

  • hyperuraemia (gout)
  • arthralgia
  • hepatitis

Ethambutol:

  • optic neuritis
  • monitor visual acuity
81
Q

Pneumonia

A

inflammation of the lungs with consolidation & interstitial infiltration most commonly caused by bacteria

82
Q

Types of pneumonia

A

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
Q

Causes of pneumonia

A

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
Q

Risk factors for pneumonia

A 
infants/young children
elderly
smoking
alcohol misuse
asthma
COPD
malignancy
immunosuppression
IVDU
hospitalisation
85
Q

Presentation of pneumonia

A 
cough with purulent sputum
fever
malaise
dyspnoea
chest pain (pleuritic)
tachycardia
hypoxia
bronchial breathing & crackles on auscultation
dullness on percussion
86
Q

Investigations for pneumonia

A

CXR
-new consolidation

FBC (↑ WCC)
CRP (↑)
U&Es
Blood cultures

87
Q

Scoring system for pneumonia

A 
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
Q

Management of Community acquired pneumonia (CAP)

A

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
Q

Management of Hospital acquired pneumonia (HAP)

A

Consider broad spectrum IV Abx
then tailor treatment when sensitivities available

generally based on local guidelines & sensitivities

90
Q

Aspiration pneumonia

A

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
Q

Risk factors for Aspiration pneumonia

A 
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
Q

Aetiology of Aspiration pneumonia

A

Similar to normal pneumonia

strep pneumoniae, staph aureus, H. influenzae, pseudomonas aeruginosa

IN alcoholics its frequently Klebsiella pneumoniae

93
Q

Presentation of Aspiration pneumonia

A 
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
Q

Investigations for Aspiration pneumonia

A

CXR

  • new consolidation
  • or atelectasis

FBC (↑WCC, neutrophilia)
sputum & blood cultures

95
Q

Management of Aspiration pneumonia

A
  • 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
Q

Sarcoidosis

A

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
Q

Epidemiology of sarcoidosis

A

most commonly seen in young adults (20-40y/o)

more common in people of african or northern european/scandinavian origin

98
Q

Presentation of sarcoidosis

A
  • 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
Q

Investigations for Sarcoidosis

A

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
Q

Pleural effusion

A

a collection of fluid between the pleural & visceral pleural surfaces in the thorax i.e. the pleural cavity

101
Q

Aetiology of pleural effusion

A

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
Q

Presentation of Pleural effusion

A

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
Q

Investigations for Pleural effusion

A

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
Q

Management of Pleural effusion

A

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
Q

Criteria for pleural effusion

A

Lights criteria

-used if protein level 25-35g/L in pleural fluid to differentiate transudate & exudate

106
Q

Criteria for pleural effusion

A

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
107
Q

Pneumothorax

A

a collection of air in the pleural cavity leading to partial or complete collapse of the lung

108
Q

Types of Pneumothorax

A

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
109
Q

Presentation of Pneumothorax

A 
dyspnoea
pleuritic chest pain with sudden onset 
ipsilateral reduced breath sounts
ipsilateral hyper resonance  on percussion
tachypnoea
hypoxia
tachycardia
110
Q

Investigations for Pneumothorax

A

CXR

  • visible rim on air between lung margin & chest wall
  • absence of lung markings

consider CT or USS
-usually for complex cases

111
Q

Management of Primary spontaneous Pneumothorax (PSP)

A

<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

112
Q

Management of Secondary spontaneous Pneumothorax (SSP)

A

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

113
Q

Tension Pneumothorax

A

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

114
Q

Obstructive sleep apnoea (OSA)

A

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

115
Q

Risk factors for Obstructive sleep apnoea (OSA)

A 
obesity***
male gender
smoking 
excess alcohol consumption 
macroglossia 
acromegaly
hypothyroidism

adenotonsilar hyperplasia especially in children

116
Q

Presentation of Obstructive sleep apnoea (OSA)

A

sleep partner complains of excessive snoring or describes apnoeas

daytime somnolence
snoring
waking headaches
unrefreshing sleep
sleep fragmentation 
irritability
117
Q

Investigations for Obstructive sleep apnoea (OSA)

A

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

118
Q

Management of Obstructive sleep apnoea (OSA)

A

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

119
Q

Driving and Obstructive sleep apnoea (OSA)

A

must inform DVLA & stop driving until adequate control is achieve i.e. ↓daytime sleepiness

120
Q

Pulmonary hypertension

A

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

121
Q

Idiopathic Pulmonary hypertension (PAH)

A

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

122
Q

Aetiology of Pulmonary hypertension

A

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

123
Q

Presentation of Pulmonary hypertension

A 
progressive dyspnoea
weakness
fatigue
exertional dizziness/syncope 
loud S2 (often split)
↑ JVP
symptoms of right HF
124
Q

Investigations for Pulmonary hypertension

A

Right heart catheterisation
-↑ PAP ≥25 mmHg at rest

CXR
-prominent R heart border

ECG, Echo, CT/MRI thorax

125
Q

Management of Pulmonary hypertension

A

treat underlying cause

pulmonary vasodilators if acute deterioratio

if idiopathic PH (PAH) give high dose calcium channel blockers

126
Q

Cor Pulmonale (Pulmonary heart disease)

A

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

127
Q

Cystic fibrosis (CF)

A

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

128
Q

Presentation of Cystic fibrosis (CF)

A
  • 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
129
Q

Investigations for Cystic fibrosis (CF)

A

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

130
Q

Genetics of Cystic Fibrosis (CF)

A

autosomal recessive disorder of cystic fibrosis transmembrane conductance regulatory gene (CFTR)

80% of cases in UK are due to delta F508 (DF508) gene

131
Q

Management of Cystic fibrosis (CF)

A

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

132
Q

Bronchiectasis

A

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

133
Q

Aetiology of Bronchiectasis

A

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

134
Q

Presentation of Bronchiectasis

A

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
135
Q

Investigations for Bronchiectasis

A

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

136
Q

Management of Bronchiectasis

A

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

137
Q

Asbestosis

A

a type of pneumoconiosis

138
Q

Asbestosis

A

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

139
Q

Causes of upper zone lung fibrosis

A

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
140
Q

Mesothelioma

A

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

141
Q

Occupational asthma

A

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

142
Q

Occupational asthma

A

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

143
Q

Silicosis

A

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

144
Q

Coal workers pneumoconiosis (Black lung disease)

A

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

145
Q

Interstitial lung disease (ILD)

A

a heterogenous group of disorders characterised by inflammation & progressive scarring (fibrosis) of the lung

146
Q

Aetiology of Interstitial lung disease (ILD)

A

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
147
Q

Medications causing Interstitial lung disease (ILD)

A
  • amiodarone
  • bleomycin
  • methotrexate
  • nitrofurantoin
  • sulfalazine
  • cabergoline
  • bromocriptine
148
Q

Presentation of Interstitial lung disease (ILD)

A 
progressive dyspnoea 
  -exertional dyspnoea → dyspnoea at rest
persistent non productive cough
fatigue
clubbing
bibasal inspiratory crackles/rales
cyanosis
149
Q

Investigations for Interstitial lung disease (ILD)

A

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

150
Q

Management of Interstitial lung disease (ILD)

A

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

151
Q

Idiopathic pulmonary fibrosis (IPF)

A

no underlying cause found
usually seen in men aged 50-75yrs

consider treating with antifibrotic agents e.g. pirfenidone

Year 3 (6 decks)

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