Respiratory Flashcards
(236 cards)
1
Q
Signs of pneumothorax on examination
A
From the end of the bed the patient may be tachypnoeic.
Diminished breath sounds on side of PTX on auscultation, and hyper-resonant on percussion.
Reduced chest expansion may be evident on side of PTX.
2
Q
What would a CXR of a tension PTX show?
But why would this not usually be seen?
A
the heart and mediastinum will be being pushed to the opposite side due to the high pressure on the side of the PTX
should not be seen because the aim is to make a diagnosis based on symptoms in order to not delay treatment
3
Q
what happens in a tension PTX?
A
A “one-way valve” establishes itself which allows air into the pleural cavity on inspiration, but closes on expiration to cause an increase in pressure
This will continue until the patient’s venous return to the heart is compressed and obstructed causing cardiac output failure and the patient will arrest
4
Q
how to make a clinical diagnosis of tension PTX
A
Severe tachypnoea, may be cyanotic
Tachycardic, hypotensive
Raised JVP
Tracheal deviation
Absent breath sounds, hyper-resonant and hyperexpanded chest unilaterally
5
Q
Immediate management of tension PTX
A
Large bore (14 or 16 gauge) needle decompression – 2nd intercostal space, mid-clavicular line.
Followed by tube thoracostomy
6
Q
Primary vs. Secondary PTX
A
Primary occurs in otherwise healthy lung tissue
Secondary occurs due to underlying lung disease
7
Q
What is asthma?
A
a disease involving bronchoconstriction and inflammation
causes variable and reversible increases in airway resistance
8
Q
What FEV1:FVC ratio suggests increased airway resistance?
A
a ratio of less than 70-80%
9
Q
Timing of symptoms of asthma
A
Symptoms tend to worsen at night or early in the morning, and symptoms tend to vary over time
10
Q
Asthma symptoms
A
wheeze, shortness of breath, chest tightness and cough
11
Q
Non-specific triggers for asthma
A
Viral infections Cigarette smoke Pollution Cold weather Emotion Exercise (sometimes)
12
Q
Specific triggers for asthma
A
Pets
Pollen
Other allergens
Occupational pollutants
13
Q
Important HPC/PMH points for asthma
A
Known precipitants
Diurnal variation in symptoms
Acid reflux symptoms (known association).
History of atopy.
History of these episodes (and establish whether they required hospital/ITU)
14
Q
Relevant DHx for asthma
A
NSAIDs (particularly aspirin) and beta-blockers, as these can cause asthma
15
Q
Relevant FH and SH for asthma
A
FH of atopy
Very important to ask about occupation (as there can be occupational pollutants such as flour or chemicals).
Days off work/school.
Smoking.
16
Q
Diagnosis of asthma
A
Requires a structured clinical assessment to see if:
Episodes are recurrent
Symptoms are variable
PMH/FH of atopy.
Recorded observation of expiratory wheeze.
Variable peak expiratory flow or FEV1
Absence of symptoms of an alternative diagnosis.
If these give a high probability of asthma – diagnose as suspected asthma and initiate treatment
17
Q
When is a diagnosis of asthma confirmed?
A
When there is objective improvement after initiating treatment.
if response to treatment is poor, refer for spirometry to test for airway obstruction with bronchodilator reversibility (FEV1/FVC <70% with bronchodilator reversibility is diagnostic)
18
Q
Diagnosis of asthma in children
A
Children <5 with suspected asthma should have symptoms treated based on observations and clinical judgement and be reviewed regularly until they are old enough to do objective testing
19
Q
Extrinsic Asthma:
A
Type I hypersensitivity reaction
Most frequently occurs in atopic individuals who show positive skin prick tests to common allergens, implying a definite extrinsic cause.
Tends to be early-onset
20
Q
Intrinsic Asthma
A
Non-immune mechanisms
Occurs in middle-aged individuals, when no causative agent can be identified
Generally more severe, and associated with quicker deterioration of lung function.
Tends to be late-onset
21
Q
Pathophysiology of asthma
A
- Spasmogens will act rapidly to cause smooth muscle contraction of the airways, leading to bronchospasm.
- Chemotaxins are released to stimulate eosinophils and mononuclear cells to go to the airways, causing an inflammatory response a few hours later.
22
Q
Persistant airway obstruction in asthma
A
can become indistinguishable from COPD
more common in intrinsic asthma
bronchoconstriction due to increased responsiveness of bronchial smooth muscle, and hyper-secretion of mucous that plugs the airways
Sputum will contain Charcot-Leyden crystals (from eosinophil granules) and Curschman spirals (mucous plugs from small airways).
Can eventually lead to pulmonary hypertension
23
Q
what is the basis of asthma treatment?
A
The use of bronchodilators reverses the bronchospasm and provides rapid relief – “relievers”.
There are also treatments to prevent more attacks – “preventers” – which are usually anti-inflammatory steroids
=> aim is to have no daytime symptoms, no night time waking, no need for rescue medication and no limitations on activity.
24
Q
beta2-adrenoceptor agonists in asthma
A
typically the first-choice drug for relief.
Can be short-acting/long-acting (SABA / LABA)
Acts on beta2-adrenoceptors on smooth muscle, which causes relaxation and in turn an increase in FEV1.
given by inhalation; localising the action and providing a rapid effect.
Prolonged use may lead to receptor down-regulation – the beta2-adrenoceptors become less responsive
25
Long-acting beta agonists
given for long term prevention and control (e.g. overnight), as it stays bound to the receptors for a lot longer than salbutamol (SABA)
26
corticosteroids in asthma
Preventative, they do not reverse an attack.
Takes 2-3 days to have an effect.
Anti-inflammatory by activation of intracellular receptors, leading to altered gene transcription (decrease cytokine production) and production of lipocortin/annexin A1.
It is thought that lipocortin/annexin A1’s action is to inhibit phospholipase A2, and therefore inhibiting the synthesis of PGs and LTs by preventing the arachidonic acid pathways from occurring.
27
Leukotriene receptor antagonists (LTRAs) in asthma
e.g. Montelukast
Increased role as add on therapy.
Have both preventative and bronchodilator uses.
Antagonises the actions of LTs by blocking their receptors
Also useful against symptoms of hayfever and eczema
28
Xanthines in asthma
e.g. theophylline, aminophylline.
These are also bronchodilators, but not as good as beta2-adrenoceptor agonists (therefore only 2nd line use).
Oral (or IV aminophylline in emergency)
Adenosine receptor antagonist.
Phosphodiesterase inhibitors, preventing the breakdown of cAMP.
29
Pharmacological treatment of SUSPECTED asthma
All patients with suspected asthma should receive a SABA.
30
Pharmacological treatment of CONFIRMED asthma
```
SABA + ICS
=>
Add LABA
(or LTRA/xanthine if this fails).
=>
Increase dose of ICS
=>
Add oral steroid
```
if salbutamol inhaler is used more than 2 times a week, this indicates that their current control is inadequate, and the care needs to move up a step
31
Moderate Acute Asthma
Increasing symptoms
PEF 50-75%
No features of acute severe asthma
32
Acute Severe Asthma
```
Requires any one of:
• PEF 33-50% predicted
• RR >25/min
• HR >110
• Inability to complete sentences in one breath
```
33
Life-threatening Asthma
```
Any one of:
• PEF <33% predicted
• SpO2 <92%
• PO2 <8kPa
• Normal PaCO2 (4.6-6)
• Silent chest
• Cyanosis
• Poor respiratory effort
• Arrhythmia
• Exhaustion
• Altered consciousness
• Hypotension
```
34
Emergency management of asthma
If a patient has ANY life-threatening feature, an arterial blood gas is the only immediate investigation required whilst treatment is initiated.
1. O2 to maintain sats at 94-98% (88-92% in COPD, 92-94% in Covid)
2. Salbutamol nebuliser (add ipratropium if required).
3. Steroids (PO prednisolone or IV hydrocortisone)
4. IV magnesium sulphate
5. IV aminophylline (senior review)
6. Referral to ITU for patients who are not improving.
35
What blood gas features are markers of a life-threatening asthma attack?
Normal PaCO2 (should normally be low due to hyperventilation).
Severe hypoxia <8 kPa
A low pH
36
What is COPD?
= Chronic Obstructive Pulmonary Disease.
Characterised by airflow obstruction, which is usually progressive and not fully reversible.
Obstruction does not change markedly over several months.
37
What causes COPD?
significant exposure to noxious particles/gases.
>90% caused by damage to the lungs from smoking.
38
pathological changes in COPD
* Chronic inflammation – chronic response to irritants
| * Structural change – repeated injury and repair
39
physiological changes in COPD
Mucous hypersecretion
Ciliary dysfunction
Airflow limitation, resulting in alveolar hyperinflation.
Impaired gas exchange
Pulmonary hypertension – due to remodelling of pulmonary arteries and veins.
40
Risk factors for COPD
SMOKING!!!!!!
Indoor air pollution
Occupational toxins
(Outdoor air pollution)
Genetic factors – alpha-1 antitrypsin deficiency.
Infections – measles, whooping cough.
Socio-economic factors – significant association with socio-economic deprivation.
Asthma and airway hyperreactivity
41
Clinical features of COPD
Chronic progressive dyspnoea
A chronic cough
Regular sputum production
Wheezing and chest tightness
These symptoms become exacerbated in acute infective episodes.
In severe cases, there may be fatigue, weight loss, anorexia, cough, syncope, depression/anxiety
42
Complications of COPD
* Acute exacerbations
* Polycythaemia
* Respiratory failure
* Cor pulmonale
* Pneumothorax
* Lung carcinoma
43
COPD - OE: observations
* Tachypnoea
* Possible cyanosis
* Flapping tremor (if CO2 retainer, >10 kPa)
* Cachexia
44
COPD - OE: inspection
* Hyperinflation
* Intercostal recession on inspiration
* Lip pursing on expiration
* Signs of respiratory distress.
* Raised JVP
* Peripheral oedema
45
COPD - OE: palpation
• Poor chest expansion
46
COPD - OE: percussion
* Hyper-resonant throughout
| * Loss of cardiac/hepatic dullness.
47
COPD - OE: auscultation
* Widespread/polyphonic wheeze, or
* Decreased breath sounds
* Prolonged expiratory phase.
48
“Pink Puffer”
Patients remaining sensitive to CO2, thus keep a low CO2 and near-normal O2.
Tachypnoeic, tachycardic, using accessory muscles to increase ventilation.
Breathless but not cyanosed.
Very thin – large amounts of calories used to breathe.
Can progress to type 1 respiratory failure.
More emphysematous.
49
“Blue Bloater”
Patients are insensitive to CO2.
Severe chronic bronchitis/COPD.
Not particularly breathless but are cyanosed and oedematous (cor pulmonale).
Blood gas will show type 2 respiratory failure (low oxygen, retaining CO2.
Oxygen should be given with care to these patients.
50
What main investigations would you order for suspected COPD?
FBC
CXR
Spirometry
51
What additional investigations could be ordered in suspected COPD?
```
Serial peak flow,
Alpha 1 antitrypsin,
Transfer factor for carbon monoxide.
Pulse oximetry,
CT thorax
ECG
Echo
```
ABG – normal in mild disease, developing to type 1/2 respiratory failure.
Sputum culture – abnormal organisms suggest bronchiectasis.
52
COPD - FBC
Secondary polycythaemia
Any anaemia?
53
Secondary polycythaemia
= the overproduction of red blood cells
due to chronic hypoxaemia, which triggers increased production of EPO by the kidneys
causes your blood to thicken, which increases the risk of a stroke.
54
COPD - CXR
Hyperinflation (>6 anterior and >10 posterior ribs)
Flattened hemidiaphragm
Rule out malignancy/other diagnoses
55
Staging of COPD by spirometry
Stage 1 – FEV1 >80% predicted (clinical diagnosis); mild.
Stage 2 – FEV1 50-79% predicted; moderate.
Stage 3 – FEV1 30-49% predicted; severe.
Stage 4 – FEV1 <30% predicted; very severe.
56
Management of COPD
Patient education - how to recognise and manage exacerbation
Lifestyle advice - diet, exercise, STOP SMOKING
Pneumococcal vaccine
Medical management
57
Medical management of COPD
Short-acting bronchodilators (SABA or SAMA)
If no features of asthma/steroid responsiveness:
- Add a long-acting beta-agonist (LABA) and muscarinic agonist (LAMA)
- Add inhaled corticosteroids if still symptomatic
- Remove ICS after 3 months if no improvement.
If features of asthma/steroid-responsiveness are present – LABA + ICS.
- LABA + LAMA + ICS if ongoing symptoms.
58
What are features of asthma/steroid-responsiveness in COPD?
Previous diagnosis of asthma/atopy, blood eosinophilia, substantial variation in FEV1 over time or diurnally.
59
Specialist treatments for COPD
Pulmonary rehabilitation – consider if someone is functionally disabled by COPD.
Oral aminophylline/theophylline – if still symptomatic after trial of triple therapy.
Mucolytics – e.g. carbocysteine
Roflumilast – PDE4 inhibitor
Nutritional supplements – consider for low BMI
Long-term oxygen therapy
Surgery
60
Acute exacerbation of COPD
Exacerbations are frequently caused by bacterial/viral infections, or exposure to pollutants.
Dyspnoea and wheeze will become worse, with increased production of purulent sputum.
Patient should have rescue medications.
Hospital admission in severe breathlessness, rapid symptom onset, acute confusion, cyanosis, low oxygen sats, or worsening peripheral oedema.
61
Steps for smoking cessation
1. ASK about smoking at every opportunity.
2. ADVISE all smokers to stop smoking.
3. Offer ASSISTANCE to all smokers to stop.
4. ARRANGE smoking cessation follow-up.
62
What are some useful things to do when helping someone to stop smoking.
* Set a date to stop completely
* Specialised stop-smoking clinics
* Review previous quit attempts (what helped/hindered)
* Plan for problems and how to manage them
* Plan for how to handle alcohol drinking situations
* Try smoking cessation treatments
63
What are some treatments to help smoking cessation?
Nicotine replacement therapy
| Bupropion
64
Epidemiology of Lung Cancer
Lung cancer is the third most common cancer in the UK.
Incidence increases with age
Lung cancer is the most common cause of cancer deaths in the UK (accountable for ~1 in 5)
79% of lung cancers are preventable.
65
Risk factors for developing lung cancer
Smoking
Second-hand/environmental smoking
Old age
Air pollution
Radon
Occupational hazards (e.g. asbestos, silica)
Family History of lung cancer in a close relative.
66
Lung cancer - Clinical Features
* Persistent cough – non-specific sign.
* Haemoptysis – less common but more specific.
* Dyspnoea
* Dysphagia
* Hoarseness
* Chest pain – pleural/chest wall involvement.
* Fatigue, Weight loss, Appetite loss, Fever
67
Lung cancer - On Examination
* Clubbing
* Cachexia
* Signs of anaemia
* Chest signs of collapse/consolidation/effusion
* Signs of metastases.
* Hypertrophic pulmonary osteoarthropathy – a paraneoplastic syndrome
68
What is the rough split between incidence of small cell and non-small cell lung cancers
Small-cell - 15%
| Non-small cell - 85%
69
Small cell (“oat cell”) carcinomas
Rarer but highly malignant, grow very quickly and metastasise early.
Rare in non-smokers.
Usually centrally located.
Originate mostly from bronchial epithelium, but differentiate into neuroendocrine cells (e.g. secreting ADH, ACTH, etc.) and causing paraneoplastic syndrome.
70
Squamous cell carcinoma
| non-small cell
Arise from squamous metaplasia of the normally pseudostratified ciliated columnar epithelium
Occur mainly in response to cigarette smoke exposure.
Usually central, close to the carina.
May secrete PTH, causing hypercalcaemia (can also be due to secondary bone metastases).
Can often be diagnosed with sputum cytology.
Tends to cause cavitating lesions.
Slow growing, may be resectable.
71
Adenocarcinoma
| non-small cell
Equal gender incidence, and less related to smoking.
Characteristically originate in peripheral locations (potentially areas of previous lung scarring).
Associated with asbestos exposure.
72
Large cell carcinoma
| non-small cell
Features showing small cell/adenocarcinomatous origins may be seen, but they are not differentiated enough to eb classified.
Poor prognosis, often widely disseminated at diagnosis.
73
Bronchoalveolar carcinoma
a special type of adenocarcinoma,
Rare but associated with better prognosis.
74
Metastatic lung tumours
the lungs are a common site of metastasis of many cancers.
secondary lung tumours will be made up of cells of the primary tumour.
75
Local complications of lung tumours
SVC compression
Recurrent laryngeal nerve palsy
Horner syndrome
76
Distant metastasis of lung tumours
Most common sites – brain, bone, liver, adrenal glands.
Symptoms will be associated to the specific organ affected
77
Lung tumours - SVC compression
Raised JVP, raised arm BP/swelling, facial swelling.
Common presenting feature of lung cancer.
Often due to local nodes rather than the tumour itself
78
Lung tumours - Recurrent laryngeal nerve palsy
voice hoarseness and left vocal cord paresis.
If present, indicates tumour inoperability.
79
Lung tumours - Horner syndrome
Miosis, ptosis, anhidrosis
Destructive lesions of the thoracic inlet, often involving the brachial plexus.
Due to Pancoast tumour
80
CXR in suspected lung cancer
For anybody with suspected lung cancer - first investigation is a CXR.
Also, ANY patient with haemoptysis should have a CXR
Symptomatic tumours are almost always visible.
A normal CXR in a symptomatic patient should warrant further investigation for central tumours
81
Blood tests in suspected lung cancer
FBC - anaemia/secondary polycythaemia
U&E - hypercalcaemia, hyponatraemia
LFTs - liver mets?
82
What are the steps in suspected lung cancer?
CXR
Bloods
Any patient presenting with any suspicion of lung cancer requires a 2-week wait referral to a lung cancer clinic for further investigation
Specialist referral for:
- sputum/pleural cytology
- contrast-enhanced CT staging
- bronchoscopy
- pulmonary function tests
- PET scan if suspected metastasis.
83
How much fluid is normally within the pleural cavity?
~15 mL of serous pleural fluid
84
What is pleural effusion?
the build-up of excess fluid between the layers of the pleura outside the lungs
85
How does pleural effusion differ from pulmonary oedema?
the location of the fluid
Pleural effusion - fluid in pleural space
Pulmonary oedema - fluid in alveolar spaces and lung tissue
86
Haemothorax
= accumulation of blood, due to trauma
87
Empyema/pyothorax
= accumulation of pus, due to infection
88
Chylothorax
= accumulation of lymph, due to thoracic duct leakage
89
Fluid effusion
= fluid accumulation, transudative or exudative
90
Transudate
Occur due to increased hydrostatic pressure/decreased oncotic pressure
Causes – cardiac failure, liver failure, renal failure, peritoneal dialysis.
Rarer causes – hypothyroidism, ovarian tumours.
91
What is the protein concentration of transudate?
Protein concentration <30 g/L
92
Exudate
Occur due to increased capillary permeability
* Infections – bacterial pneumonia, TB
* Neoplasm – lung primary/secondary, mesothelioma.
* Pulmonary Embolism
* Autoimmune disease – RA/SLE
* Abdominal disease
93
What is the protein concentration of transudate?
Protein concentration >30 g/L
94
If protein level of pleural fluid is 25-30 g/L, what criteria are needed to suggest it is an exudate (not transudate)?
one positive element of Light’s criteria will suggest an exudate:
* Pleural fluid protein/serum protein >0.5.
* Pleural fluid LDH/serum LDH >0.6.
* Pleural fluid LDH more than two-thirds the upper limit of normal serum LDH.
95
Symptoms of pleural effusion
A small amount of fluid is completely asymptomatic
```
As the volume of fluid increases, the patient will experience:
• Shortness of breath
• Cough
• Pleuritic chest pain
• Reduced exercise tolerance
```
96
Pleural effusion - percussion
dull due to underlying fluid
97
Pleural effusion - auscultation
quieter breath sounds and vocal fremitus
98
What is the first-line investigation on suspicion of a pleural effusion?
CXR
99
What is the issue in using a CXR in ?pleural effusion
PA and AP erect X-ray films are insensitive to small amounts of fluid – as much as 250-600 mL of fluid is required before it becomes evident.
100
CXR features indicating pleural effusion
* blunting of the costophrenic angle
* blunting of the cardiophrenic angle
* fluid within the horizontal or oblique fissures
* eventually, a meniscus will be seen (note: if a hydropneumothorax is present, no such meniscus will be visible)
* with large volume effusions, mediastinal shift occurs away from the effusion
101
Pleural effusion - ultrasound
allows the detection of small amounts of pleural locular fluid, with positive identification of amounts as small as 3-5 mL.
It is it is effective in guiding thoracocentesis (even in small fluid collections) and can be used to assess pleural fluid volume.
102
Treatment of pleural effusion
The treatment of pleural effusions is usually targeted to the underlying condition.
Ultrasound-guided aspiration is reliable and fast and enables loculated effusions to be drained. Symptomatic patients with large effusions may be treated by therapeutic aspiration/pleural tap.
Fluid can be sent to microbiology and also be assessed for clinical chemistry (protein, LDH, glucose) and cytology. It can also be run through a blood gas machine to assess pH.
103
Community-acquired pneumonia definition
Clinical lower respiratory tract infection AND
New pneumonic changes on CXR AND
Onset of symptoms in the community OR within 48 hours of hospital admission.
104
CAP is more common in...
* Males
* Winter/early spring
• The elderly – peak age 50-70 years; most severe in age >65.
* Alcoholics
* Smokers
* People with established chronic disease
105
CAP presentation
The patient presents with symptoms of LRTI – cough, sputum, breathlessness, pleuritic chest pain, occasionally haemoptysis
These symptoms are similar to bronchitis, and for a diagnosis of CAP you need evidence of lung parenchymal involvement (confirmation with CXR).
106
CAP presentation in the elderly
Elderly populations may present with very few symptoms, but be very unwell and usually acutely confused
107
Causes of CAP
```
Conventional bacteria (60-80%)
=> S. pneumoniae, H. influenzae
```
‘Atypical’ bacteria (10-20%)
Viruses (10-20%)
108
What are the "atypical" bacteria causing CAP?
Mycoplasma pneumoniae,
Chlamydia pneumoniae
Legionella pneumophila
109
CAP - on examination
Inspection:
• Tachypnoea
Palpation:
• Decreased chest expansion on the affected side.
Percussion:
• Dullness over the affected area
Auscultation:
• Coarse crackles and pleural rub over the affected area
• Bronchial breathing
• Increased vocal resonance – “111” / “99” can be heard better due to consolidation.
ALSO there can be upper abdominal tenderness in lower lobe pneumonia.
110
Investigations for CAP
* Confirm diagnosis – CXR
* Assess severity of disease – CURB65
• Identify complications
=> Often linked to respiratory failure (T1RF/T2RF)
=> Can lead to multi-organ failure, septic shock and death.
=> Will the patient need supplementary oxygen therapy to maintain PO2 >94 (or >88 COPD)?
=> Bloods – LFTs, FBC, CRP, Arterial Blood Gas.
111
Microbiological investigations for CAP
• Sputum analysis and culture
• Immunofluorescence on sputum/nasopharyngeal samples
=> Viruses (influenza), mycoplasma, legionella
• Blood cultures
• Urinary pneumococcal and legionella antigen
=> For any patient with moderate/severe CAP!
112
CURB65 criteria
Confusion – mini-mental test score of 8 or less (new)
Urea >7 mmol/L (new)
Respiratory Rate >30 breaths per minute
Blood Pressure – systolic BP <90 mmHg or diastolic BP <60 mmHg
65 or more years old
113
Low-severity CAP
CURB score 0 or 1
114
Management of Low-severity CAP
PO Amoxicillin, managed as outpatients.
| PO doxycycline if penicillin allergy.
115
Moderate-severity CAP
CURB score 2
116
Management of Moderate-severity CAP
Higher mortality – ~5-10%
PO amoxicillin + clarithromycin, usually admitting the patient
117
Severe CAP
CURB score >2
118
Management of Severe CAP
Can be >20% mortality if established failure in another organ system.
Requires admission to at least Level 01 unit or even HDU/ICU.
IV co-amoxiclav + clarithromycin.
Penicillin allergy/MRSA suspicion – vancomycin and levofloxacin.
Treatment for at least 10 days.
119
Pneumonia follow-up
Patients should always have a follow-up CXR at 6 weeks to ensure resolution of consolidation and assess for persistent abnormalities of the lung parenchyma
120
CAP non-resolution
?endobronchial obstruction as cause of pneumonia (e.g. lung cancer)
121
Definition of hospital-acquired pneumonia
Clinical lower respiratory tract infection AND
New pneumonic changes on CXR AND
onset of symptoms > 48 hours after admission OR admission in the last 7 days
122
when is there increased risk of HAP?
prolonged hospital stays, poor mobility, age >70 years and severe underlying disease.
123
What are the causes of HAP?
Tends to be more gram negative pathogens
Enteric gram-negative bacilli – ~60% HAP cases
Also:
Strep. pneumoniae
H. influenzae
Staph. aureus
124
Management of HAP
Assess MRSA risk factors
Assess HAP severity
Mild HAP – oral doxycycline.
Severe HAP – IV Tazocin.
125
Aspiration pneumonia
Aspiration of gastric contents leading to chemical inflammation and infection.
126
When should you suspect aspiration pneumonia?
Does not always show on CXR!!
Suspect it for example in someone who has a low GCS and evidence of vomiting (so at risk of aspirating).
127
What should you do in suspected aspiration pneumonia?
If suspected can add metronidazole for HAP or CAP – this is to cover anaerobic bacteria.
128
Complications of pneumonia
Sepsis
Septic shock
Lung abscess
Empyema
129
Complications of pneumonia - empyema
= pus-filled collection in the pleural space.
Seen especially in streptococcus pneumonia
130
Complications of pneumonia - lung abscess
= pus-filled collection in the lung parenchyma
Seen especially in Staph. aureus pneumonia.
131
When should you suspect lung abscess/empyema?
if there is a persistent swinging pyrexia and rising CRP despite treatment.
132
characteristics of Mycobacterium tuberculosis
an aerobic bacillus:
Non-motile
Cell envelope which resists gram staining.
Known as “acid fast bacilli” or AFBs
Very slow growing.
133
In which groups in the UK is TB particularly common?
immigrant ethnic groups,
the socially disadvantaged,
HIV +,
Londoners
134
How is TB transmitted?
The person with pulmonary TB can cough and expel infectious droplets. Infectious particles can remain suspended in the air for several hours and inhaled aerosolised droplets lodge in the alveoli.
135
What are factors that determine the probability of TB transmission?
Susceptibility of exposed person - e.g. HIV+
Infectiousness - number of bacilli expelled into the air
Environment - e.g. enclosed spaces
Exposure - proximity, frequency, duration
136
Primary TB infection
occurs when a non-immune host (never met TB before) is exposed to M. tuberculosis
137
The process of primary TB infection
1. TB containing droplets reach the alveoli and are taken up by macrophages
2. If macrophages fail to kill TB, primary infection occurs.
=> TB bacilli then slowly multiply inside the macrophages.
=> macrophages can carry TB to local lymph nodes or further around the body.
=> granulomatous lesions beginning to develop in the lungs.
3. At this point a complex interplay between host and bacteria occurs to determine whether active or latent disease occurs.
=> Factors such as number of TB bacteria inhaled and whether the host is immunocompetent.
138
When do the caseating granulomas of TB develop?
The tissue reaction in the lungs and lymph nodes changes to form caveating granulomas ~1-2 weeks after infection.
139
Latent TB infection
LTB occurs when the host defences are able to contain the TB infection.
Over around 2-6 weeks the adaptive immune response kicks in and and a granuloma forms to contain the TB infection.
The TB within the granuloma is DORMANT, therefore, latent TB can always be reactivated
but people with LTB do not have active disease and are not infectious
140
Post-primary TB infection
occurs when latent TB becomes reactivated.
This may stay local or spread to more distant sites, causing extra-pulmonary TB.
Cavities and progressive lung destruction lead to cough and systemic symptoms (patient is infectious again)
141
Which people are at a higher risk of TB reactivation?
Untreated HIV+
Immunosuppressed for other reasons – e.g. long-term steroids, organ transplant.
Comorbidities – e.g. diabetes and CKD
Aging
142
% risk of LTB reactivation
LTB + no risk factors – 10% risk of reactivation over lifetime
LTB + untreated HIV – 7-10% risk of reactivation per year.
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Investigating TB
1. Culture:
=> Pulmonary TB – several sputum samples (at least one in early morning) to look for acid fast bacilli down the microscope and then culture.
=> PCR if rapid diagnostic results required or suspected MDR-TB
=> Culture is gold-standard test but takes 6 months.
=> Non-Pulmonary TB – a sample from the suspected site to culture
2. Histology – classically will find caseating granuloma
3. Imaging
=> CXR – different findings for primary, latent and post-primary, but also significant overlap!
144
CXR in Primary TB
Caseating granulomas/Ghon focus
=> These represent healing of a primary TB infection.
Lobar or patchy consolidation
Effusions and regional lymphadenopathy
145
Ghon focus and complex
Calcified caseating granulomas
if seen with regional lymphadenopathy then called Ghon complex
146
miliary TB
where the TB spreads rapidly though the body
looks like ‘Millet seeds’ on CXR
more common if immunosuppressed
147
CXR in Post-primary TB
characterised by:
- necrosis and cavitation formation
- Progressive lung destruction
Cavities now tend to be apical (more oxygen).
148
CXR in latent TB
Should be normal!
Very occasionally a few nodules.
There should be no signs of active TB disease.
149
When would you investigate for Latent TB?
close contacts of active TB patient (contact tracing);
someone who has come from a high incidence TB country
150
How do you investigate for latent TB?
Mantoux test/tuberculin skin test
=> can get false positives if prior BCG vaccine or false negatives with HIV infection
Interferon-gamma release assay (IGRA) test
=> no false negatives with HIV or cross reaction with BCG
Positive results should lead to assessment for active TB (as these tests cannot differentiate between active/latent disease). If no evidence of active TB, treat as latent TB.
151
Presentation of pulmonary TB
Cough
Haemoptysis
Fever
Systemic symptoms – night sweats, weight loss, fatigue.
152
Presentation of extra-pulmonary TB
Common sites include the larynx, pleura, brain, kidneys and bone.
Presentation varies, as it depends on the site
153
Management of active TB
Therapy consists of 6 months of treatment, which can be divided into:
1. “bactericidal” phase in which the majority of organisms are killed = four drugs for two months
2. “sterilising” phase in which persisting organisms are eliminated = two drugs for four months.
Standard therapy in the UK (BTS 1998) is:
1. Rifampicin, isoniazid, pyrazinamide and ethambutol given for a two-month period.
2. Followed by Rifampicin and isoniazid for four months.
154
What is given as a supplement with isoniazid?
given with pyridoxine supplements to prevent peripheral neuropathy.
155
Why is combination therapy essential in treating active TB?
Mycobacteria mutate to develop single drug resistance.
in a bacillary population of sufficient size, single drug therapy will always select resistant organisms.
156
Management of latent TB
Isoniazid for 6 months
OR
Rifampicin and Isoniazid for 3 months
157
TB resistance / MDR TB
The most common drug resistance in the UK is isolated Isoniazid resistance, with rifampicin being the marker for multi-drug resistant TB
158
Who is at risk of MDR TB?
Individuals previously treated for TB
Known contact with a case of drug resistant TB
Acquisition of infection in a country or group with high prevalence of drug resistance (e.g. Tanzania).
Patients who fail to make a satisfactory response to adequate conventional treatment
Co-existing HIV infection
159
What is bronchiectasis?
a disease involving inflammation which causes permanent dilation of the subsegmental airways (bronchi and bronchioles)
leads to a build-up of excess mucous.
160
How is there a two-fold effect of deadspace created in bronchiectasis?
1. The damage will significantly reduce the surface area to volume ratio.
2. Airways become filled with secretion, so less oxygen can reach the alveoli.
161
What are the types of bronchiectasis?
Cylindrical (most common)
Varicose
Cystic (most severe, least common)
162
Cylindrical bronchiectasis
airways are widened, but structure tends to be the same
163
Varicose bronchiectasis
architecture is also damaged as well as widened ariways
164
Cystic bronchiectasis
development of out-pouches/bulges, which can impinge on healthy airways
165
Vicious cycle hypothesis of bronchiectasis
an initial insult leads to the start of the chain reaction of:
```
Respiratory tract infection
&
Bronchial Inflammation
&
Respiratory tract damage
```
166
What can be the initial insult of bronchiectasis?
Congenital (e.g. CF)
Infective (viruses, bacteria, fungi)
Obstruction (e.g. COPD, tumours, foreign bodies, irritants)
Other (e.g. Idiopathic)
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Long-term consequences of bronchiectasis
Recurrent pneumonia
Pleural effusions – accumulated inflammatory transudate.
Secondary pneumothorax
Massive haemoptysis – larger vessel eroded by chronic disease
Right heart failure – increased pulmonary resistance.
Rarely – cerebral abscess and amyloidosis
168
Typical Presentation of bronchiectasis
Shortness of Breath
Fatigue
```
Copious amounts (“cupfuls”) of sputum, sometimes with blood.
=> Productive cough
```
Previous infection/history of lung disease – e.g. pneumonia
169
Atypical Presentation of bronchiectasis
Idiopathic bronchiectasis – no history of lung disease.
Dry bronchiectasis – no excessive sputum production
COPD-bronchiectasis overlap
170
What is the difference between the early stages of COPD and bronchiectasis?
COPD is a functional/physiological diagnosis – due to poor reversible airflow obstruction.
Bronchiectasis is a structural diagnosis – presence of airway dilatation on CT
=> initially restrictive due to widening of airways,
=> then obstructive as airways fill up with fluid/mucous,
=> eventually mixed deficit towards the advanced stages of disease
171
Bronchiectasis - on examination
Acute signs:
- Rronchi (loud expiratory wheezing)
- Mid-inspiratory squeaks
- Coarse crackles
Chronic signs – maybe acute signs, but also potentially:
- Generalised wheezing
- Clubbing
- RHF (raised JVP, oedema)
172
Bronchiectasis - investigations
Routine bloods – FBC, U&E, CRP, coagulation.
Sputum Microbiology – identify causative or propagating organism
=> Treat with broad spectrum initially, target once known.
=> If negative, consider fungal infection.
CXR
=> ?pneumonia, ?effusion,
=> might see some bronchial thickening,
Pulmonary function tests – will show obstructive picture (FEV1/FVC <0.7)
173
What would a high resolution CT scan of a patient with bronchiectasis show?
Signet ring pattern
174
Restrictive Lung Disease
= physical reduction in potential maximum lung volume
Can be:
- A problem of compliance – e.g. fibrosis
- An increase in dead space – e.g. effusion, pus
175
Obstructive lung disease
= increased effort to reach near-normal lung volume, due to narrowing of airways
Can be:
- obstruction of large airways – asthma, COPD, bronchitis
- obstruction of small airways – bronchiolitis, bronchiectasis
176
What is FEV1?
| What is considered normal?
= the volume exhaled in the first second after deep inspiration and forced expiration
Normal is >80%
177
What is FVC?
| What is considered normal?
= the total volume of air that can be forcibly exhaled in one breath from maximal inhalation
Normal is >80%
178
What is FEV1/FVC?
| What is considered normal?
a ratio used to identify restrictive/obstructive deficit.
Normal is >70%
179
Spirometry in obstructive lung disease
FEV1 <80%
FVC >80%
FEV1/FVC <0.7
180
Spirometry in restrictive lung disease
FEV1 <80%
FVC <80%
FEV1/FVC >0.7 (i.e. normal)
181
What causes non-lung related restrictive deficit?
Pregnancy, obesity, kyphoscoliosis
182
What is pulmonary fibrosis?
a condition in which there is diffuse scarring of the lung parenchyma
183
Focal pulmonary fibrosis
The occupational Lung Diseases (OLD)
| => affects lymphoid tissue
184
Interstitial pulmonary fibrosis
Extrinsic Allergic alveolitis
| => affects parenchyma
185
Replacement pulmonary fibrosis
RA, TB, connective tissue disorders
| => direct damage due to disease
186
Apical pulmonary fibrosis
| A TEA SHOP
```
Allergic Bronchopulmonary Aspergillosis
Tuberculosis
Extrinsic allergic alveolitis
Ankylosing Spondylosis
Sarcoid
Histiocytosis
Occupational (berylliosis, silicosis)
Pneumoconiosis
```
187
Basal pulmonary fibrosis
| DR CIA
```
Drugs
Rheumatoid Arthritis
Connective Tissue Disease
Idiopathic Pulmonary fibrosis
Asbestosis
```
188
Which drugs can cause pulmonary fibrosis?
amiodarone, bleomycin, busulfan, methotrexate, vincristine, nitrofurantoin
189
Which occupational lung diseases cause direct fibrosis?
Berylliosis – beryllium inhalation
Silicosis – silica/silicon inhalation
Asbestosis – asbestos inhalation
190
Which occupational lung diseases cause extrinsic allergic alveolitis?
Pigeon Fancier’s Lung – Bird dander/droppings
Farmer’s Lung – hay/crop mould
Malt worker’s lung – hop moulds
Hot tub lung – M. avium from hot tub mist.
Saxophonist’s lung – mixed fungi from uncleaned instruments
191
Pulmonary fibrosis - investigations
Bloods:
• ABG
• CRP
• Special tests
Imaging:
• CXR – reduced lung volume
• CT – classic signs of fibrosis: honeycombing.
Spirometry – restrictive deficit.
Lung biopsy – to assess for any fibrotic change ONLY if the CT scan and other tests are equivocal and diagnosis is uncertain.
192
what does pulmonary fibrosis look like on a high resolution CT?
Honeycombing
193
Prognosis of pulmonary fibrosis
Condition is progressive and life-limiting - prognosis is poor if untreated.
Treatment depends on the cause, and is often very limited.
Lung transplants can be done, but there is still risk of developing fibrosis in the new lung.
194
What are the three main buffering systems for H+ in the body?
1. Intra- and extracellular buffers
2. Ventilation
3. Renal regulation of H+ and HCO3-
195
How does the body deal with an excess of H+?
buffers can combine with H+ to reduce levels
ventilation can increase to excrete CO2
Excreting H+ as free hydrogen ions or in phosphate/ammonia buffers
196
What pH is acadaemia and what pH is alkalaemia?
<7.35 is acidaemic
| >7.45 is alkalaemic
197
Steps to interpreting an ABG
1. How is the patient?
2. Assess oxygenation
3. Determine the pH
4. Determine the respiratory component
5. Determine the metabolic component
6. Is there any evidence of compensation?
7. Base excess
198
What should oxygenation on an ABG be?
PaO2 should be >10kPa on air, or
PaO2 should be ~10kPa less than the % inspired concentration.
199
What would respiratory acidosis look like on an ABG?
acidaemic
| PaCO2 >6
200
What would respiratory alkalosis look like on an ABG?
alkalaemic
| HCO3- >26
201
What does base excess look like on an ABG?
Negative in metabolic acidosis
| Positive in metabolic alkalosis
202
What is base excess?
the theoretical amount of acid needed to bring a patient’s fully oxygenated blood to normal pH at room temperature
203
Respiratory Acidosis
Decrease in gaseous exchange leading to retention of CO₂
High PCO₂ leads to renal retention of bicarbonate to buffer excess H⁺
Compensation by the kidneys results in an increase in secretion of H⁺ over 3-5 days leading to increase in plasma bicarbonate level
204
Causes of respiratory acidosis
Drugs e.g. morphine and sedatives
Stroke
Infection
Asthma
COPD
Pneumoconiosis
Bronchitis
Acute respiratory distress syndrome (ARDS)
Poliomyelitis
Kyphoscoliosis
Myasthenia gravis
Muscular dystrophies
Obesity
Hypertension
205
Respiratory Alkalosis
Alveolar hyperventilation leads to excess exhalation of CO₂, resulting in low PCO₂
Compensation by the kidneys results from decreased ammonium (NH₄⁻) excretion, leading to a fall in bicarbonate
206
Causes of respiratory alkalosis
```
Pain, anxiety, psychosis
Fever
Cerebrovascular accident/stroke
Meningitis/encephalitis
Trauma
```
```
High altitude
Pneumonia
Pulmonary oedema
Aspiration
Severe anaemia
```
Pregnancy, progesterone
Salicylates
Haemothorax, flail chest
Cardiac failure, PE
Septicaemia
Mechanical hyperventilation
Hepatic failure, heat exposure
207
Metabolic Acidosis
Results from the body producing too much acid or the kidneys failing to excrete enough H⁺.
Initially this creates a decrease in bicarbonate as carbonic acid is produced to buffer the H⁺
The lungs compensate by hyperventilation and blowing of the CO₂
The anion gap can be used to differentiate causes – if gap is normal, bicarbonate is being lost either by GI loss (e.g. diarrhoea) or renal disease allowing loss.
High anion gap results from increased production of acids (e.g. lactic acid, urate or diabetic ketoacidosis) or large amounts of acid (e.g. aspirin overdose)
208
Causes of metabolic acidosis
HIGH anion gap
Lactic acidosis
Ketoacidosis – diabetic, alcohol abuse, starvation
Renal failure – acute/chronic
Toxins – e.g. methanol, salicylates
NORMAL anion gap
Bicarbonate loss from GI tract
Renal acidosis (proximal/distal tubular acidosis)
Drug-induced (NSAIDs, ACEi, spironolactone, etc)
Rapid saline infusion
209
Metabolic Alkalosis
Results from increased bicarbonate due to either decreased H⁺ concentration (e.g. due to vomiting) or a direct increase in bicarbonate.
Bicarbonate shift can occur from retention, an intracellular shift in H⁺ or by ingestion of large amounts of alkali (e.g. antacids).
The lungs compensate by slower breathing to retain more CO₂
210
Causes of metabolic alkalosis
```
Milk-alkali syndrome
Vomiting
Nasogastric suction
Villous adenoma
Hypercalcaemia
Recovery from lactic acidosis/ketoacidosis
High renin – renal artery stenosis
Accelerated hypertension
Aldosteronism
Cushing’s Syndrome
Steroids
```
211
ABG - type 1 respiratory failure
PaO2 <10
| PaCO2 <6
212
ABG - type 2 respiratory failure
PaO2 <10
| PaCO2 >6
213
Respiratory History - Dyspnoea
When did it start?
Sudden or gradual?
How long has this been going on for?
can they speak in full sentences?
Is it impacting on day-to-day activities?
How far can they walk?
Does it fluctuate?
Does anything make it better or worse?
214
Respiratory History - specific PMH
Asthma/COPD or other respiratory conditions
Hx of atopy
Recurrent chest infections in childhood
215
Respiratory History - relevant drug history
Inhalers – reliever/preventer
Beta-blockers/NSAIDs – bronchoconstriction
ACE inhibitors – dry cough
Cytotoxic agents – interstitial lung disease
Oestrogen – increased risk of PE
Amiodarone/methotrexate – pleural effusions/ interstitial lung disease
216
Respiratory History - relevant family history
e.g. asthma / atopy / lung cancer / CF
217
How many cigarettes are 1 pack year?
20 cigarettes/day
218
Respiratory History - social history
Smoking status - current/past/never
Alcohol
Illicit drugs - cannabis increased risk of lung cancer
```
Employment - occupational lung disease
Hobbies pets (e.g. bird fancier disease)
```
Overseas travel - long haul flights (PE), TB risk
Ability to complete activities of daily living (ADL)
219
What type of cells line the respiratory tract normally?
Columnar epithelial cells
220
How will emphysema appear histologically?
there will be loss of the solid architecture (“moss eaten” appearance)
also unequal size and enlargement of the alveoli (due to dilatation).
221
What is the difference between congenital and functional alpha1-antitrypsin deficiency?
Congenital - gene defect causes inactivation of antiproteiases
Functional - Smoking causes reactive oxygen species/free radicals, which cause inactivation of antiproteases
222
Saddle embolism
a large pulmonary embolism that straddles the bifurcation of the pulmonary trunk extending to the left and right pulmonary arteries
223
What pathogens tend to cause interstitial pneumonia?
The atypical organisms
SARS coronaviruses
224
What is the most likely organism causing pneumonia in a previously healthy individual?
S. pneumoniae
225
What is the most likely organism causing pneumonia in pre-existing viral infection?
Staph. aureus or S. pneumoniae
226
What is the most likely organism causing pneumonia in COPD?
Haemophilus influenzae or S. pneumoniae
227
What is the most likely organism causing pneumonia in HIV+?
Pneumocystis carinii, cytomegalovirus, TB
228
What is the most likely organism causing pneumonia in Cystic Fibrosis?
Pseudomonas, Berkholderia species
229
What is the most likely organism causing pneumonia in a child?
Haemophilus influenzae
230
What is the most likely organism causing pneumonia in someone who also has a maculopapular skin rash in their extremities?
Mycoplasma pneumoniae
| extra-pulmonary manifestations are common
231
What is the most likely organism causing pneumonia developed during hospital admission?
E. coli, Klebsiella spp., proteus spp., S. pneumoniae, S. aureus (MSSA or MRSA).
232
what is a the lead time between asbestos exposure and development of mesothelioma?
normally >20 years
233
which sites does mesothelioma most commonly spread to from the pleural cavity?
other pleural cavity
lung
hilar lymph nodes
234
what type of room is best to prevent the spread of airborne microbes?
negative pressure isolation room
235
What is a cavitating lung mass?
| what are the causes?
= gas-filled spaces surrounded by consolidation, a lung mass or nodule.
Causes:
- bacterial lung abscess
- metastatic squamous cell carcinoma
- granulomatosis
- pulmonary infarct
236
what organisms may cause a caveatting lung abscesS?
anaerobic spp.
| mycobacterium tuberculosis
