Longen Flashcards
1
Q
What is the differential diagnosis for an intrapulmonary mass on a CXR?
A
1) lung cancer
2) TB
3) abscess
4) foreign body
5) pulmonary hamartoma
2
Q
Chronic bronchitis definition
A
defined clinically
cough with sputum production on most days for 3 months over 2 successive years.
3
Q
Emphysema definition
A
defined histologically as enlarged air spaces distal to terminal bronchioles, with destruction of alveolar walls.
4
Q
Obstructive Sleep Apnoea
A
Recurrent episodes of partial or complete upper airway obstruction during sleep, causing intermittent hypoxia and sleep fragmentation
5
Q
Obstructive Sleep Apnoea Syndrome
A
apnoea with daytime somnolence (sleepiness)
6
Q
Mechanism of Obstructive Sleep Apnoea Syndrome
A
pharynx narrows, creating negative airway pressure due to the airway closure
this causes cessation of air flow, which leads to sleep disruption and arousal
Results in: o Fragmented sleep o Daytime sleepiness o BP surge - increased risk of stroke/heart attack o Reduced QOL o RTA if untreated
7
Q
Obstructive Sleep Apnoea investigations
A
Limited Polysomnography (Limited Sleep Study) o home study. Looks at: Oxygen Saturations Heart Rate Flow (through nose and mouth) Thoracic and Abdominal effort Position
FULL POLYSOMNOGRAPHY
• Inpatient investigation
8
Q
Apnoea
A
the (near) complete cessation of airflow
4% oxygen desaturation, lasting ≥ 10 secs
9
Q
Hypopnoea
A
a reduction of airflow to a degree insufficient to meet the criteria for an apnoea
10
Q
Apnoea-Hypopnoea Index (AHI)
A
Determines how many events patients are having per hour
• AHI ≥15 is diagnostic of OSA
11
Q
Factors predisposing to OSA
A
High BMI
underlying conditions - tonsils, hypothyroidism, nasal obstruction
triggering factors - alcohol
age
male gender
12
Q
OSAS treatment
A
- Explain OSAS
- Weight loss
- Avoid triggering factors - alcohol
- Treat underlying conditions - tonsils, hypothyroidism, nasal obstruction
CPAP
13
Q
Untreated OSAS
A
Most common presentation – hypertension that is refractory to anti-hypertensives
Cardiovascular disease
Increased risk of CVA
o Increased accidents at work/poor concentration
o 4 times more likely to have a RTA (must inform DVLA)
14
Q
Why does pneumothorax cause lung collapse?
A
Any breach of the pleural space leads to collapse of the elastic lung because there is loss of the negative pressure required for inspiration
15
Q
pneumothorax
A
Air within the pleural cavity
16
Q
types of pneumothorax
A
1) Traumatic - penetrating/blunt injury
o Stabbing
o Fractured rib
2) Iatrogenic
o lung biopsy
o pleural aspiration
3) Spontaneous - no preceding trauma/event
o Primary
Classically happens in tall, thin young men with apical surface blebs. No underlying lung disease
o Secondary
underlying lung disease (e.g. COPD, cystic fibrosis)
bullae may rupture
17
Q
Tension pneumothorax
A
‘One way valve’ leads to increased intrapleural pressure (exceeds atmospheric pressure)
Venous return impaired, cardiac output and blood pressure fall
Patients become hypoxic and hypotensive
18
Q
Where would you insert a chest drain to relieve the pressure of a tension pneumothorax?
A
2nd intercostal space midclavicular line
19
Q
Pneumothorax risk factors
A
Smoking
male gender
height
• Underlying lung disease (secondary)
20
Q
primary pneumothorax pathophysiology
A
Spontaneous rupture of subpleural blebs leads to tear in visceral pleura
Air flows from airways to pleural space (down the pressure gradient)
Elastic lung then collapses
21
Q
signs and symptoms of pneumothorax
A
Pleuritic chest pain
Breathlessness (can be minimal if primary)
Respiratory distress (especially if secondary)
Reduced air entry on affected side
Hyper-resonance to percussion
barrel chest
Reduced vocal resonance
Tracheal deviation if tension (+/- circulatory collapse)
22
Q
Differential diagnosis: pneumothorax
A
PTE, musculoskeletal pain, pleurisy/ pneumonia
23
Q
Pneumothorax management
A
Primary spontaneous pneumothorax may be treated conservatively if symptoms are minimal
- Observation (serial CXR) - can be as outpatient
Secondary pneumothorax more frequently requires treatment by aspiration or intercostal chest drain (ICD)
Tension pneumothorax ALWAYS requires ICD insertion
If not resolved by a chest drain within 5-7 days, consider surgical intervention
24
Q
After a spontaneous pneumothorax has resolved on CXR, how long should the patient wait before flying?
A. ≥ 7 days
B. ≥ 14 days
C. ≥ 28 days
A
≥ 7 days
If there is residual air in the pleural space, as they ascend and descend the air can expand and contract –> increased risk of recurrence
25
After a spontaneous pneumothorax has resolved on CXR, how long should the patient wait before diving?
A. ≥ 2 weeks
B. ≥ 6 weeks
C. should not dive again
should not dive again
With a spontaneous pneumothorax, there is at least a 30% risk of recurrence because there is probably an ongoing pathological process that can predispose to further pneumothoraxes
The pressures on scuba diving are far greater than those on flying
26
Spirometry
Forced expiratory manoeuvre from total lung capacity to residual volume, followed by a full inspiration
Most common pulmonary function test
method of differentiating between obstructive airways disorders and restrictive diseases
27
What is the most effective way of determining the severity of COPD?
spirometry
28
which limb of the Flow/ Volume Loop is effort dependent?
Inspiratory limb
Expiratory limb is effort independent - Relies on the elastic recoil of the lung
29
why does air trapping occur?
Expiration is effort independent.
If you increased the pressure outside the lungs, it leads to dynamic airway collapse
no matter how hard you squeeze, you can’t get more air out
30
What is considered to be a "normal" FEV1?
FEV1 of 85% predicted may be considered “normal”
31
Obstructive lung disease on pulmonary function tests
FEV1/FVC ratio <70% (0.7)
FVC is relatively well preserved, but they only manage to get it out very slowly – i.e. there is obstruction to air flow, i.e. decreased FEV1
“church and steeple pattern” on flow/volume loop
32
How do you determine COPD severity?
The severity of COPD is stratified by percentage predicted FEV1
– mild > 80%
– moderate 50-80%
– severe 30-50%
– very severe <30%
33
Reversibility testing
Nebulised or inhaled salbutamol is given
Spirometry is measured before and 15 minutes after salbutamol
15% change AND 400ml reversibility in FEV1 are suggestive of asthma
34
restrictive lung disease on pulmonary function tests
* Both FEV1 AND FVC are reduced
* FEV1/ FVC ratio >70% (normal)
* Flow/volume and volume/time loops appear normal but smaller (absolute volume reduction)
35
Causes of restrictive lung disease
– Interstitial lung disease
– Kyphoscoliosis/ chest wall abnormality
* Neuromuscular disease – GBS, polymyositis
* Obesity – one of the more common causes
36
Transfer factor
measure of gas exchange in the lungs
Anything that impacts gas exchange will cause a low transfer factor
Give px single breath of very low [carbon monoxide]
CO has very high affinity to Hb
Measure concentration in expired gas to derive uptake in the lungs
37
Name 4 things that will caused a reduction in transfer factor
– Emphysema
– Interstitial lung disease
– Pulmonary vascular disease
– Anaemia (increased in polychthaemia)
38
Oximetry
Non-invasive measurement of saturation of haemoglobin by oxygen
NB: Depends on adequate perfusion
– Not accurate in shock or cardiac failure
Does NOT measure carbon dioxide, so therefore no measurement of ventilation
39
Main causes of Hypoxaemia
Ventilation/ perfusion mismatch (eg COPD, pneumonia)
Hypoventilation (eg drugs, neuromuscular disease)
Shunt (eg congenital heart disease)
Low inspired oxygen (altitude, flight)
40
Ventilation & perfusion
Ventilation refers to the movement of gas into and out of alveoli.
Perfusion refers to the flow of blood through the pulmonary capillaries.
must be matched for efficient gas exchange.
41
Alveolar oxygen equation
The difference between the calculated alveolar pO2 and the arterial pO2 is the alveolar arterial (A-a) oxygen gradient
Difference between alveolar and arterial oxygen partial pressures should be <2-4 kPa
more than this suggests V/Q mismatch
42
Hypoxemic respiratory failure (type I)
* failure of oxygen exchange (perfusion problem)
* generally caused by V/Q mismatch
* characterized by PaO2 < 60 mmHg
* normal PaCO2
e.g.
o pulmonary oedema
o pneumonia
43
Hypercapnic respiratory failure (type II)
* failure to remove CO2
* generally caused by problems with ventilation
* characterized by a PaCO2 > 50 mmHg.
* Hypoxemia is common
Common causes include:
o drug overdose
o neuromuscular disease
o chest wall abnormalities
Remember: type 2 has 2 problems: low O2 AND high CO2 = HYPOXIA + HYPERCAPNIA
44
acute respiratory failure
characterized by life-threatening derangements in arterial blood gases and acid-base status
o develops over minutes to hours
o pH is less than 7.3
45
chronic respiratory failure
manifestations are less dramatic
develops over several days or longer, allowing time for renal compensation and an increase in bicarbonate concentration.
Therefore, the pH usually is only slightly decreased.
46
Blood gas analysis (respiratory perspective)
Always look at the pO2 first
– Is the patient in respiratory failure requiring additional oxygen?
Then look at the PCO2 (type 1 vs type 2 respiratory failure)
– High in type 2 respiratory failure
Then consider acid base balance
Acute respiratory acidosis
– elevated pCO2
– normal bicarbonate
– acidosis
Compensated respiratory acidosis
– elevated pCO2
– elevated bicarbonate (renal compensation)
– not acidotic
47
What type of respiratory failure does cardiac failure cause?
type 1
48
What type of respiratory failure does pneumonia cause?
type 1
49
What type of respiratory failure does severe fatigue cause?
type 2
50
What type of respiratory failure does pulmonary embolism cause?
type 1
51
What is the appearance of emphysematous lungs on CXR?
emphysema causes hyperinflation – lungs appear bigger on CXR
```
CXR features:
• >9 posterior ribs above the diaphragm
• >6 anterior ribs above the diaphragm
• Heart looks long and thin because the lung volume has increased
• Hemidiaphragms are flat
```
• lungs are blacker due to loss of lung tissue
52
What level of oxygen therapy is recommended for patients with hypercapnic tendency?
24-28% oxygen is usually recommended
patients with hypercapnic tendency will become more hypercapnic and drowsy if you give them too much oxygen
aim for SpO2 88–92 % (targeted oxygen therapy)
Over 92% - higher risk for developing hypercapnia
53
How do you treat COPD exacerbation?
Remember: ONAP
* Oxygen
* Nebulised bronchodilators
* Antibiotics
* Prednisolone
54
pCO2 high and the HCO3 low
respiratory acidosis and metabolic acidosis
55
pCO2 low and the HCO3 high
respiratory alkalosis and metabolic alkalosis
56
NON-INVASIVE VENTILATION IN COPD
Provides positive pressure to the airways to support breathing
* Reduces respiratory rate
* Improves dyspnoea and gas exchange
* Lowers mortality
* Reduces need for ventilation in ITU
* Reduces length of hospital stay
57
COR PULMONALE
Clinical syndrome of:
• Right heart failure secondary to lung disease
• Salt and water retention leading to peripheral oedema
treat with diuretics and oxygen therapy
58
signs of cor pulmonale
* Peripheral oedema
* Raised jugular venous pressure
* A systolic parasternal heave
* Loud pulmonary second heart sound
59
Chronic Obstructive Pulmonary Disease (COPD) Definition
• COPD is characterised by airflow obstruction.
The airflow obstruction is:
• usually progressive
• not fully reversible
• does not change markedly over several months.
60
Chronic Bronchitis
defined clinically
production of sputum on most days for at least 3 months in at least 2 years
affects the larger airways > 4mm
inflammation leads to scarring and thickening of airways
61
Emphysema
abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles
defined histologically
62
Bronchiolitis
small airways disease
narrowing of the bronchioles due to:
• mucus plugging
• inflammation
• fibrosis
63
Effects of Cigarette Smoking on the lungs
damages cilia, causing decreased motility and decreased mucous clearance. This predisposes to infections and neutrophilic infiltration -> decreased lung function
goblet cell hyperplasia -> chronic cough
Activation of proteases and inactivation of antiproteinases -> tissue destruction
Free radicals
Squamous metaplasia
64
Mechanisms of Airflow Obstruction in COPD
smoking & inflammatory response destroy interstitial tissue -> loss of elasticity
airways collapse on expiration -> causes air trapping and hyperinflation
Goblet cell metaplasia with mucus plugging of lumen
Thickening of the bronchiolar wall due to inflammation
65
Diagnosis of COPD
Consider the diagnosis of COPD for people who are:
◦ over 35
◦ smokers or ex-smokers
```
with any of:
exertional breathlessness
chronic cough
regular sputum production
frequent winter ‘bronchitis’
wheeze
```
66
Treatment of COPD
Remember: ABCS + oxygen
A - anticholinergics (muscarinic agonists: tiotropium)
B - bronchodilators (SABA: salbutamol; LABA: salmeterol)
C - Inhaled Corticosteroids (Budesonide and fluticasone – combination inhalers)
S = smoking cessation
Oxygen therapy for patients with very severe lung disease
67
phenotypes of end-stage COPD
Blue Bloater
| Pink Puffer
68
Blue bloater
chronic bronchitics
cyanosis
warm peripheries
bounding pulse due to hypercapnia
flapping tremor
confusion, drowsiness – due to raised CO2
right heart failure - due to chronic pulmonary HTN
Oedema, raised JVP
low respiratory drive, loss of sensitivity to CO2
Type 2 respiratory failure - ↓PaO2, ↑PaCO2,
Become more hypercapnic with oxygen therapy
cyanosed but not breathless
69
Pink Puffer
Emphasematous patients
high respiratory drive
Type 1 respiratory failure - ↓PaO2
pursed lips – improve efficiency of breathing
use accessory muscles – stabilise the chest wall to make breathing more efficient
wheeze
indrawing of intercostals
tachypnoea
Breathless but not cyanosed
70
inflammatory processes in COPD vs asthma
asthma
- mainly eosinophilic
- CD4+ T lymphocytes
COPD
- neutrophilic
- increased numbers of macrophages and CD8+ T lymphocytes.
71
SARCOIDOSIS
multisystem inflammatory disease of unknown aetiology
predominantly affects the lungs and intrathoracic lymph nodes
characterised by non-necrotising granulomatous inflammation
diagnosis of exclusion
72
What kind of inflammation is typically seen in sarcoidosis?
non-necrotising granulomatous inflammation
73
What are Asteroid bodies?
filaments of cytokeratin
only ever see asteroid bodies in relation to sarcoidosis
74
causes of Pulmonary Fibrosis
* Smoking
* Radiation
* RA
* Idiopathic
* Drug Induced – Amiodarone, Nitrofurantoin, Methotrexate, Cocaine
75
Usual Interstitial Pneumonia (UIP)
used interchangeably with idiopathic pulmonary fibrosis (IPF)
form of interstitial lung disease characterized by progressive fibrosis (scarring) of both lungs.
76
Radiological features of idiopathic pulmonary fibrosis
* PERIPHERAL Interstitial pattern of fibrosis
| * Subpleural honeycombing
77
symptoms of idiopathic pulmonary fibrosis
* Breathlessness (worse with exercise)
* Hacking dry cough
* Fatigue and weakness
* Appetite and weight loss
* Clubbing
78
diagnosis of idiopathic pulmonary fibrosis
High-resolution CT (HRCT) - honeycombing
If classical signs are not seen on HRCT, then the patient will have Video-Assisted Thoracoscopic Surgery (VATS)
• Used to biopsy the lung
79
pathophysiology of idiopathic pulmonary fibrosis
Unknown
Theory that free radicals perpetuate damage and fibrosis
progression of fibroblast proliferation leads to scar tissue formation = fibroblast focus
collagen gets laid down (irreversible damage) --> progressive breathlessness
80
Extrinsic Allergic Alveolitis (EEA)
= Hypersensitive Pneumonitis (HSP)
Delayed allergic response (type III & IV hypersensitivity)
lungs develop immune response (hypersensitivity) to something inhaled -> inflammation of the lung (pneumonitis)
Body generates antibodies (sensitisation) against trigger
Repeat exposure causes immune complexe formation
-> deposit in kidneys and small capillaries of the lungs
Immune complexes activate complement -> destruction of the lungs; sets up a process of remodelling/repair -> fibrosis and emphysema
Non-necrotizing granulomatous inflammation can occur
81
Differentiation between sarcoidosis and EEA
Both have non-necrotising granulomatous inflammation in the lung
The difference is that in sarcoidosis the inflammation (and thereby the granulomas) is in the interstitium alone
In hypersensitive pneumonitis, the inflammation is in the alveolar air spaces
• This is because the allergen is being inhaled, and it stays in the air spaces, therefore this is where the inflammatory reaction occurs
82
Which form(s) of lung cancer are most closely linked to smoking?
squamous and small cell lung cancer
83
Risk factors for lung cancer
* smoking
* Environmental tobacco smoke
* Ionising radiation
* Air pollution
* Asbestos
84
Signs and Symptoms of Lung Cancer
* Cough
* Haemoptysis
* Shortness of Breath
* Chest pain
* Weight loss/Anorexia
* General malaise
NB: There will be different symptoms depending on where the tumour is
85
symptoms of central lung tumours
Central tumours arise in and around hilus of the lung (carina and main airways) and are usually squamous or small cell carcinomas
Haemoptysis – more likely to invade into blood vessels if central
Bronchial obstruction
SOB
retention pneumonia – secretions will be retained behind site of obstruction, and this can be superimposed by infection
Cough
86
symptoms of peripheral lung tumours
predominantly adenocarcinomas
probably few symptoms as the main airways and blood vessels are unaffected
Pain if pleura or chest wall involved
may be picked up on routine CXR
87
symptoms of SVC obstruction by a tumour
o Oedema of face and arms
o Raised JVP
o Dilated veins on chest wall
o Plethoric face – headache worse on stooping
88
What are 3 possible effects of local spread of a lung tumour?
1) SVC obstruction
2) phrenic nerve paralysis – hemidiaphragm paralysis
3) recurrent laryngeal nerve paralysis - causes hoarse voice
89
Common sites of lung tumour metastasis
Haematogenous spread --> liver, bone, brain, adrenal
Lymphatic spread --> Cervical lymph nodes
90
What are possible non-metastatic effects of a lung tumour?
ACTH secretion -> Cushing's syndrome
ADH secretion -> hyponatraemia due to water retention
PTHrP secretion -> hypercalcaemia
91
What is the most aggressive form of lung cancer?
small cell carcinoma
* Metastasizes early and widely
* Often initial good response to chemotherapy – but most patients relapse
92
Which form of lung cancer is associated with keratinzation and/or intercellular bridges?
squamous cell carcinoma
93
Which form of lung cancer is most commonly seen in females and non-smokers?
adenocarcinoma
94
Which Molecular Target has been Identified in non-small cell lung cancer?
Epidermal Growth Factor Receptor (EGFR) with ALK fusion gene
Chromosomal translocation
Puts the ALK gene right next to EML4 -> leads to a constitutive activation of a tyrosine kinase leading to increased cell proliferation
• Inhibit with Crizotinib
Others:
• Cetuximab
• Erlotinib
95
Which drug can be used to treat PDL1 positive lung tumours?
Nivolumab
PDL1 stops T cells killing tumour cells
Blocking PDL1 stops tumour cells evading the immune system
96
Common sources of metastases to the lung
```
Almost any cancer can spread to the lung but common sites of origin are:
• Breast
• Colorectal
• Kidney
• Head and neck
• Testicular
• Bone (osteosarcoma) – Sarcomas
• Melanoma
• Thyroid
```
97
differential diagnosis for a lung mass on CXR
```
cancer
TB granuloma
abscess
cyst
pulmonary hamartoma
```
98
Mesothelioma
Primary pleural tumour
also occurs in peritoneum, pericardium and tunica vaginalis testis
* Almost always due to asbestos exposure
* Very long lag period before disease develops
Tumour has either an epithelial or sarcomatoid appearance, or a mixture of both (biphasic)
99
atelectasis
lung collapse
100
4 causes of Bilateral Hilar adenopathy (=enlargement of mediastinal lymph nodes)
1) Sarcoidosis
2) Lymphoma
3) TB
4) Malignancy
101
Causes of whiteout of hemithorax
- Pneumonectomy
- Effusion ->Fluid pushes mediastinum away
- Collapse -> creates a space, mediastinal structures move towards it
i.e. in a white lung:
if the mediastinum is pushed to the opposite side it’s a PLEURAL EFFUSION
If the mediastinum is towards the affected side, it’s a PNEUMONECTOMY or a LUNG COLLAPSE
102
What kinds of lung pathology cause a shift of mediastinal structures towards the affected side?
- Collapse
- Post pneumonectomy
- Pulmonary agenesis & hypoplasia
103
What kinds of lung pathology cause a shift of mediastinal structures away from the affected side?
- Pleural effusion
| - Diaphragmatic hernia
104
What kinds of lung pathology cause the mediastinal structures to remain central?
- Consolidation
- Mesothelioma
remember: Consolidation is Central
105
What should you be concerned about with a CXR showing a dark lung with mediastinal shift?
Dark lung with mediastinal shift = pneumothorax until proven otherwise
106
How can a minor change in calibre of the airway lead to airway collapse?
Tiny changes in calibre/radius of the airway leads to massive changes in resistance to air flow
This means that much more pressure needs to be generated to expire air
this pressure causes airway collapse
107
What is allergy?
an immune system mediated intolerance of an external factor
Requires exposure to a specific trigger
108
What is the effect of chronic allergy?
Chronic exposure to allergens leads to changes in structure due to activation of healing and repair pathways (tissue remodelling)
This leads to changes in cells, and scarring/fibrosis in airways
results in a thickened, chronically narrowed airway
that becomes less sensitive to asthma treatments over time
109
hyperreactivity
a normal process that is heightened in some people
the more of the stimulus there is, the bigger the reaction will be
110
effect of allergy on the airways
Increases resistance
Causes wheeze/stridor – turbulence
Due to changes in airway calibre and air flow
Turbulence happens at junctions
Turbulence occurs where the flow is disrupted by asymmetrical narrowing
111
Extrathoracic airway disease
airways held open by cartilage rings e.g. larynx
Disease in this area affects the flow of air in
Not affected by expiration because they are held open by cartilage rings
i.e. not susceptible to changes in intra-thoracic pressure because of the cartilage rings
Disease in these airways affects the flow of air into the lungs
o Disease here causes STRIDOR (inspiratory)
112
Intrathoracic airway disease
Airways are soft and flaccid. Susceptible to intra-thoracic pressure because there are no supportive cartilage rings
o Collapse very easily upon deep expiration
o Disease in this region causes WHEEZE (expiratory)
o These are the airways affected by asthma
o Sputum due to decreased mucous clearance
113
Stepwise management of asthma
Step 1: occasional relief bronchodilator: SABA as required
Step 2: regular inhaled preventer therapy - ICS
Step 3: ICS + LABA. If LABA not working, add one of:
o Leukotriene receptor antagonist
o oral theophylline
Step 4: high-dose ICS + regular bronchodilators - e.g. nebulised therapy, anti-muscarinics
Step 5: regular corticosteroid tablets
114
Clinical Definition of asthma
chronic inflammatory condition of the airways that causes recurrent episodes of:
o Wheezing
o Breathlessness
o chest tightness
o cough
o particularly at night and/or early morning
symptoms are usually associated with widespread but variable bronchoconstriction and airflow limitation that is at least partly reversible
Key Features:
increased airway hyper-responsiveness resulting in episodic bronchoconstriction
inflammation of the bronchial walls
increased mucus secretion
115
Airway pathology in acute severe asthma
Lumen of airways filled with mucous/eosinophils
Thick basement membrane
smooth muscle hypertrophy – infiltrated by MAST CELLS
airway oedema
Destruction of epithelium
116
Diagnosis of asthma
Appropriate clinical history + Supportive physiological tests
- variable peak flow
- Bronchial Hypersensitivity when tested with methacholine
- Reversible Airflow Obstruction: ≥ 15% improvement in FEV1 after 5mg nebulised salbutamol
117
Pleural Effusion
accumulation of abnormal volume of fluid in the pleural space
Normal volume of pleural fluid < 15ml
difficult to detect < 500ml clinically
118
Symptoms of Pleural Effusion
may be asymptomatic
SOB
cough
pleuritic chest pain
119
clinical signs of Pleural Effusion
```
Reduced chest expansion
Reduced tactile vocal fremitus
Stony dull percussion note
Quiet breath sounds
Bronchial breathing above fluid level
Rub with pleural inflammation
```
120
causes of Pleural Effusion
Increased hydrostatic pressure (congestive cardiac failure)
Decreased osmotic pressure (hypoalbuminaemia, e.g. in liver disease/nephrotic syndrome)
Increased vascular permeability (pneumonia) may cause damage to the underlying blood vessels
Decreased lymphatic drainage (mediastinal carcinoma)
121
bilateral pleural effusion
cause is usually obvious
– Usually transudate
– No need to sample initially
– Treat underlying cause (e.g. increase diuretics for heart failure) and repeat imaging
do not drain these patients because fluid will keep on accumulating
122
Unilateral pleural effusion
• Should be investigated
```
Many causes, main causes to think about:
– Infection
– Malignancy
– PTE
– Inflammatory causes
– TB
```
123
Transudate vs Exudate
requires paired serum sample - apply Light's criteria
Transudate:
- protein <30g/L
- LDH <2/3 of upper limit of normal
- often bilateral
- usually clear
Exudate:
- protein >30g/L
- LDH >2/3 of upper limit of normal
- often unilateral
- clear, cloudy or blood stained
124
Common causes of transudate
cardiac failure
nephrotic syndrome
liver cirrhosis
hypoalbuminaemia
125
Common causes of exudate
bacterial pneumonia
TB
malignancy
mesothelioma
126
Investigation procedure for pleural effusion
1) history/exam/CXR
2) aspirate if exudate suspected
3) CT if no diagnosis from aspirate
4) VATS/biopsy if still no diagnosis
127
MANAGEMENT OF LIFE THREATENING ACUTE EXACERBATION OF ASTHMA
High flow oxygen
Nebulised bronchodilators (salbutamol + ipatropium bromide)
Oral prednisolone
Oral doxycycline
IV magnesium
Consider IV aminophylline infusion
128
Anti-muscarinics: Mechanism of Action
Inhibition of cholinergic M1 and M3 receptors in lung
This causes a reduction in cGMP
Result is an inhibition of parasympathetic-mediated bronchoconstriction
129
Side Effects of Anti-muscarinics
Blurred vision, dry mouth, urinary retention
cant see, cant pee, cant spit
130
Mechanism of Action: theophylline
Non-selective inhibition of phosphodiesterase
causes increased intracellular cAMP -> bronchial smooth muscle relaxation
Immunomodulatory action - improved mucociliary clearance and anti-inflammatory effect
NB: Narrow therapeutic window
131
List two factors that affect theophylline dosing
Metabolised in the liver
- caution in liver disease
- caution with concomitant use of enzyme inducers (rifampicin) and inhibitors (clarithromycin, ciprofloxacin)
Smoking increases theophylline clearance – dose may need adjusted following smoking cessation
132
Most common cause of pneumonia (typical)
streptococcus pneumoniae
Also:
Haemophilus influenzae
Moraxella cattharalis
Staphylococcus aureus
133
Typical presentation of pneumonia
e.g. streptococcus pneumoniae infection
```
often presents with signs of sepsis and chest symptoms:
o cough
o purulent sputum
o pleuritic chest pain
o dyspnoea
```
134
Atypical organisms causing pneumonia
Legionella pneumophila
Mycoplasma pneumonia
Coxiella burnetti (Q fever).
135
How would you assess pneumonia severity?
CURB65 scoring system
C - Confusion (new disorientation to place, person & time)
U -Blood urea >7mmol/L
R - Respiratory rate >30 breaths per minute
B - Diastolic BP <60mmHg
65 - Age ≥ 65 years
outpatient treatment can be considered in patients with a CURB65 score of 0 to 1
136
What trumps CURB 65? (i.e. you have severe pneumonia regardless of CURB score)
o Sepsis
o Multi-lobar consolidation
o Hypoxia
137
Complications in CAP
depend on the infecting pathogen and the patient’s baseline health.
Pleural effusions in pneumococcal pneumonia are relatively common
Can develop into empyema if infected
Patients with CAP who have impaired splenic function may develop overwhelming pneumococcal
sepsis, potentially leading to death
138
How can you induce a sputum sample?
nebulise with isotonic saline to induce coughing.
139
Presentation of advanced HIV
manifests as recurrent, severe infections and/or opportunistic malignancies.
signs and symptoms are those of the presenting illness, meaning
HIV infection should be suspected as an underlying illness when unusual infections present in apparently healthy individuals.
140
What increases the risk of sexual transmission of HIV?
```
o high HIV viral load
o trauma (including sexual assault)
o co-existing STIs
o ulcerative conditions - HSV/syphilitic chancre
o if the index male is uncircumcised
```
141
High risk groups for HIV
MSM who have had unprotected sex
Individuals from high prevalence countries with sexual or vertical transmission risk
IVDU, especially those from high prevalence area
Individuals exposed to blood via injection, tattoo, piercing or transfusion in high-risk countries or nonprofessional settings
Sexual contacts of the above
Anyone diagnosed with a STI
142
Barriers to HIV testing
```
Patient barriers:
May not think they are at risk
Worried regarding confidentiality, stigma, immigration issues
Employment issues
Criminalisation issues
Insurance
```
Doctor barriers:
May not think of testing
May assume patient is not at risk
Fear of embarrassing/offending patient
Lack of time
Perceived lack of counselling skills
Logistic issues to get result back to patient
143
What pre-test discussion is required prior to a HIV test?
Why testing is indicated i.e. due to clinical presentation or symptoms
Benefits to testing i.e. if positive the success of HIV therapy, if negative the ability to concentrate on other investigations/diagnoses
How/when result will be available
144
Name 4 opportunistic infections
o CMV
o Candida
o PCP
o Toxoplasma
145
How does HIV affect the immune system?
HIV gains entry to Th by binding to CD4 and other glycoproteins and co-receptors (i.e. CXCR4/CCR5).
Th are depleted as HIV progresses, causing:
o Impaired B cell activation
o Impaired antibody production
o impaired cytotoxic T cell immunity.
At CD4 <350 individuals begin to become symptomatic
<200 - increased risk of opportunistic infections- PCP.
<100 risk of serious infections - mycoplasma and CMV
146
Name 4 AIDS defining illnesses
PCP
CMV
Mycoplasma infections (TB)
Candidiasis
147
Definition of an exacerbation of COPD
a sustained worsening of the patient's symptoms from their usual stable state which is beyond normal day-to-day variations, and is acute in onset.
```
Common symptoms:
worsening breathlessness
cough
increased sputum production
change in sputum colour
```
148
Management of an Exacerbation of COPD
Assess severity: Symptoms, ABG, CXR
Controlled oxygen therapy
Bronchodilators: Air-driven nebulised salbutamol
and ipratropium bromide
Corticosteroids oral prednisolone
Antibiotics: if signs of bacterial infection (purulent sputum, increased sputum volume, ++ WCC, ++CRP)
149
Describe the clinical signs and CXR changes of a pleural effusion.
A pleural effusion is fluid in the pleural space
Clinical signs:
decreased breath sounds
stony dull to percussion
decreased tactile or vocal fremitus
```
CXR:
need >300 ml of fluid to be present to see on CXR
uniformly white appearance
blunting of costophrenic angles.
A meniscus at the upper edge
```
150
Which patients are candidates for long term oxygen therapy?
In (COPD) patients who have:
PaO2 <7.3 kPa when stable
OR PaO2 7.3 – 8 kPa
```
AND any of:
secondary polycythaemia
nocturnal hypoxaemia
peripheral oedema
pulmonary hypertension
```
Must be NON-SMOKERS FOR >3 MONTHS
151
Name three cell types and three inflammatory mediators involved in airway inflammation in asthma.
Eosinophils - degranulate releasing leukotrienes -> damage the epithelium -> cell loss causes bronchial hyper-responsiveness
Mast cells - degranulate releasing histamine → bronchoconstriction
Dendritic cells - present allergens to T lymphocytes
IL-4 stimulates IgE production by plasma cells
IL-5 - activates eosinophils
IL-13 stimulates mucus secretion
152
Pathological Features in the Asthmatic Airways
```
Plasma exudation
Oedema
Smooth Muscle hypertrophy
Mucus plugging
Shedding of epithelium
thickened basement membrane
Inflammatory cell infiltration
```
153
Symptoms Suspicious of Lung Cancer
* Cough - that doesn’t go away, or a long-standing cough gets worse
* Recurrent infections
* Breathlessness – lobar/lung collapse (co-existing COPD)
* Haemoptysis
* Unexplained weight loss
* Night sweats
* Chest and/or shoulder pains
* Hoarse voice -> invasion of RLN
154
Signs Suspicious of Lung Cancer
* Finger clubbing
* Dull percussion/Reduced air entry
* Cachexia
From metastases
o Hepatomegaly
o Cervical lymphadenopathy (supraclavicular)
o bony tenderness
* Horner's syndrome (Pancoast tumour)
* Evidence of superior vena cava obstruction (SVCO)
* Evidence of spinal cord compression (SCC)
* Cushingoid
155
What are the main risk factors for the development of lung cancer?
- Smoking in 85%
- Passive smoking
- occupational asbestos
- silica and nickel exposure
- pulmonary fibrosis
156
Common sites for lung cancer metastasis
* Lymph nodes
* Liver
* Bone
* Brain
* Adrenals
157
Common Non-Metastatic Manifestations of Lung Cancer
Metabolic – weight loss, anorexia, lassitude
Endocrine
o ectopic ACTH – Cushingoid appearance
o SIADH – hyponatraemia
o Hypercalcaemia – PTHrP, bony metastases
Neurological – Lambert-Eaton syndrome
Skeletal – finger clubbing, hypertrophic osteoarthropathy
158
Emergencies Associated with Lung Cancer
Superior vena cava obstruction
• due to mediastinal nodes compressing SVC
Spinal cord compression
159
signs and symptoms of Superior vena cava obstruction
```
Symptoms
o Breathless
o Dysphagia
o Stridor
o swollen oedematous face and right arm
```
Signs
o venous congestion in the neck
o dilated veins in the arm
160
TNM Staging
```
T = tumour size
N = LN involvement
M = metastases
```
161
small cell carcinoma
central tumour
highly malignant and associated with worse prognosis
generally present at advanced stage
treat with chemotherapy only
162
Non small cell carcinoma subtypes
adenocarcinoma
large cell carcinoma
squamous cell carcinoma
may be managed surgically in stages I/II. Radiotherapy with palliative/curative intent in later stages. Generally less responsive to chemotherapy.
Adenocarcinoma may have specific mutations in EGFR/PD-L1/ALK
163
Large cell carcinoma
peripheral tumour
undifferentiated epithelial tumour
may be resectable
164
adenocarcinoma
peripheral tumour
more common in women and non-smokers
mucin production
may have mutations in EGFR/PD-L1/ALK
165
squamous cell carcinoma
central tumour
associated with smoking
keratinisation
166
Idiopathic Pulmonary Fibrosis
specific form of chronic fibrosing interstitial pneumonia of unknown aetiology
limited to the lung
histopathological appearance of usual interstitial pneumonia (UIP) on surgical lung biopsy
known causes of ILD such as drugs, environmental exposure and connective tissue disease have been excluded
167
Name 2 Drugs that can Induce ILD
amiodarone
nitrofurantoin
168
What changes would you expect in Total lung capacity (TLC) in obstructive and restrictive lung disease?
obstructed = TLC more or less preserved
Reduced in restrictive
169
Serum angiotensin converting enzyme
o Test of sarcoid
| o Raised in sarcoid patients
170
Describe the histological and radiological changes seen in idiopathic pulmonary fibrosis (usual interstitial pneumonia)
honeycombing
ground glass changes
traction bronchiectasis
171
what does ground glass changes on CXR indicate?
partial filling of air spaces in the lungs by exudate or transudate
caused by alveolar wall inflammation or thickening and/or partial air-space filling
172
key histological features of IPF
Histological pattern of fibrosis is usual interstitial pneumonia (UIP)
patchy interstitial fibrosis, varies in intensity and age (temporal heterogeneity)
fibroblastic foci in early fibrosis
honeycomb change
• Stiffening around the lung with trapping of air
• Deposition of collagen and inflammatory cells -> produce mucin, which blocks the lumen of the airways
173
Pathogenesis of IPF
unknown agent causes repeated epithelial cell injury
this leads to inflammation and cell damage
chronic inflammation causes structural changes and fibrosis
alveolar epithelium becomes dysfunctional
174
Which treatments are available for IPF?
pirfenidone = antifibrotic and anti-inflammatory
Nintedanib = intracellular inhibitor of multiple tyrosine kinases
Steroids and immunosuppressants are not routinely recommended. Azithioprine may worsen prognosis
Symptom control:
- LTOT
- Diuretics
- Antibiotics
- Lung transplantation in younger patients
175
dull percussion note
collapse
consolidation
fibrosis
pleural effusion (stony dull)
176
hyperresonant percussion note
pneumothorax
hyperinflation (COPD)
177
fine crackles
pulmonary oedema
178
coarse crackles
bronchiectasis
179
pleural rub
pneumonia
180
increased vocal resonance
consolidation (sound conducts better through solid)
181
decreased vocal resonance
COPD
pleural effusion
pneumothorax
