Resp Flashcards

1
Q

how many lobes in the lungs?

A

The left lung has two lobes and the right has three.

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2
Q

sputum sample descriptions

A

clear and colourless (chronic bronchitis), yellow-green or brown (pulmonary infection), red (haemoptysis), black (smoke, coal dust), or frothy white-pink (pulmonary oedema).

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3
Q

Define Tidal volume

A

Amount of air inhaled or exhaled in one breath - 500ml a breath

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4
Q

Define Inspiratory Reserve Volume (IRV)

A

Amount of air in excess of tidal inspiration that can be inhaled with maximum effort

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5
Q

Expiratory Reserve Volume (ERV)

A

Amount of air in excess of tidal expiration that can be exhaled with maximum effort

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6
Q

Residual Volume (RV)

A

Amount of air remaining in the lungs after maximum expiration; keeps alveoli inflated between breaths and mixes with fresh air on next inspiration

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7
Q

Vital Capacity (VC)

A

Amount of air that can be exhaled with maximum effort after maximum inspiration (ERV + TV + IRV); used to assess strength of thoracic muscles as well as pulmonary function

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8
Q

Functional Residual Capacity (FRC)

A

Amount of air remaining in the lungs after a normal tidal expiration (RV + ERV)

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9
Q

Inspiratory Capacity (IC)

A

Maximum amount of air that can be inhaled after a normal tidal expiration (TV + IRV)

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10
Q

Total Lung Capacity (TLC)

A

Maximum amount of air the lungs can contain (RV + VC)

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11
Q

FEV1

A

Forced expiratory volume in 1 second. In which a person takes a maximal inspiration and then exhales maximally as fast as possible. The important value is the fraction of the total “forced” vital capacity expired in 1 second

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12
Q

What is Peak expiratory flow (pef)?

A

Measured by a maximal forced expiration through a peak flow meter. It correlates well with the forced expiratory volume in 1 second (fev1) & is used as an estimate of airway calibre in asthma, but is effort-dependent.

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13
Q

abnormal FEV1?

A

if the FEV1 is less than 80% of the predicted value

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14
Q

abnormal FVC?

A

if the FVC is less than 80% of the predicted value.

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15
Q

what does a low FVC indicate?

A

airway restriction

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16
Q

what is FEV1/FVC ratio?

A

The proportion of FVC exhaled in the 1st second. If the ratio is below 0.7 = airway obstruction. If the ratio is high i.e. normal but the FVC is low = airway restriction

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17
Q

obstructive vs restrictive lung disease difference?

A

obstructive lung disease includes conditions that hinder a person’s ability to exhale all the air from their lungs. Those with restrictive lung disease experience difficulty fully expanding their lungs. Obstructive and restrictive lung disease share one main symptom–shortness of breath with any sort of physical exertion.Obstructive lung disease and its characteristic narrowing of pulmonary airways hinder a person’s ability to completely expel air from the lungs. The practical result is that by the end of every breath, quite a bit of air remains in the lungs.
People suffering from restrictive lung disease have a hard time fully expanding their lungs when they inhale. That is, it’s more difficult to fill lungs with air. This is a result of the lungs being restricted from fully expanding. This can occur when tissue in the chest wall becomes stiffened, or due to weakened muscles or damaged nerves.

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18
Q

normal ranges of O2 sats?

A

Target oxygen saturations are usually 94–98% in a well patient or 88–92% in those with certain pre-exisiting lung pathology (eg copd). Oxygen saturation of <92% in a normally well person is a serious sign and arterial blood gases (abgs) should be checked. Causes of erroneous readings: poor perfusion, movement, skin pigmentation, nail varnish, dyshaemoglobinaemias, and carbon monoxide poisoning

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19
Q

Ideal arteries to use for ABGs?

A

radial or femoral artery. The brachial artery is used less because of median nerve proximity and it is an end artery

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20
Q

Signs of CO2 retention

A

bounding pulse, drowsy, tremor (flapping), headache

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21
Q

what are the reference ranges in an ABG?

A

pH: 7.35 – 7.45
PaCO2: 4.7 – 6.0 kPa
PaO2: 11 – 13 kPa
HCO3–: 24-30 mmol/L
Base excess (BE): -2 to +2 mmol/L
anion gap: 12-16 mmol/L

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22
Q

Why is context king in ABG interpretation (and in general)?

A
  • A ‘normal’ PaO2 in a patient on high flow oxygen: this is abnormal as you would expect the patient to have a PaO2 well above the normal range with this level of oxygen therapy.
  • A ‘normal’ PaCO2 in a hypoxic asthmatic patient: a sign they are tiring and need ITU intervention.
  • A ‘very low’ PaO2 in a patient who looks completely well, is not short of breath and has normal O2 saturations: this is likely a venous sample.
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23
Q

What to look at 1st in an ABG?

A
  • 1st look at oxygenation. hypoxia most immediate threat to life
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24
Q

if the patient is receiving oxygen therapy, what should their PaO2 be?

A

If the patient is receiving oxygen therapy their PaO2 should be approximately 10kPa less than the % inspired concentration FiO2

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25
Q

What percentage of oxygen does a nasal cannula deliver at flow rates 1,2,3 and 4L/min?

A

1L / min – 24%
2L/ min – 28%
3L/ min – 32%
4L / min – 36%

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26
Q

What percentage of oxygen does a simple face mask deliver at a flow rate of 15L/min?

A

Simple face masks can deliver a maximum FiO2 of approximately 40%-60% at a flow rate of 15L/min. These masks should not be used with flow rates less than 5L/min.

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27
Q

What percentage of oxygen does a Reservoir mask (also known as a non-rebreather mask) deliver at a flow rate of 10 - 15L/min?

A

Reservoir masks deliver oxygen at concentrations between 60% and 90% when used at a flow rate of 10–15 l/min. These masks are most suitable for trauma and emergency use where carbon dioxide retention is unlikely.

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28
Q

What are the things that can affect oxygen delivery through a device?

A

patient’s breathing rate, depth and how well the oxygen delivery device is fitted.

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29
Q

What percentages of oxygen can a venturi mask deliver and what is the advantage of using them?

A

A Venturi mask will give an accurate concentration of oxygen to the patient. Venturi masks are available in the following concentrations: 24%, 28%, 35%, 40% and 60%. They are suitable for all patients needing a known concentration of oxygen, but 24% and 28% Venturi masks are particularly suited to those at risk of carbon dioxide retention

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30
Q

At what partial pressure of oxygen is a patient considered to be hypoxaemic and at what point in respiratory failure?

A

If PaO2 is <10 kPa on air, a patient is considered hypoxaemic.

If PaO2 is <8 kPa on air, a patient is considered severely hypoxaemic and in respiratory failure.

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31
Q

diff bw type 1 and type 2 resp failure?

A

Type 1 respiratory failure involves hypoxaemia (PaO2 <8 kPa) with normocapnia (PaCO2 <6.0 kPa).

Type 2 respiratory failure involves hypoxaemia (PaO2 <8 kPa) with hypercapnia (PaCO2 >6.0 kPa).

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32
Q

What can cause type 1 resp failure?

A

occurs as a result of ventilation/perfusion (V/Q) mismatch. Examples of VQ mismatch include:

  • Reduced ventilation and normal perfusion (e.g. pulmonary oedema, bronchoconstriction)
  • Reduced perfusion with normal ventilation (e.g. pulmonary embolism)
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33
Q

what can cause type 2 resp failure?

A

occurs as a result of alveolar hypoventilation.
Hypoventilation can occur for a number of reasons including:

  • Increased resistance as a result of airway obstruction (e.g. COPD).
  • Reduced compliance of the lung tissue/chest wall (e.g. pneumonia, rib fractures, obesity).
  • Reduced strength of the respiratory muscles (e.g. Guillain-Barré, motor neurone disease).
  • Drugs acting on the respiratory centre reducing overall ventilation (e.g. opiates).
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34
Q

What are the signs of pulmonary oedema on a CXR?

A

ABCDE -

  • Alveolar oedema (bat wings)
  • kerley B lines (interstitial oedema)
  • Cardiomegaly
  • Diversion of blood to upper lobes (where vessels in upper zone are larger than vessels in lower zone)
  • pleural Effusions
35
Q

How to calculate a normal PaO2 for a patient on oxygen?

A

This is done approximately by subtracting 10 from the FiO2 and, if the PaO2 exceeds this calculated number, then the patient is not hypoxic; if the PaO2 is lower, then the patient is hypoxic.

36
Q

Causes of respiratory alkalosis

A

rapid breathing (due to organic disease or anxiety)

37
Q

Causes of Metabolic alkalosis

A

vomiting, diuretics, and Conn’s syndrome.

38
Q

causes of metabolic acidosis

A

Metabolic acidosis has multiple causes and the most frequent are lactic acidosis, DKA, renal failure, and ethanol/methanol/ethylene glycol intoxication. One can use the anion gap to narrow the cause.

39
Q

what is a pneumothorax

A

air in pleural space separating the lung from the chest wall.

40
Q

causes of pneumothorax

A
spontaneous (classically young tall thin male)
trauma 
iatrogenic (lung biopsy, mechanical ventilation or central line insertion)
lung pathology (infection,asthma,COPD) [acute severe asthma may have an underlying pneumothorax!]
41
Q

investigation of choice for simple pneumothorax

A

erect CXR is the investigation of choice for simple pneumothorax

**CT thorax for complex or uncertain cases
also do an ABG

42
Q

how to measure size of pneumothorax

A

measuring horizontally from the lung edge to the inside of the chest wall at the level of the hilum.

43
Q

management of simple pneumothorax

A

Oxygen should be given
If no SOB and there is a < 2cm rim of air on the chest xray then no treatment required as it will spontaneously resolve. Follow up in 2-4 weeks is recommended.
If SOB and/or there is a > 2cm rim of air on the chest xray then it will require aspiration and reassessment.
If aspiration fails twice it will require a chest drain.
Unstable patients or bilateral or secondary pneumothoraces generally require a chest drain.

**if any suspicion of tension pneumothorax then ABCDE followed by oxygen and emergency needle decompression

44
Q

tension pneumothorax?

A

Tension pneumothorax is caused by trauma to chest wall that creates a one-way valve that lets air in but not out of the pleural space. more air keeps getting drawn into the pleural space with each breath and cannot escape. This is dangerous as it creates pressure inside the thorax that will push the mediastinum across, kink the big vessels in the mediastinum and cause cardiorespiratory arrest.

Severe symptoms and signs of respiratory distress suggest the presence of tension pneumothorax

45
Q

signs of tension pneumothorax

A

Tracheal deviation away from side of pneumothorax
Reduced air entry to affected side
Increased resonant to percussion on affected side
haemodynamic instability (Tachycardia, Hypotension)

46
Q

symptoms of pneumothorax

A

SOB
pleuritic chest pain
asymptomatic
in tension pneumothorax patient will be very unwell

47
Q

Management of Tension Pneumothorax

A

ABCDE approach
oxygen and emergency needle decompression (insert large bore cannula/needle (standard cannula may be insufficiently long) into the 2nd intercostal space at the mid clavicular line)
If a tension pneumothorax is suspected do not wait for any investigations. Once the pressure is relieved with a cannula then a chest drain is required for definitive management.

48
Q

triangle of safety?

A

Chest drains are inserted into the “triangle of safety”. This triangle is formed by:
5th intercostal space
mid axillary line
anterior axillary line

The needle is inserted just above the rib to avoid the neurovascular bundle that runs just below the rib. Once the chest drain is inserted obtain a chest xray to check the positioning.

49
Q

Typical clinical situations where tension pneumothorax arise

A

Ventilated patients.
Trauma patients.
Resuscitation patients (CPR).
Lung disease, especially acute presentations of asthma and COPD.
Blocked, clamped or displaced chest drains.
Patients receiving non-invasive ventilation.
Patients undergoing hyperbaric oxygen treatment.

50
Q

RFs for pneumothorax

A

smoking
lung conditions, including COPD, tuberculosis, sarcoidosis, cystic fibrosis, asthma

51
Q

presentation of COPD

A

Suspect COPD in a long term smoker presenting with chronic shortness of breath, cough, sputum production, wheeze and recurrent respiratory infections, particularly in winter.

52
Q

ddx to consider alongsied COPD

A

lung cancer, fibrosis or heart failure. COPD does NOT cause clubbing. It is unusual for it to cause haemoptysis (coughing up blood) or chest pain.

53
Q

MRC dyspnoea scale?

A

MRC (Medical Research Council) Dyspnoea Scale is a 5 point scale that NICE recommend for assessing the impact of breathlessness esp in COPD:

Grade 1 – Breathless on strenuous exercise
Grade 2 – Breathless on walking up hill
Grade 3 – Breathless that slows walking on the flat
Grade 4 – Stop to catch their breath after walking 100 meters on the flat
Grade 5 – Unable to leave the house due to breathlessness

54
Q

how is copd diagnosed

A

based on clinical presentation plus spirometry.
Spirometry will show an “obstructive picture”. FEV1/FVC ratio <0.7 and the obstructive picture does not show a dramatic response to reversibility testing with beta-2 agonists such as salbutamol during spirometry testing. If there is a large response to reversibility testing then consider asthma as an alternative diagnosis.

55
Q

how is severity of airflow obstruction graded?

A

The severity of the airflow obstruction can be graded using the FEV1:

Stage 1: FEV1 >80% of predicted
Stage 2: FEV1 50-79% of predicted
Stage 3: FEV1 30-49% of predicted
Stage 4: FEV1 <30% of predicted

56
Q

other investigations to consider in someone who is suspected to have copd

A

Chest xray to exclude other pathology such as lung cancer.
Full blood count for polycythaemia or anaemia. Polycythaemia (raised haemoglobin) is a response to chronic hypoxia.
Body mass index (BMI) as a baseline to later assess weight loss (e.g. cancer or severe COPD) or weight gain (e.g. steroids).
Sputum culture to assess for chronic infections such as pseudomonas.
ECG and echocardiogram to assess heart function.
CT thorax for alternative diagnoses such as fibrosis, cancer or bronchiectasis.
Serum alpha-1 antitrypsin to look for alpha-1 antitrypsin deficiency. Deficiency leads to early onset and more severe disease.
Transfer factor for carbon monoxide (TLCO) is decreased in COPD. It can give an indication about the severity of the disease and may be increased in other conditions such as asthma.

57
Q

Long Term Management of COPD

A
  1. smoking cessation
  2. pneumococcal vaccine and annual flu vaccine
  3. MDT involvement - PT,OT, Resp specialist nurses, resp physicians, GP, etc.
  4. consider pulmonary rehab
  5. co-develop personalised self-management plan
  6. optimise treatment of comorbidities
  7. inhaler management -
    STEP 1: Short acting bronchodilators: beta-2 agonists (salbutamol or terbutaline) or short acting antimuscarinics (ipratropium bromide).
    STEP 2:
    If they do not have asthmatic or steroid responsive features they should have a combined long acting beta agonist (LABA) plus a long acting muscarinic antagonist (LAMA). (plus SABA)
    If they have asthmatic or steroid responsive features they should have a combined long acting beta agonist (LABA) plus an inhaled corticosteroid (ICS). (plus SABA or SAMA)
    STEP 3:
    LAMA plus LABA plus ICS
  8. In more severe cases additional options are:
    Nebulisers (salbutamol and/or ipratropium)
    Oral theophylline
    Oral mucolytic therapy to break down sputum (e.g. carbocisteine)
    Long term prophylactic antibiotics (e.g. azithromycin)
    Long term oxygen therapy at home

**Long term oxygen therapy is used for severe COPD that is causing problems such as chronic hypoxia, polycythaemia, cyanosis or heart failure secondary to pulmonary hypertension (cor pulmonale). It can’t be used if they smoke

58
Q

ix for exacerbation of COPD

A

ABG
theophylline level on admission in people who are taking theophylline therapy
Sputum MC&S
blood cultures if pt pyrexic
Chest xray to look for pneumonia or other pathology
ECG to look for arrhythmia or evidence of heart strain (heart failure)
FBC to look for infection (raised white cells)
U&E to check electrolytes which can be affected by infection and medications

59
Q

usual trigger for exacerbation of COPD?

A

viral or bacrerial infection

60
Q

how to diff bw acute and chronic CO2 retention on ABG

A

acute retention - acidosis and raised CO2 only
chronic retention - resp acidosis with raised bicarb - partial/full compensation

61
Q

what is special abt venturi masks?

A

Venturi masks are designed to deliver a specific percentage concentration of oxygen. Environmental air contains 21% oxygen. Venturi masks deliver 24% (blue), 28% (white), 31% (orange), 35% (yellow), 40% (red) and 60% (green) oxygen. useful in COPD

62
Q

rules to target O2 sats in someone with known COPD

A
  • If retaining CO2 aim for oxygen saturations of 88-92% titrated by venturi mask
  • If not retaining CO2 and their bicarbonate is normal (meaning they do not normally retain CO2) then give oxygen to aim for oxygen saturations - 94% to 98%
63
Q

treatment of exacerbation of COPD

A

if treating at home:

  1. oral prednisolone
  2. regular inhalers or home nebs
  3. abx if bacterial infection suspected

if treating in hospital:

  1. nebulised bronchodilators
  2. appropriate oxygen therapy
  3. abx if bacterial infection suspected
  4. oral prednisolone or parenteral hydrocortisone
  5. physiotherapy to help clear sputum

options in severe cases where 1st line fails -

  1. IV aminophylline
  2. NIV
  3. intubation and ventilation with admission to Intensive care
  4. Doxapram can be used as a respiratory stimulant where NIV or intubation is not appropriate
64
Q

pneumonia

A

infection of lung tissue causing inflammation of lung tissue. it can be seen as consolidation on a CXR

65
Q

classification of pneumonia

A

If the pneumonia developed outside of hospital it is labeled labelled “community acquired pneumonia”. If it develops more than 48h after hospital admission it is labelled “hospital acquired pneumonia”. If it develops as a result of aspiration, meaning after inhaling foreign material such as food, then it is labelled “aspiration pneumonia”.

hospital acquired pneumonia -
Infection occurring less than five days after hospital admission is usually caused by S. pneumoniae.
Infection occurring after this time is usually caused by H. influenzae , methicillin-resistant Staphylococcus aureus (MRSA), Pseudomonas aeruginosa and other non-pseudomonal Gram-negative bacteria.

66
Q

presentation of pneumonia

A

Shortness of breath
Cough productive of sputum
Fever
Haemoptysis (coughing up blood)
Pleuritic chest pain (sharp chest pain worse on inspiration)
Delirium (acute confusion associated with infection)
Sepsis
malaise, fatigue, anorexia and abdo pain or other non-specific symptoms may also be the niitial presentation

These can indicate sepsis secondary to the pneumonia:

Tachypnoea (raised respiratory rate)
Tachycardia (raised heart rate)
Hypoxia (low oxygen)
Hypotension (shock)
Fever
Confusion

There are characteristic chest signs of pneumonia:

Bronchial breath sounds. These are harsh breath sounds equally loud on inspiration and expiration. These are caused by consolidation of the lung tissue around the airway.
Focal coarse crackles. These are air passing through sputum in the airways similar to using a straw to blow in to a drink.
Dullness to percussion due to lung tissue collapse and/or consolidation.

67
Q

severity assessment of pneumonia

A

CRB-65 out of hospital and CURB-65 in hospital
CURB65 score is calculated by giving 1 point for each of the following prognostic features:

confusion (abbreviated Mental Test score 8 or less, or new disorientation in person, place or time). For guidance on delirium, see the NICE guideline on delirium

raised blood urea nitrogen (8 or more mmol/litre)

raised respiratory rate (30 breaths per minute or more)

low blood pressure (diastolic 60 mmHg or less, or systolic less than 90 mmHg)

age 65 years or more.

CRB-65 score of anything other than 0 NICE suggest considering referring to the hospital.

Score 0/1: Consider treatment at home
Score ≥ 2: Consider hospital admission
Score ≥ 3: Consider intensive care assessment

68
Q

causes of pneumonia

A
common - 
 Streptococcus pneumoniae (50%)
 Haemophilus influenzae (20%)

Other Causes and Associations

Moraxella catarrhalis in immunocompromised patients or those with chronic pulmonary disease
Pseudomonas aeruginosa in patients with cystic fibrosis or bronchiectasis
Staphylococcus aureus in patients with cystic fibrosis

atypical pneumonia is pneumonia caused by an organism that cannot be cultured in the normal way or detected using a gram stain. They don’t respond to penicillins and can be treated with macrolides (e.g. clarithomycin), fluoroquinolones (e.g. levofloxacin) or tetracyclines (e.g. doxycycline). causes -
Legions of psittaci MCQs -

Legionella pneumophila (Legionnaires’ disease). This is typically caused by infected water supplies or air conditioning units. It can cause hyponatraemia (low sodium) by causing an SIADH. The typical exam patient has recently had a cheap hotel holiday and presents with hyponatraemia.

Mycoplasma pneumoniae. This causes a milder pneumonia and can cause a rash called erythema multiforme characterised by varying sized “target lesions” formed by pink rings with pale centres. It can also cause neurological symptoms in young patient in the exams.

Chlamydophila pneumoniae. The presentation might be a school aged child with a mild to moderate chronic pneumonia and wheeze. Be cautious though as this presentation is very common without chlamydophilia pneumoniae infection.

Coxiella burnetii AKA “Q fever”. This is linked to exposure to animals and their bodily fluids. The MCQ patient is a farmer with a flu like illness.

Chlamydia psittaci. This is typically contracted from contact with infected birds. The MCQ patient is a from parrot owner.

fungal pneumonia - 
Pneumocystis jiroveci (PCP) pneumonia occurs in patients that are immunocompromised. It is particularly important in patients with poorly controlled or new HIV with a low CD4 count. It usually presents subtly with a dry cough without sputum, shortness of breath on exertion and night sweats. Treatment is with co-trimoxazole
69
Q

ix for somone presenting with suspected pneumonia

A

hx and exam
vital signs
Chest xray
FBC (raised white cells)
U&Es (for urea)
CRP (raised in inflammation and infection)
AMT

pts with moderate/severe cases shd also have -
Sputum cultures
Blood cultures
Legionella and pneumococcal urinary antigens (send a urine sample for antigen testing)

Inflammatory markers such as white blood cells and CRP are roughly raised in proportion to the severity of the infection. The trend can be helpful in monitoring the progress of the patient towards recovery. For example, repeating WBC and CRP after 3 days of antibiotics may show a downward trend suggesting the antibiotics are working. CRP commonly shows a delayed response so may be low on first presentation then spike very high a day or two later despite the patient improving on treatment. WBC typically responds faster than CRP and give a more “up to date” picture.

Patients that are immunocompromised may not show an inflammatory response and may not have raised inflammatory markers.

70
Q

general mx of pneumonia

A

CRB/CURB56 - decide on whether to admit to hospital

oxygen for hypoxia
fluids for dehydration
analgesics like paracetamol
Antibacterials are recommended in all suspected cases of pneumonia, starting as soon as possible.

71
Q

abx for pneumonia

A

follow local area guidelines
usual abx -

Mild CAP: 5 day course of oral antibiotics (amoxicillin or macrolide)
Moderate to severe CAP: 7-10 day course of dual antibiotics (amoxicillin and macrolide)
Moderate or severe pneumonia or septic patients usually start with IV antibiotics.

72
Q

complications of pneumonia

A

Sepsis
Pleural effusion
Empyema
Lung abscess
Death

73
Q

RFs for pneumonia

A

Age: especially infants, young children and the elderly.
Lifestyle: smoking, alcohol.
Preceding viral infections - eg, influenza predisposing to Streptococcus pneumoniae infection.
Respiratory: asthma, chronic obstructive pulmonary disease (COPD), malignancy, bronchiectasis, cystic fibrosis.
Immunosuppression, AIDS, cytotoxic therapy - increased risk of infection with Staphylococcus spp., tuberculosis, Gram-negative bacilli and P. jirovecii.
Intravenous drug abuse, often associated with Staphylococcus aureus infection.
Hospitalisation - often involving Gram-negative organisms.
Aspiration pneumonia: patients with impaired consciousness, neurological disease such as cerebrovascular or Parkinson’s disease, or patients with oesophageal obstruction are at risk of aspiration pneumonia which usually affects the right lung and is caused by anaerobes from the oropharynx.
Underlying predisposing disease: diabetes mellitus, cardiovascular disease.

74
Q

VTE RFs

A

Immobility
Recent surgery
Long haul flights
Pregnancy
Hormone therapy with oestrogen
Malignancy
Polycythaemia
Systemic lupus erythematosus
Thrombophilia

75
Q

VTE prophylaxis options

A

Every patient admitted to hospital should be assessed for their risk of venous thromboembolism (VTE). If they at increased risk of VTE they should receive prophylaxis with a low molecular weight heparin such as enoxaparin unless contraindicated. Contraindications include active bleeding or existing anticoagulation with warfarin or a NOAC. Anti-embolic compression stockings are also used unless contraindicated. The main contraindication for compression stockings is significant peripheral arterial disease.

76
Q

presentation of PE

A

Shortness of breath
tachypnoea
Cough with or without blood (haemoptysis)
Pleuritic chest pain
Hypoxia
Tachycardia
Raised respiratory rate
Low grade fever
Haemodynamic instability causing hypotension

There may also be signs and symptoms of a deep vein thrombosis such as unilateral leg swelling and tenderness.

77
Q

ix and diagnosis of PE

A

hx, exam
IX -
ppl with suspected PE -
vital signs
D-dimer +/- CTPA (Computed tomographic pulmonary angiography ) (gold standard for diagnosis)
CXR
ECG
U&Es and serum creatinine
FBC

well’s score and proceed according to outcome:
PE Likely: perform a CT pulmonary angiogram
PE Unlikely: perform a d-dimer and if positive perform a CTPA

Ventilation-perfusion (VQ) scan - They are used in patients with renal impairment, contrast allergy or at risk from radiation where a CTPA is unsuitable. involves using radioactive isotopes and a gamma camera to compare the ventilation with the perfusion of the lungs.

Echocardiography — for people with hypotension (clinically ‘massive’ PE). The absence of right heart failure excludes PE.

78
Q

possible ABG findings in PE and 1 differential for this

A

resp alkalosis
ddx - hyperventilation syndrome.

Patients with a pulmonary embolism often have a respiratory alkalosis when an ABG is performed. This is because the high respiratory rate causes them to “blow off” extra CO2. As a result of the low CO2, the blood becomes alkalotic. It is one of the few causes of a respiratory alkalosis, the other main cause being hyperventilation syndrome. Patients with a PE will have a low pO2 whereas patients with hyperventilation syndrome will have a high pO2.

79
Q

Mx of PE

A

Initial management -
ABCDE
admit to hospital
Oxygen as required
Analgesia if required
Adequate monitoring for any deterioration
The initial recommended treatment is apixaban or rivaroxaban. It should be started immediately before confirming the diagnosis in patients where DVT or PE is suspected and there is a delay in getting the scan. Low molecular weight heparin (LMWH) is an alternative where these are not suitable, or in antiphospholipid syndrome. Examples are enoxaparin and dalteparin.

Long term anticoagulation - NOAC, LMWH or warfarin
The target INR for warfarin is 2-3. When switching to warfarin continue LMWH for 5 days or until the INR is 2-3 for 24 hours on warfarin (whichever is longer).
NOACs - “non-vitamin K oral anticoagulants”. This is changing to DOACs, standing for “direct-acting oral anticoagulants”. The main three options are apixaban, dabigatran and rivaroxaban.
LMWH long term is first line treatment in pregnancy or cancer.

Continue anticoagulation for:
3 months if there is an obvious reversible cause (then review)
Beyond 3 months if the cause is unclear, there is recurrent VTE or there is an irreversible underlying cause such as thrombophilia. This is often 6 months in practice.
6 months in active cancer (then review)

massive PE with haemodynamic compromise - thrombolysis using fibrinolytic agent. significant risk of bleeding. eg streptokinase, alteplase and tenecteplase.

two ways thrombolysis can be performed:
Intravenously using a peripheral cannula.
Directly into the pulmonary arteries using a central catheter. This is called catheter-directed thrombolysis.

80
Q

DVT well’s criteria

A

The risk of DVT is likely if the score is two points or more, and unlikely if the score is one point or less.
For people who are likely to have DVT -
Offer a proximal leg vein ultrasound scan with the results available within 4 hours if possible. If a proximal leg vein ultrasound scan cannot be carried out within 4 hours of being requested, offer:

A D-dimer test, then
Interim therapeutic anticoagulation (if possible, choose an anticoagulant that can be continued if DVT is confirmed) and
A proximal leg vein ultrasound scan with the results available within 24 hours.

For people who are unlikely to have DVT (based on the results of the two-level DVT Wells score):
Offer a D-dimer test with the results available within 4 hours. If the results cannot be obtained within 4 hours:
Offer interim therapeutic anticoagulation while awaiting the result (if possible, choose an anticoagulant that can be continued if DVT is confirmed).

81
Q

2 level PE Wells score

A

For people with a Wells score of more than 4 points (PE likely), arrange hospital admission for an immediate computed tomography pulmonary angiogram (CTPA) and, where necessary, other investigations.
If CTPA cannot be carried out immediately, offer interim therapeutic anticoagulation (if possible, choose an anticoagulant that can be continued if PE is confirmed), and arrange hospital admission.

For people with a Wells score of 4 points or less (PE unlikely), offer a D-dimer test with the result available within 4 hours:

If the test result cannot be obtained within 4 hours, offer interim therapeutic anticoagulation while awaiting the result (if possible, choose an anticoagulant that can be continued if PE is confirmed).
If the test is positive, arrange admission to hospital for an immediate CTPA and, where necessary, other investigations

82
Q

lung cancer

A

third most common cancer in the UK behind breast and prostate cancer. Smoking is the biggest cause. Around 80% of lung cancers are thought to be preventable.

histological types:

broadly divided into:

  • Small cell lung cancer (SCLC) (around 20%)
  • Non-small cell lung cancer (around 80%). Non-small cell lung cancer can be further divided into:
    • Adenocarcinoma (around 40% of total lung cancers)
    • Squamous cell carcinoma (around 20% of total lung cancers)
    • Large-cell carcinoma (around 10% of total lung cancers)
    • Other types (around 10% of total lung cancers)

Small cell lung cancer cells contain neurosecretory granules that can release neuroendocrine hormones. This makes SCLC responsible for multiple paraneoplastic syndromes.

Mesothelioma:

Mesothelioma is a lung malignancy affecting the mesothelial cells of the pleura. It is strongly linked to asbestos inhalation. There is a huge latent period between exposure to asbestos and the development of mesothelioma of up to 45 years. The prognosis is very poor. Chemotherapy can improve survival, but it is essentially palliative.

Presentation of lung cancers:

  • Shortness of breath
  • Cough
  • Haemoptysis (coughing up blood)
  • Finger clubbing
  • Recurrent pneumonia
  • Weight loss
  • Lymphadenopathy – often supraclavicular nodes are the first to be found on examination

Extrapulmonary Manifestations: Sometimes they can be the first evidence of lung cancer in an otherwise asymptomatic patient.

  1. Recurrent laryngeal nerve palsy presents with a hoarse voice. It is caused by a tumour pressing on or affecting the recurrent laryngeal nerve as it passes through the mediastinum.
  2. Phrenic nerve palsy, due to nerve compression, causes diaphragm weakness and presents with shortness of breath.
  3. Superior vena cava obstruction is a complication of lung cancer. It is caused by direct compression of the tumour on the superior vena cava. It presents with facial swelling, difficulty breathing and distended veins in the neck and upper chest. “Pemberton’s sign” is where raising the hands over the head causes facial congestion and cyanosis. This is a medical emergency.
  4. Horner’s syndrome is a triad of partial ptosis, anhidrosis and miosis. It can be caused by a Pancoast tumour (tumour in the pulmonary apex) pressing on the sympathetic ganglion.
  5. Syndrome of inappropriate ADH (SIADH) can be caused by ectopic ADH secreted by a small cell lung cancer. It presents with hyponatraemia.
  6. Cushing’s syndrome can be caused by ectopic ACTH secretion by a small cell lung cancer.
  7. Hypercalcaemia can be caused by ectopic parathyroid hormone secreted by a squamous cell carcinoma.
  8. Limbic encephalitis is a paraneoplastic syndrome where small cell lung cancer causes the immune system to make antibodies to tissues in the brain, specifically the limbic system, causing inflammation in these areas. This causes symptoms such as short term memory impairment, hallucinations, confusion and seizures. It is associated with anti-Hu antibodies.
  9. Lambert-Eaton myasthenic syndrome can be caused by antibodies produced by the immune system against small cell lung cancer cells. These antibodies also target and damage voltage-gated calcium channels sited on the presynaptic terminals in motor neurones. This leads to weakness, particularly in the proximal muscles but can also affect intraocular muscles causing diplopia (double vision), levator muscles in the eyelid causing ptosis and pharyngeal muscles causing slurred speech and dysphagia (difficulty swallowing). Patients may also experience dry mouth, blurred vision, impotence and dizziness due to autonomic dysfunction.

The NICE guidelines on suspected cancer (updated January 2021) recommend offering a chest x-ray, carried out within 2 weeks, to patients over 40 with:

  • Clubbing
  • Lymphadenopathy (supraclavicular or persistent abnormal cervical nodes)
  • Recurrent or persistent chest infections
  • Raised platelet count (thrombocytosis)
  • Chest signs of lung cancer

They also recommend considering a chest x-ray in patients over 40 years old who have:

Two or more unexplained symptoms in patients that have never smoked

One or more unexplained symptoms in patients that have ever smoked

The unexplained symptoms that the NICE guidelines list are:

  • Cough
  • Shortness of breath
  • Fatigue
  • Chest pain
  • Weight loss
  • Loss of appetite

Ix:

Chest x-ray is the first-line investigation in suspected lung cancer. Findings suggesting cancer include:

  • Hilar enlargement
  • Peripheral opacity – a visible lesion in the lung field
  • Pleural effusion – usually unilateral in cancer
  • Collapse

Staging CT scan of chest, abdomen and pelvis is used to assess the stage, lymph node involvement and presence of metastases. This should be contrast-enhanced, using an injected contrast to give more detailed information about different tissues.

PET-CT

Bronchoscopy with endobronchial ultrasound (EBUS). This allows detailed assessment of the tumour and ultrasound-guided biopsy.

Histological diagnosis requires a biopsy to check the type of cells in the tumour. This can be either by bronchoscopy or percutaneous biopsy (through the skin)

Mx:

MDT involvement

Surgery is offered first-line in non-small cell lung cancer to patients that have disease isolated to a single area. The intention is to remove the entire tumour and cure the cancer.

Radiotherapy can also be curative in non-small cell lung cancer when diagnosed early enough.

Chemotherapy can be offered in addition to surgery or radiotherapy in certain patients to improve outcomes (“adjuvant chemotherapy”) or as palliative treatment to improve survival and quality of life in later stages of non-small cell lung cancer (“palliative chemotherapy“).

Treatment for small cell lung cancer is usually chemotherapy and radiotherapy. Prognosis is generally worse for small cell lung cancer compared with non-small cell lung cancer.

Endobronchial treatment with stents or debulking can be used as part of palliative treatment to relieve bronchial obstruction caused by lung cancer.

Lung Cancer Surgery:

options -

  • Segmentectomy or wedge resection
  • Lobectomy (most common method)
  • Pneumonectomy involves removing an entire lung

types of surgery -

  • Thoracotomy - open surgery
  • Video-assisted thoracoscopic surgery (VATS) – minimally invasive “keyhole” surgery
  • Robotic surgery

Minimally invasive surgery (i.e., VATS or robotic surgery) is generally preferred as it has a faster recovery and fewer complications.

There are three main thoracotomy incisions:

  • Anterolateral thoracotomy with an incision around the front and side
  • Axillary thoracotomy with an incision in the axilla (armpit)
  • Posterolateral thoracotomy with an incision around the back and side (the most common approach to the thorax)

TOM TIP: If you see a patient with a thoracotomy scar in your OSCEs, they are likely to have had a lobectomy, pneumonectomy or lung volume reduction surgery for COPD. If they have no breath sound on that side, this indicates a pneumonectomy rather than lobectomy. If they have absent breath sound in a specific area on the affected side (e.g., the upper zone), but breath sounds are present in other areas, this indicates a lobectomy. Lobectomies and pneumonectomies are usually used to treat lung cancer. In the past, they were often used to treat tuberculosis, so keep this in mind in older patients. If it is a cardiology examination and they have a right-sided mini-thoracotomy incision, this is more likely to indicate previous minimally invasive mitral valve surgery.

A chest drain will be left in after thoracic surgery. The chest drain allows air and fluid to exit the thoracic cavity and the lungs to expand. A chest drain pump can be used to suck fluid and air out of the chest. They are removed when they are no longer required to drain air or fluid.

The external end of the drain is placed underwater, creating a seal to prevent air from flowing back through the drain, into the chest. Air can exit the chest cavity and bubble through the water, but the water prevents air from re-entering the drain and chest. During normal respiration, the water in the drain will rise and fall due to changes in pressure in the chest (described as “swinging”).

83
Q

basic lung anatomy

A

Air enters the lung through the trachea, which splits into the left main bronchus and right main bronchus. These bronchi then split into lobar bronchi, segmental bronchi, the segmental bronchi give rise to many conducting bronchioles, which eventually lead into terminal bronchioles. Each terminal bronchiole gives off respiratory bronchioles, which feature thin walled outpocketings that extend from their lumens. These are the alveoli.

The right lung has three lobes. The left lung has two lobes. The heart is on the left, leaving less room for an extra lobe. Both lungs have an oblique fissure separating the lobes. The right lung also has a horizontal fissure. Fluid may be seen in the fissures in acute heart failure and pulmonary oedema.

There is a membrane that surrounds the lungs called the pleura. There are two layers of this membrane, with a small amount of fluid between them (less than 20mls). These layers separate the lungs from the chest wall. Lubrication between the two layers allows the lungs to expand and move without creating friction with the chest wall.

Between the two layers, there is a potential space, called the pleural cavity. The two layers are usually touching each other, which is why it is only a potential space. There is negative pressure within the pleural cavity, pulling the two layers of the pleura together. As the chest wall expands, the negative pressure within the pleural cavity pulls the lungs outwards with the chest wall, causing them to expand.

A pleural effusion is when the potential space of the pleural cavity fills with excess fluid. This creates an inward pressure on the lungs, reducing the lung volume. A pneumothorax is when air gets into the pleural cavity.

84
Q
A