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MRCP I > resp > Flashcards

resp Flashcards

1
Q

Control of respiration

A

Central regulatory centres
* Central and peripheral chemoreceptors
* Pulmonary receptors

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2
Q

Central regulatory centres

A
  • Medullary respiratory centre
  • Apneustic centre (lower pons)
  • Pneumotaxic centre (upper pons)
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3
Q

Central and peripheral chemoreceptors

A

Central: raised [H+] in ECF stimulates respiration
* Peripheral: carotid + aortic bodies, respond to raised pCO2 & [H+], lesser extent low pO2

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4
Q

Pulmonary receptors

A
  • Stretch receptors, lung distension causes slowing of respiratory rate (Hering-Bruer reflex)
  • Irritant receptor, leading to bronchoconstriction
  • Juxtacapillary receptors, stimulated by stretching of the microvasculature
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5
Q

Chloride shift

A

CO2 diffuses into RBCs
* CO + H O —- carbonic anhydrase -→ HCO - + H+ 223
* H+ combines with Hb
* HCO - diffuses out of cell,- Cl- replaces it

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6
Q

Bohr Effect

A

Increasing acidity (or pCO2) means O2 binds less well to H

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7
Q

Haldane effect

A

↑ pO2 means CO2 binds less well to Hb

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8
Q

Tidal Volume (TV)

A

Volume inspired or expired with each breath at rest
* 500ml in ♂s, 350ml in ♀s

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9
Q

Inspiratory Reserve Volume (IRV) = 2-3 L

A

Maximum volume of air that can be inspired after normal tidal inspiration
* Inspiratory capacity = TV + IRV

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10
Q

Expiratory Reserve Volume (ERV) = 750ml

A

Maximum volume of air that can be expired after normal tidal expiration

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11
Q

Residual volume (RV) = 1.2L

A

Volume of air remaining after maximal expiration
* ↑ with age
* RV = FRC – ERV (Functional Residual Capacity - Expiratory Reserve Volume)

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12
Q

Vital Capacity (VC) = 5L

A

Maximum volume of air that can be expired after a maximal inspiration
* 4,500ml in ♂s, 3,500 mls in ♀s
* ↓ with age
* VC=IC+ERV

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13
Q

Obstructive lung disease

A

FEV1 - significantly ↓ FVC - ↓ or normal (FEV1/FVC) - ↓

Asthma
COPD
Bronchiectasis Bronchiolitis obliterans

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14
Q

Restrictive lung disease

A

FEV1 - ↓
FVC - significantly ↓ (FEV1/FVC) - normal or ↑

Pulmonary fibrosis
Asbestosis
Sarcoidosis
Acute respiratory distress syndrome Infant respiratory distress syndrome Kyphoscoliosis
Neuromuscular disorders

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15
Q

Causes of ↑ compliance

A

of ↑ compliance * Age
* Emphysema

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16
Q

Causes of ↓ compliance

A
  • Pulmonary edema
  • Pulmonary fibrosis * Pneumonectomy
  • Kyphosis
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17
Q

Oxygen dissociation curve shifts

A

Shifts Right - Raised oxygen delivery - Raised acidity, Temp, 2-3 DPG
* Shifts Left - Lower oxygen delivery - Lower acidity, Temp, 2-3 DPG - also HbF,
carboxy/methemoglobin

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18
Q

Oxygen Dissociation Curve

A

describes the relationship between the percentage of saturated hemoglobin and partial pressure of oxygen in the blood. It is not affected by hemoglobin concentration, but affected by its quality (HbF, methemoglobin).
Basics

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19
Q

Oxygen Dissociation Curve RIGHT

A

Shifts to right = for given oxygen tension there is ↓ saturation of Hb with oxygen i.e. Enhanced oxygen delivery to tissues

Shifts to Right = Raised oxygen delivery
* Raised [H+] (acidity)
* Raised PCO2
* Raised 2,3-DPG
* Raised temperature

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20
Q

Oxygen Dissociation Curve LEFT

A

Shifts to left = for given oxygen tension there is ↑ saturation of Hb with oxygen i.e. ↓ oxygen delivery to tissues

  • HbF, methemoglobin, carboxyhemoglobin
  • Low [H+] (alkali)
  • Low PCO2
  • Low 2,3-DPG
  • Low temperature
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21
Q

Left shift - affinrt

A

Left shift of the curve is a sign of hemoglobin’s ↑ affinity for oxygen (eg. at the lungs). Similarly, right shift shows ↓ affinity, as would appear with an ↑ in body temperature, hydrogen ion, 2,3- diphosphoglycerate (also known as bisphosphoglycerate) or carbon dioxide concentration (the Bohr effect)

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22
Q

Transfer factor

A

Raised: asthma, hemorrhage, left-to-right shunts, polycythemia
* Low: everything else

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23
Q

Transfer factor

A

he transfer factor describes the rate at which a gas will diffuse from alveoli into blood. Carbon monoxide is used to test the rate of diffusion. Results may be given as the total gas transfer (TLCO) or that corrected for lung volume (transfer coefficient, KCO)

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24
Q

Causes of a raised TLCO

A

Asthma
* Pulmonary hemorrhage (wegener’s, goodpasture’s)
* Left-to-right cardiac shunts
* Polycythemia
* Hyperkinetic states
* ♂ gender, exercise

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25
Q

Causes of a lower TLCO

A
  • Pulmonary fibrosis
  • Pneumonia
  • Pulmonary emboli
  • Pulmonary edema
  • Emphysema
  • Anemia
  • Low cardiac output
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26
Q

KCO also tends to ↑ with age (used to diagnose or R/O interstitial lung disease). Some conditions may cause ↑ KCO with a normal or ↓ TLCO

A

Pneumonectomy/lobectomy * Scoliosis/kyphosis
* Neuromuscular weakness
* Ankylosis of costovertebral joints e.g. Ankylosing spondylitis

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27
Q

ulmonary arteries vasoconstrict

A

vasoconstriction of the pulmonary arteries. This allows blood to be divered to better aerated areas of the lung and improves the efficiency of gaseous exchange

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28
Q

The following can cause Asthma:

A

Isocyanates
* Platinum salts
* Soldering flux resin
* Glutaraldehyde
* Flour
* Epoxy resins
* Proteolytic enzymes

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29
Q

↑ possibility of asthma

A

Wheeze, breathlessness, chest tightness and cough, worse at night/early morning
* History of atopic disorder
* Wheeze heard on auscultation
* Unexplained peripheral blood eosinophilia

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30
Q

↓ possibility of asthma

A

Prominent dizziness, light-headedness, peripheral tingling
* Chronic productive cough in the absence of wheeze or breathlessness
* Repeatedly normal physical examination
* Significant smoking history (i.e. > 20 pack-years)
* Normal PEF or spirometry when symptomatic

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31
Q

For patients with an intermediate probability of asthma further investigations are suggested. The guidelines state that spirometry is the preferred initial test:

A

FEV1/FVC < 0.7: trial of treatment
* FEV1/FVC > 0.7: further investigation/consider referral

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32
Q

Stepwise management of stable asthma

A

1st Inhaled short-acting β2 agonist as required (e.g Sulbutamol PRN)

2nd Add inhaled steroid at 200-800 mcg/day (beclometasone dipropionate or equivalent)
400 mcg is an appropriate starting dose for many patients. Start at dose of inhaled steroid appropriate to severity of disease

. Add inhaled long-acting β2 agonist (LABA)
2. Assess control of asthma:
* Good response to LABA - continue LABA
* Benefit from LABA but control still inadequate: continue LABA and ↑ inhaled
steroid dose to 800 mcg/day* (if not already on this dose)
* No response to LABA: stop LABA and ↑ inhaled steroid to 800 mcg/ day.* If control
still inadequate, institute trial of other therapies, leukotriene receptor antagonist or SR theophylline

Consider trials of:
* Increasing inhaled steroid up to 2000 mcg/day
* Addition of a fourth drug e.g. Leukotriene receptor antagonist, SR theophylline, β2
agonist tablet

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33
Q

Leukotriene Receptor Antagonists:

A

.g. Montelukast (causes Churg-Strauss syndrome), zafirlukast
* Have both anti-inflammatory and bronchodilatory properties
* Should be used when patients are poorly controlled on high-dose inhaled corticosteroids and a
long-acting β2 agonist
* Particularly useful in aspirin-induced asthma
* Associated with the development of churg-strauss syndrome

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34
Q

Fluticasone

A

s more lipophilic and has a longer duration of action than beclometasone

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35
Q

Hydrofluoroalkane

A

now replacing chlorofluorocarbon as the propellant of choice. Only half the usually dose is needed with hydrofluoroalkane due to the smaller size of the particles

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36
Q

Long acting β2 agonists (LABA)

A

bronchodilators but also inhibit mediator release from mast cells. Recent meta- analysis showed adding salmeterol improved symptoms compared to doubling the inhaled steroid dose

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37
Q

Moderate asthma

A

PEF > 50% best or predicted
* Speech normal
* RR < 25 / min
* Pulse < 110 bpm

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38
Q

severe asthma

A

PEF 33 - 50% best or predicted
* Can’t complete sentences
* RR > 25/min
* Pulse > 110 bpm

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39
Q

life threatening asthma

A
  • PEF < 33% best or predicted
  • SpO2 < 92%
  • Silent chest, cyanosis or feeble respiratory effort
  • Bradycardia, dysrhythmia or hypotension * Exhaustion, confusion or coma
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40
Q

asthma non responding to treatment

A

British Thoracic Society guidelines 2003 (updated 2004)
* Magnesium sulphate recommended as next step for patients who are not responding (e.g. 1.2 -
2g IV over 20 mins)
* Little evidence to support use of IV aminophylline (although still mentioned in management
plans)
* If no response consider IV salbutamol
* If the patient is developing respiratory acidosis (pH <7.35) consider intubation

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41
Q

COPD causes

A

Smoking.
* Alpha-1 antitrypsin deficiency
* Cadmium (used in smelting)
* Coal
* Cotton
* Cement

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42
Q

The following investigations are recommended in patients with suspected COPD:

A

To demonstrate airflow obstruction: post- bronchodilator spirometry: FEV1/FVC < 70%
* Chest x-ray: hyperinflation, bullae, flat hemidiaphragm. Also important to exclude lung cancer
* Full blood count: exclude secondary polycythemia
* Body mass index (BMI) calculation

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43
Q

Chronic Management: COPD

A

General management
* Smoking cessation advice
* Annual influenza vaccination
* Pneumococcal vaccination

Bronchodilator therapy
* Short-acting β2-agoinst (SABA) or short-acting muscarinic antagonist (SAMA) is 1st line Rx.
* For patients who remain breathless or have exacerbations despite using short-acting
bronchodilators the next step is determined by the FEV1

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44
Q

COPD treatment
FEV1 > 50% (Stage I and II)

A

Long-acting β2-agoinst (LABA), for
example salmeterol, or:
* Long-acting muscarinic antagonist
(LAMA), for example tiotropium

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45
Q

COPD treatment
FEV1 < 50% (stage III and IV)

A

LABA + inhaled corticosteroid (ICS) in a
combination inhaler, or: * LAMA

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46
Q

For patients with persistent exacerbations or breathlessness

A
  • If taking a LABA then switch to a LABA + ICS combination inhaler
  • Otherwise give a LAMA and a LABA + ICS combination inhaler
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47
Q

Oral theophylline

A
  • NICE only recommends theophylline after trials of short and long-acting bronchodilators or to
    people who cannot use inhaled therapy
  • The dose should be reduced if macrolide or fluroquinolone antibiotics are coprescribed
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48
Q

Cor pulmonale

A

Features include peripheral oedema, raised
JVP, systolic parasternal heave, loud P2
* Use a loop diuretic for oedema, consider
long-term oxygen therapy
* ACE-inhibitors, calcium channel blockers
and alpha blockers are NOT recommended by NICE

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49
Q

Factors which may improve survival in patients with stable COPD

A

Smoking cessation - the single most important intervention in patients who are still smoking
* Long term oxygen therapy in patients who fit criteria
* Lung volume reduction surgery in selected patients

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50
Q

long-term oxygen therapy (L TOT).

A

sess
* Very severe airflow obstruction (FEV1 <
patients if any of the following:
30% predicted). Assessment should be ‘considered’ for patients with severe airflow obstruction (FEV1 30-49% predicted)
* Cyanosis
* Polycythaemia
* Peripheral oedema
* Raised jugular venous pressure
* Oxygen saturations ≤ 92% on room ai

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51
Q

LTOT

A

Assessment is done by measuring arterial blood gases on 2 occasions at least 3 weeks apart in patients with stable COPD on optimal management.

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52
Q

Offer LTOT to patients with

A

< 7.3 kPa or tothosewithapO2 of7.3-8kPaandoneofthe following:
* Secondary polycythaemia
* Nocturnal hypoxaemia
* Peripheral oedema
Pulmonary hypertension

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53
Q

Benefits of LTOT:

A
  • ↓ secondary polycythemia
  • ↓ sympathetic activity → ↓ cardiac
    arrhythmia
  • Improve sleep quality
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54
Q

Oxygen saturation targets

A

Acutely ill patients: 94-98%
* Patients at risk of hypercapnia (e.g. COPD patients): 88-92% (see below)
* Oxygen should be ↓ in stable patients with satisfactory oxygen saturation

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55
Q

Management of COPD patients O2 saturation

A

Prior to the availability of blood gases, use a 28% Venturi mask at 4 l/min and aim for an oxygen saturation of 88-92% for patients with risk factors for hypercapnia but no prior history of respiratory acidosis
* Adjust target range to 94-98% if the pCO2 is normal

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56
Q

Situations where oxygen therapy should not be used routinely if there is no evidence of hypoxia:

A

Myocardial infarction and acute coronary syndromes
* Stroke
* Obstetric emergencies
* Anxiety-related hyperventilation

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57
Q

Non-invasive ventilation - key indications

A

COPD with respiratory acidosis pH 7.25-7.35
* Type II respiratory failure secondary to chest wall deformity, neuromuscular disease or
obstructive sleep apnoea
* Cardiogenic pulmonary edema unresponsive to CPAP
* Weaning from tracheal intubation.

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58
Q

Recommended initial settings for bi-level pressure support in COPD

A

Expiratory Positive Airway Pressure (EPAP): 4-5 cm H2O
* Inspiratory Positive Airway Pressure (IPAP): RCP advocate 10 cm H20 whilst BTS suggest 12-
15 cm H2O
* FiO2: not > 40%
* Back up rate: 15 breaths/min
Back up inspiration:expiration ratio: 1:3
* Keep SpO2: 88-92%
* ABG every 1-2 hours

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59
Q

INVESTIGATION: The British Thoracic Society (BTS) published guidelines in 2003 on the
investigation of patients with suspected pulmonary embolism (PE)

A

Computed Tomographic Pulmonary Angiography (CTPA) is now the recommended initial
lung-imaging modality for non-massive PE. Advantages compared to V/Q scans include speed, easier to perform out-of-hours, a ↓ need for further imaging and the possibility of providing an alternative diagnosis if PE is excluded
* If the CTPA is negative then patients do not need further investigations or treatment for PE
* Ventilation-Perfusion scanning (V/Q) MAY BE USED INITIALLY IF appropriate facilities exist, the chest x-ray is normal, and there is no significant symptomatic concurrent
cardiopulmonary disease

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59
Q

Massive PE + hypotension →

A

thrombolyse

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60
Q

Ongoing anticoagulation with warfarin (Target INR 2 – 3) length of treatment:

A

Calf DVT: at least 6 weeks
* Proximal DVT or PE where there is transient risk factors: at least 3 months
* Idiopathic venous thromboembolism or permanent risk factors: at least 6 months

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61
Q

Thrombolysis

A

Thrombolysis is now recommended as the first-line treatment for massive PE where there is
circulatory failure (e.g. Hypotension). Other invasive approaches should be considered where appropriate facilities exist

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62
Q

CAP) may be caused by the following organisms:

A

Streptococcus pneumoniae (accounts for around 80% of cases)
* Hemophilus influenzae
* Staphylococcal aureus
* Atypical pneumonias (e.g. due to Mycoplasma pneumoniae)
* Viruses

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63
Q

Streptococcus pneumoniae commonly causes

A

reactivation of the herpes simplex virus resulting in ‘cold sores and associated with foreign travel

64
Q

Klebsiella pneumoniae

A

(Friedlander’s pneumonia) is classically in alcoholics. CXR features may include abscess formation in the middle/upper lobes and empyema. The mortality approaches 30-50%

65
Q

Staphylococcus aureus:

A

normally causes pneumonia only AFTER a preceding influenzal viral infection. Characteristically causes multiple abscesses in up to 25% of patients and empyema in 10%, septicemia develops with metastatic abscess in other organs such as brain and bones.

66
Q

Characteristic features of pneumococcal pneumonia

A

Rapid onset
* High fever
* Pleuritic chest pain
* Herpes labialis

67
Q

Antibiotic choices The British Thoracic Society published guidelines in 2009:

A

Low or moderate severity CAP: oral amoxicillin. A macrolide should be added for patients
admited to hospital
* High severity CAP: intravenous co-amoxiclav + clarithromycin OR cefuroxime +
clarithromycin OR cefotaxime + clarithromycin

68
Q

CURB-65 criteria of severe pneumonia

A
  • Confusion (abbreviated mental test score < 8/10)
  • Urea > 7 mmol/L
  • Respiratory rate = 30 / min
  • BP: systolic < 90 or diastolic < 60 mmHg
  • age > 65 years
69
Q

most common cause of CAP

A

Streptococcus Pneumoniae (pneumococcus)

70
Q

Bacterial organisms that cause infective exacerbations of COPD

A

Hemophilus influenzae (most common cause)
* Streptococcus pneumoniae
* Moraxella catarrhalis

71
Q

Mycoplasma pneumoniae

A

It is associated with a number of characteristic complications such as erythema multiforme (target lesion) and cold autoimmune hemolytic anemia (pneumococcus may also cause erythema multiforme). Epidemics of Mycoplasma pneumoniae classically occur every 4 years. It is important to recognise atypical pneumonias as they may not respond to penicillins or cephalosporins.

72
Q

Mycoplasma pneumoniae features

A

Features
* Flu-like symptoms classically PRECEDE a dry cough
* Bilateral consolidation on x-ray
*

73
Q

Mycoplasma pneumoniae complications

A

Complications:
o Cold agglutins (IgM) may cause an hemolytic anemia, thrombocytopenia o Erythema multiforme, erythema nodosum
o Meningoencephalitis, Guillain-Barre syndrome
o Bullous myringitis: painful vesicles on the tympanic membrane
o Pericarditis/myocarditis
o Gastrointestinal: hepatitis, pancreatitis o Renal: acute glomerulonephritis

74
Q

Mycoplasma pneumoniae Diagnosis

A

Mycoplasma serology
* Can be differentiated from other types of pneumonia by the relatively slow progression of
symptoms, a positive coombs in 50-70% after 10 days of infection (should be used with caution or not at all since 50% of the tests are false-positive), lack of bacteria in a gram-stained sputum, and a lack of growth on blood agar.
* PCR has also been used

75
Q

Mycoplasma pneumoniae Management

A
  • Erythromycin/clarithromycin
  • Tetracyclines such as doxycycline are an alternative
76
Q

Pneumocystis carinii pneumonia (PCP):

A

Dyspnea
* Dry cough
* Fever
* Very few chest signs

77
Q

Pneumocystis carinii pneumonia (PCP): features

A

Pneumocystis jiroveci is an unicellular eukaryote, generally classified as a fungus but some authorities consider it a protozoa
* PCP is the most common opportunistic infection in AIDS
* All patients with a CD4 count < 200/mm3 should receive PCP prophylaxis

78
Q

Young Patient
* Signs & Symptoms of chest infection * Hematuria

A

Mycoplasma Pneumonia

79
Q

PCP Extrapulmonary manifestations are rare (1-2% of cases), may cause

A
  • Hepatosplenomegaly
  • Lymphadenopathy
  • Choroid lesions
80
Q

PCP Management

A

Co-trimoxazole
* IV pentamidine in severe cases
* Steroids if hypoxic (if pO2 < 9.3kPa (9.3*7.5=71mmHg) then steroids ↓ risk of respiratory
failure by 50% and death by a third)

81
Q

Legionella pneumonia

A

egionnaire’s disease is caused by the intracellular bacterium Legionella pneumophilia (Gram –ve bacilli). It is typically colonizes water tanks (hint → air- conditioning systems, showers or foreign holidays) Person-to-person transmission is not seen

82
Q

Legionella pneumonia

A

Features
* Flu-like symptoms
* 50% of cases have GI symptoms such as nausea, vomiting, diahrrhea and abdominal pain.
* Dry cough
* Lymphopenia
* Hyponatremia
* Deranged LFTs
* Hematuria occurs and occasionally renal failur

83
Q

Legionella is suggested if 3 of the following 4 features are present:

A
  • Prodormal viral like illness
  • Dry cough, confusion or diarrhea
  • Lymphopenia without marked leukocytosis. * Hyponatremia
84
Q

Legionella diagnosis

A

Diagnosis
* Urinary antigen Management
* Treat with erythromycin

85
Q

Non-invasive ventilation - key indications

A
  • COPD with respiratory acidosis pH 7.25-7.35
  • Type II respiratory failure secondary to chest wall deformity, neuromuscular disease or
    obstructive sleep apnoea
  • Cardiogenic pulmonary edema unresponsive to CPAP
  • Weaning from tracheal intubation.
86
Q

PE Ongoing anticoagulation with warfarin (Target INR 2 – 3) length of treatment:

A
  • Calf DVT: at least 6 weeks
  • Proximal DVT or PE where there is transient risk factors: at least 3 months
  • Idiopathic venous thromboembolism or permanent risk factors: at least 6 months
87
Q

Characteristic features of pneumococcal pneumonia

A
  • Rapid onset
  • High fever
  • Pleuritic chest pain
  • Herpes labialis
88
Q

CURB-65 criteria of severe pneumonia

A
  • Confusion (abbreviated mental test score < 8/10)
  • Urea > 7 mmol/L
  • Respiratory rate = 30 / min
  • BP: systolic < 90 or diastolic < 60 mmHg
  • age > 65 years
89
Q

pneumonia - characteristic complications such as erythema multiforme (target lesion) and cold autoimmune hemolytic anemia

A

Mycoplasma pneumoniae

90
Q
  • Prodormal viral like illness
  • Dry cough, confusion or diarrhea
  • Lymphopenia without marked leukocytosis. * Hyponatremia
A

Legionella pneumophili

91
Q

Extrinsic Allergic Alveolitis (EAA)

A

condition caused by hypersensitivity induced lung damage due to a variety of inhaled organic particles. It is thought to be largely caused by immune- complex mediated tissue damage (type III hypersensitivity = acute phase) although delayed hypersensitivity (type IV = chronic phase)

92
Q

Extrinsic Allergic Alveolitis (EAA) - Examples

A

Examples
* Bird fanciers’ lung (avian proteins)
* Farmers lung (spores of micropolyspora faeni)
* Malt workers’ lung (aspergillus clavatus)
* Mushroom workers’ lung (thermophilic actinomycetes*)

93
Q

Lung Fibrosis that predominately affecting the UPPER ZONES

A
  • Extrinsic allergic alveolitis
  • Coal worker’s pneumoconiosis/progressive massive fibrosis
  • Silicosis
  • Sarcoidosis
  • Ankylosing spondylitis (rare)
  • Histiocytosis
  • Tuberculosis
94
Q

Fibrosis predominately affecting the LOWER ZONES

A
  • Cryptogenic fibrosing alveolitis
  • Most connective tissue disorders (except ankylosing spondylitis)
  • Drug-induced: amiodarone, bleomycin, methotrexate
  • Asbestosis
95
Q

Asbestosis:

A

The latent period is typically 15-30 years. Asbestosis typically causes lower lobe fibrosis. As with other forms of lung fibrosis the most common symptoms are shortness-of-breath and reduced exercise tolerance. Crocidolite (blue) asbestos is the most dangerous form

96
Q

Asbestosis:

A

Possible features
* Progressive SOB
* Chest pain
* Pleural effusion

  • Pleural thickening in a similar pattern to that seen following an empyema or hemothorax. The
    underlying pathophysiology is not fully understood.
  • Pleural plaques also seen (not premalignant). They are the most common form of asbestos
    related lung disease and generally occur after a latent period of 20-40 years.
97
Q

Primary pneumothorax:

A

If the rim of airis <2cm and the patient is not
short of breath then discharge should be
considered
* Otherwise aspiration should be attempted
* If this fails then repeat aspiration should be
considered
* If this fails then a chest drain should be
inserted

98
Q

Secondary pneumothorax:

A

If the patient is > 50 years old and the rim of air is > 2cm and the patient is short of breath then
a chest drain should be inserted.
* Otherwise aspiration should be attempted. If aspiration fails a chest drain should be inserted. All
patients should be admitted for at least 24 hours

99
Q

Lung cancer: Risk Factors:

A
  • ↑ risk of lung ca by a factor of 10
    Other factors
  • Asbestos - ↑ risk of lung ca by a factor of 5
  • Arsenic
  • Radon
  • Nickel
  • Chromate
  • Aromatic hydrocarbon
  • Cryptogenic fibrosing alveolitis
100
Q

Smoking +asbestos are synergistic, risk

A

a smoker with asbestos exposure has a 10 x 5 = 50 times ↑ risk

101
Q

Lung cancer The 2005 NICE cancer referral guidelines gave the following advice: Consider immediate referral for patients with:

A

Signs of superior vena caval obstruction (swelling of the face/neck with fixed elevation of jugular venous pressure)
* Stridor

102
Q

Lung cancer Refer urgently patients with:

A

Persistent hemoptysis (in smokers or ex-smokers aged 40 years and older)
* A chest x-ray suggestive of lung cancer (including pleural effusion and slowly resolving
consolidation)
* A normal chest x-ray where there is a high suspicion of lung cancer
* A history of asbestos exposure and recent onset of chest pain, shortness of breath or
unexplained systemic symptoms where a chest x-ray indicates pleural effusion, pleural mass or any suspicious lung pathology

103
Q

Refer urgently for chest x-ray for patients with any of the following:

A

Hemoptysis
* Unexplained or persistent (longer than 3 weeks): chest and/or shoulder pain, dyspnea, weight
loss, chest signs, hoarseness, finger clubbing, cervical or supraclavicular lymphadenopathy, cough, features suggestive of metastasis from a lung cancer (for example, secondaries in the brain, bone, liver, skin)
Factors that are NOT related * Coal dust

104
Q

Types of lung cancer

A
  • Squamous: 35%
  • Adenocarcinoma: 30%
  • Small (oat) cell: 15%
  • Large cell: 10%
  • Other: 5%
105
Q

types of lung cancer most common

A

Squamous is the most common in UK, Adenocarcinoma is the most common in US

106
Q

Paraneoplastic features of lung cancer

A
  • Squamous cell: PTHrp, clubbing, HPOA
  • Small cell: ADH, ACTH, Lambert-Eaton syndrome
107
Q

Small Cell Lung Cancer features

A

Features
* Usually central
* Arise from APUD* cells
* ADH → Hyponatremia
* ACTH → cushing’s syndrome
* ACTH secretion can cause bilateral adrenal hyperplasia, the high levels of cortisol can lead to
hypokalaemic alkalosis
* Lambert-eaton syndrome: antibodies to voltage gated calcium channels causing myasthenic like
syndrome

108
Q

Small Cell Lung Cancer management

A

Management
* Usually metastatic disease by time of diagnosis
* Surgery: only used for debulking
* Radiotherapy: only used for debulking
* Chemotherapy (being the mainstay of treatment): good response to combination chemotherapy,
may extend life by approximately 4 months

109
Q

Contraindications to lung cancer surgery

A

include SVC obstruction, FEV < 1.5, MALIGNANT pleural effusion, and vocal cord paralysis

cal Cord Paralysis → extracapsular spread to mediastinal nodes and is an indication of inoperability.

110
Q

Lung cancer - 1. Squamous cell cancer

A
  • Typically central
  • Associated with ectopic PTH secretion 􏱐 HYPERCALCAEMIA
  • Strongly associated with finger clubbing
  • Hypertrophic pulmonary osteoarthropathy (HPOA)
111
Q

Lung cancer Surgery contraindications

A
  • Assess general health
  • Stage IIIb or IV (i.e. Metastases present)
  • FEV1 < 1.5 litres is considered a general cut-off point*
  • Malignant pleural effusion
  • Tumour near hilum or within 2 cm of bronchus
  • Vocal cord paralysis
  • SVC obstruction
111
Q

Lung cancer - 2. Adenocarcinoma

A

Most common type of lung cancer in non-smokers, although the majority of patients who develop lung adenocarcinoma are smokers
* Typically located on the lung periphery

112
Q

Bronchial Carcinoma

A

20-30% of cases with bronchial carcinoma are of the small (oat) cell type and arise from endocrine (Kulchitsky) cells.

113
Q

Bronchial Carcinoma Paraneoplastic manifestations:

A

Paraneoplastic manifestations:
* Syndrome of inappropriate ADH secretion (SIADH) 5-10%
* Ectopic secretion of ACTH 5%
* Ectopic atrial natriuretic peptide (ANP) secretion can also occur

114
Q

CXR Cavitations:

A

Differential
* Tuberculosis
* Lung cancer (especially squamous cell)
* Abscess (staph aureus, klebsiella and Pseudomonas)
* Wegener’s granulomatosis
* Pulmonary embolism
* Rheumatoid arthritis
* Aspergillosis, histoplasmosis, coccidioidomycosis

115
Q

Sarcoidosis:

A

is a multisystem disorder of unknown aetiology characterized by non-caseating granulomas. It is more common in young adults and in people of African descent. Sarcoidosis remits without treatment in approximately two-thirds of people.

116
Q

ACE levels Sarcoidosis:

A

ACE levels have a sensitivity of 60% and specificity of 70% and are therefore not reliable in the diagnosis of sarcoidosis although they may have a role in monitoring disease activity.

117
Q

Sarcoidosis Other investigations*

A
  • Spirometry: may show a restrictive defect
  • Tissue biopsy: non-caseating granulomas
  • Gallium-67 scan - not used routinely
    *the Kveim test (where part of the spleen from a patient with known sarcoidosis is injected under the skin) is no longer performed due to concerns about cross-infection
118
Q

in sarcoidosis Erythema nodosum is associated with

A

good prognosis

119
Q

Factors associated with poor prognosis sarcoidosis

A
  • Insidious onset, symptoms > 6 months
  • Absence of erythema nodosum
  • Extrapulmonary manifestations: e.g. Lupus pernio, splenomegaly
  • CXR: stage III-IV features
  • Black people
120
Q

Mikulicz syndrome

A

is a chronic condition characterized by the abnormal enlargement of parotids, lacrimal and salivary glands. The tonsils and other glands in the soft tissue of the face and neck may also be involved. It is associated with sarcoidosis

121
Q

Indications for steroids

A
  • Hypercalcemia
  • Worsening lung function
  • Eye (bilateral posterior uveitis is common eye manifestation)
  • Heart or neuro involvement
122
Q

BHL: = (bulky mediastinum), the most common causes of Bilateral Hilar Lymphadenopathy are sarcoidosis and tuberculosis

A

Causes include:
* Sarcoidosis
* Tuberculosis
* Lymphoma/other malignancy
* Pneumoconiosis e.g. Berylliosis
* Fungi e.g. Histoplasmosis, coccidioidomycosis (VHL + Cavitation in CXR)

123
Q

Lofgren’s syndrome

A

acute form sarcoidosis characterized by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia. It typically occurs in young ♀s and carries an excellent prognosis

124
Q

Lofgren’s syndrome features

A

Transient CXR shadowing and blood eosinophilia
* Thought to be due to parasites such as Ascaris lumbricoides causing an alveolar reaction
* Presents with a fever, cough and night sweats which often last for less than 2 weeks.
* Generally a self-limiting disease

125
Q

Causes of pulmonary Eosinophilia

A
  • Churg-Strauss syndrome (eosinophilia + asthma + hemorrhage)
  • Allergic bronchopulmonary aspergillosis (ABPA)
  • Loffler’s syndrome
  • Eosinophilic pneumonia
  • Hypereosinophilic syndrome
  • Tropical pulmonary eosinophilia
  • Drugs: nitrofurantoin, sulphonamides
  • Less common: Wegener’s granulomatosis
  • Tropical pulmonary eosinophilia
  • Associated with Wuchereria bancrofti infection
126
Q

COPD Causes:

A
  • Smoking!
  • α-1 antitrypsin deficiency
  • Cadmium (used in smelting)
  • Coal
  • Cotton
  • Cement
  • Grain
127
Q

Asthma Causes:

A
  • Isocyanates
  • Platinum salts
  • Soldering flux resin
  • Glutaraldehyde
  • Flour
  • Epoxy resins
  • Proteolytic enzymes
128
Q

Silicosis is a risk factor for

A

for developing TB (silica is toxic to macrophages) Features
* Fibrosing lung disease
* ‘Egg-shell’ calcification of hilar lymph nodes

129
Q

Respiratory Alkalosis

A

Common causes
* Anxiety leading to hyperventilation
* Pulmonary embolism
* Salicylate poisoning*
* CNS disorders: stroke, subarachnoid hemorrhage, encephalitis
* Altitude
* Pregnancy

130
Q

*salicylate overdose leads to a

A

mixed respiratory alkalosis and metabolic acidosis. Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis

131
Q

Bronchiectasis

A

Causes
* Post-infective: tuberculosis, measles, pertussis, pneumonia
* Cystic fibrosis
* Bronchial obstruction e.g. Lung cancer/foreign body
* Immune deficiency: selective IgA, hypogammaglobulinemia
* Allergic bronchopulmonary aspergillosis (ABP A)
* Ciliary dyskinetic syndromes: kartagener’s syndrome, young’s syndrome
* Yellow nail syndrome (associated with pleural effusion - exudates)

132
Q

Symptom control in non-CF bronchiectasis

A

inspiratory muscle training + postural drainage

133
Q

Pseudomonas aeruginosa:

A
  • Insensitive for Amoxicillin
  • IV Ticarcillin + IV Gentamycin
  • IV Colistin for resistant cases
134
Q

Most common organisms isolated from patients with bronchiectasis:

A

Hemophilus influenzae (most common)
* Pseudomonas aeruginosa
* Klebsiella spp.
* Streptococcus pneumoniae

135
Q

Obstructive Sleep Apnoea/Hypopnoea Syndrome predisposing factors

A

Predisposing factors
* Obesity
* Macroglossia: acromegaly, hypothyroidism, amyloidosis
* Large tonsils
* Marfan’s syndrome

136
Q

OSA acessment

A

ssessment of sleepiness
* Epworth Sleepiness Scale - questionnaire completed by patient +/- partner
* Multiple Sleep Latency Test (MSLT) - measures the time to fall asleep in a dark room (using
EEG criteria) Diagnostic tests
* Sleep studies - ranging from monitoring of pulse oximetry at night to full polysomnography where a wide variety of physiological factors are measured including EEG, respiratory airflow, thoraco-abdominal movement, snoring and pulse oximetry

137
Q

OSA management

A

Management
* W eight loss
* CPAP is first line for moderate or severe OSAHS
* Intra-oral devices (e.g. Mandibular advancement) may be used if CPAP is not tolerated or for
patients with mild OSAHS where there is no daytime sleepiness
* Limited evidence to support use of pharmacological agents

138
Q

Acute Respiratory Distress Syndrome - ARDS

A

Caused by ↑ permeability of alveolar capillaries leading to fluid accumulation in alveoli i.e. Non-cardiogenic pulmonary edema

139
Q

ARDS criteria

A

Criteria (American-European Consensus Conference)
* Acute onset
* Bilateral infiltrates on CXR
* Non-cardiogenic (pulmonary artery wedge pressure needed if doubt)
* pO2/FiO2 < 200 mmHg

140
Q

ARDS causes

A

auses
* Infection: sepsis, pneumonia
* Massive blood transfusion
* Trauma
* Smoke inhalation
* Pancreatitis
* Cardio-pulmonary bypass

141
Q

Allergic bronchopulmonary aspergillosis (ABPA)

A

llergy to Aspergillus spores. In the exam questions often give a history of bronchiectasis and eosinophilia.
Features
* Bronchoconstriction: wheeze, cough, dyspnea
* Bronchiectasis (proximal)

142
Q

Allergic bronchopulmonary aspergillosis (ABPA) investigations

A

Investigations
* Eosinophilia
* Flitting CXR changes
* Positive radioallergosorbent (RAST) test to aspergillus
Positive IgG precipitins (not as positive as in aspergilloma)
* Raised IgE

143
Q

Aspergilloma

A

ungus ball which often colonises an existing lung cavity (e.g. secondary to TB, lung cancer or cystic fibrosis)
Usually asymptomatic but features may include * Cough
* Hemoptysis (may be severe)
Investigations
* CXR containing a rounded opacity
* High titres Aspergillus precipitins

144
Q

Cystic fibrosis (CF)

A

autosomal recessive disorder causing ↑ viscosity of secretions (e.g. lungs and pancreas). It is due to a defect in the cystic fibrosis transmembrane conductance regulator gene (CFTR), which codes a cAMP-regulated chloride channel. The most common inherited lethal condition in Caucasians

145
Q

In the UK 80% of CF cases are due

A

In the UK 80% of CF cases are due to a deletion at delta F508 on the long arm of chromosome 7. Cystic fibrosis affects 1 per 2500 births, and the carrier rate is c. 1 in 25

146
Q

Organisms which may colonise CF patients

A
  • Staph aureus
  • Pseudomonas aeruginosa (Rx: Inhaled Tobramycin)
  • Burkholderia cepacia*
  • Aspergillus
147
Q

Cepacia Syndrome in CF:

A

characterized by a rapidly progressive fever, uncontrolled bronchopneumonia, septicemia, weight loss, and poor outcomes.
Management:
* Aminoglycosides + Ceftazidime
* Ceftazidime + Cholramphenicol
* Cholramphenicol + Minocycline

148
Q

CF presentation

A

Neonatal period (around 20%): meconium ileus, less commonly prolonged jaundice
* Recurrent chest infections (40%)
* GI Manifestation: malabsorption (30%) steatorrhoea, liver disease, cholesterol gall stones,
peptic ulcers, ↑ GI malignancy.
* Other features: failure to thrive.

149
Q

CFswear test

A
  • Sweat test: 2 reliable positive results on 2 separate days is diagnostic for CF. it is positive when chloride is > 60
150
Q

Other features of cystic fibrosis

A

Other features of cystic fibrosis
* Short stature
* Diabetes Mellitus
* Delayed puberty
* Rectal prolapse (due to bulky stools)
* Nasal polyps
* ♂ infertility, ♀ subfertility

151
Q

Management of cystic fibrosis involves a multidisciplinary approach. Key points:

A

Management of cystic fibrosis involves a multidisciplinary approach. Key points:
* Regular (at least twice daily) chest physiotherapy and postural drainage. Parents are usually
taught to do this. Deep breathing exercises are also useful
* High calorie diet, including high fat intake*
* Vitamin supplementation
* Pancreatic enzyme supplements taken with meals
* Heart and lung transplant

152
Q

Bronchiolitis obliterans:

A

term used to describe fibrous scarring of the small airways. It is seen following: toxic-fume inhalation; mineral-dust exposure; viral infection; mycoplasma and legionella infection; bone marrow, heart–lung and lung transplantation; rheumatoid arthritis; SLE; and as a side-effect of penicillamine. It presents as a dry cough and dyspnea. Physical examination is unremarkable. Expiratory wheeze may be audible. The chest X-ray findings can vary from normal to a reticular or reticulonodular pattern. The diagnosis can be confirmed by lung biopsy. Patients rarely respond to steroids. The prognosis is poor

153
Q

Pleural Effusion: Exudate - (> 30g/L protein)

A
  • Infection: pneumonia, TB, subphrenic abscess
  • Connective tissue disease: RA ( glucose < 1.6, LDH > 700, pH < 7.2,↑ R.F > 1:320, ↑ cholesterol), SLE
  • Neoplasia: lung cancer, mesothelioma, metastases
  • Pancreatitis
  • Pulmonary embolism
  • Dressler’s syndrome
  • Yellow nail syndrome
154
Q

Pleural effusion - Transudate - (< 30g/L protein)

A
  • Heart failure
  • Hypoalbuminemia (liver disease, nephrotic syndrome, malabsorption)
  • Hypothyroidism
  • Meigs’ syndrome: triad of ascites, pleural effusion (right side) and benign ovarian tumor
    (fibroma). It resolves after the resection of the tumor. For reasons unknown.
155
Q

Indications for chest tube insertion

A

in patients with infected pleural effusions are: presence of organisms on a Gram stain of the pleural fluid, a frankly purulent pleural fluid, pleural pH < 7.2 in the setting of an infected pleural effusion, loculated pleural effusions and poor clinical progress despite antibiotic treatment.

156
Q

Transfusion Related Acute Lung Injury (TRALI

A

caused by anti-HLA, Human Neutrophil Antigens (HNA) or antigranulocytes antibody in donor blood.
Donor’s blood sensitization occurs in:
* Multiparous ♀ develop these antibodies through exposure to fetal blood
* Previous transfusion
* Transplantation patient

157
Q

Transfusion Related Acute Lung Injury (TRALI ) diagnosis

A

Diagnosis anti-HLA or anti-Neutrophil antibody in donors’ or recipient blood.

MRCP I (21 decks)

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