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RESP Flashcards

1
Q

Describe the pathophysiology of Asthma

A

-Normal airway with bronchial epithelium, some matrix and some smooth muscle under it

-Allergen sensitises airway — causes inflammation and airway remodelling

  • Recruitment of inflammatory cells into airway (mostly eosinophils)
  • structural changes in airway is increase in goblet cells which produce mucus
    -Amount of matrix increases too and amount + size of smooth muscle cells increase
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2
Q

what genes are expressed according to GWAS study of asthma?

A

GSDMB
IL33

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3
Q

How does type 2 immunity reaction come about in allergic asthma?

A

Allergen exposure - lung dendritic cells – MHC II – Mediastinal lymph nodes — Naive T cells – T helper cells - IL 4, 5, 13

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4
Q

What does il 4 do?

A

B cellls differentiate and produce IgE cells

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5
Q

What does il 5 do?

A

Eosinophil recruitment and survival

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6
Q

What does il 13 do?

A

Mucous secretion

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7
Q

How do we test for allergic sensitisation? (2)

A

Blood test for specific IgE antibodies
Skin prick test

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8
Q

How do we test for eosinophil levels?

A
  • Blood eosinophil count when stable → ≥300 cells/mcl is abnormal
  • Induced sputum eosinophil count: ≥2.5% eosinophils is abnormal
  • Exhaled nitric oxide-
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9
Q

What objective tests are done to diagnose asthma? (3)

A
  • Reversible airway obstruction- bronchodilator reversibility ≥12%
  • Airway obstruction on spirometry- FEV1/FVC ratio <0.7
  • Exhaled NO (FeNO) >35ppb (children), >40ppb (adults)
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10
Q

Reduce airway eosinophilic inflammation of asthma- how? (2)

A
  • Inhaled corticosteroids- target and reduce eosinophilic inflammation
  • Leukotriene receptor antagonists- can reduce type 2 inflammation
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11
Q

Acute symptomatic relief of asthma- how? (2)

A
  • Beta-2 agonists (smooth muscle relaxation)
  • Anticholinergic therapies (smooth muscle relaxation)
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12
Q

How does anti-IgE antibody therapy work?

A
  • Reduction in serum IgE over time means the therapy may not need be used indefinitely
    • Binds and captures circulating IgE- prevents its interaction with mast cells and basophils to stop allergic cascade
      -IgE production can decrease with time when patients given anti-IgE Ab
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13
Q

What is Omalizumab?

A
  • The commonly used anti-IgE antibody given as subcutaneous injections
  • Is very expensive
  • Is effective at reducing exacerbations compared to placebo

When is it used?
Severe, persistent allergies (IgE mediated) asthma in patients ≥6 years who need continuous or frequent treatment with oral corticosteroids
Have to have optimised standard therapy with good adherence with no response

  • What serum IgE level is it prescribed for?
    Total serum IgE between 30-1500
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14
Q

Mepolizumab

A
  • Anti-IL5-antibody
  • Reduces IL-5 effect, reducing eosinophilic inflammation in severe eosinophilic asthma
  • Licensed for adults and children ≥6
  • When is it trialled?
    Blood eosinophils ≥300 cells/mcl in the last 12 monthsAt least 4 exacerbations requiring oral steroids in the last 12 monthsFor 12 months- 50% reduction in attacks, then continue
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15
Q

Dupilumab

A

Anti IL4 / IL13 receptor

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16
Q

Define respiratory failure

A

Syndrome of inadequate gas exchange due to dysfunction of ≥1 components of respiratory system
Respiratory system:
Nervous
Muscular
Pulmonary

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17
Q

According to Berlin’s Classificatio. how do you identify ARDS?

A
  1. Timing: Within 1 week of known clinical insult or new or worsening respiratory symptoms
  2. Chest Imaging: Bilateral opacities - not fully explained by effusions, lung collapse
  3. Origin of odema: Not fully explained by cardiac failure or fluid overload - echocardiogram
  4. Oxygenation:
    Severe <100
    Moderate 100 -200
    Mild 200 - 300
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18
Q

Explain how perfusion and ventilation changes across the lung?

A

Ventilation: Not impacted by gravity so aveoli at the apex of lung show less compression , larger diameter and less compliant. Greater pleural pressure. Less ventilation

Perfusion: Impacted by gravity so at the base of the lung more compression, more blood vessels, more perfusion. Higher intravascular pressure, higher flow rate, less resistance

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19
Q

How would you describe the ventilation perfusion matching according to zones of the lung?

A

Zone 1- Alveolar pressure is higher than arterial and venous

2- arterial pressure is higher than alveolar and venous

3- arterial and venous are higher than alveolar

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20
Q

Complaince vs elastance

A

Compliance is the volume per unit pressure- ease of stretching
AV/AP

Elastance is the amount of pressure required to distend by a volume- resistance to being stretched

-The elastic recoil of the chest and lung tissue
AP/AV

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21
Q

What is the formula for minute ventilation and when is it used?

A

Tidal volume (L) x Breaths/min = L/min
Gas entering and leaving lung

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22
Q

What is the formula for alveoli ventilation and when is it used?

A

(Tidal volume - dead space) x breath per minute

Gas entering and leaving the alveoli

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23
Q

Type 1 or Hypoxemic resp failure- what does this mean?

A
  • Failure of oxygen exchange
  • PaO2 <60 at sea level
  • Increased shunt fraction (QS/QT)
  • Due to alveolar flooding in heart/CVD failure patients
  • Hypoxemic refractory to supplemental oxygen
24
Q
  • Increased shunt fraction (QS/QT)- what does this mean?
A

More blood transported through lungs without taking part in gas exchange

25
Q

Causes of Type I respiratory failure

A
  • Collapse of lobe
  • Aspiration
  • Fibrosis
  • Pulmonary oedema
  • Pulmonary embolism
  • Pulmonary hypertension
26
Q

Type 2 or Hypercapnic resp failure- what does this mean?

A
  • Failure to exchange or remove CO2
  • Decreased alveolar minute ventilation
  • Dead space ventilation
27
Q

Causes of Type 2 respiratory failure

A
  • Nervous system issues
  • Neuromuscular issues
  • Muscle failure- muscles too tired to maintain tidal volume
  • Airway obstruction
  • Chest wall deformity
28
Q

Type 3 or perioperative failure- what does this mean?

A
  • Increased atelectasis (collapse of entire lung or lobe) due to low functional residual capacity (FRC) with abnormal abdominal wall mechanics
  • You can have hypoxemia or hypercapnia
29
Q

How do we prevent type 3 respiratory failure?

A
  • Anaesthetic or operative technique
  • Posture
  • Incentive spirometry
  • Analgesia
  • Attempts to lower intraabdominal pressure
30
Q

Type 4 resp failure aka shock- what does this mean?

A
  • This happens in intubated and ventilated patients during shock (septic/cardiogenic/neurologic)
  • Poor perfusion of the lung so gas can’t come into blood
    Optimise ventilation improve gas exchange and to unload the

respiratory muscles, lowering their oxygen consumption

31
Q

What are the effects of the ventilator on the left ventricle and right ventricle in type 4 respiratory failure?

A

Reduces LV afterload, Increased RV pre and after load

32
Q

What occurs in acute lung injury?

A

The complex interaction- the lung can be injured from either direction

From the lung or to the lung.

Within the lung infection will lead to macrophage and neutrophil activation, triggering release of cytokines such as TNF and IL-6, IL-8 for example.

These result in activation of a cascade of inflammatory responses which are key to resolution of lung injury but may often become disruptive.

In additional to the biological consequences at the receptor level, these responses drive inflammation and alveolar fluid leak across the endothelium.

As the endothelium becomes oedematous this secondarily impairs gas exchange.

33
Q

What in vivo evidence do we have for acute lung injury? (5)

A
  • TNF signalling implicated- reduced injury of alveolar lung injury by blocking TNFR-1 signalling pathway with Ab or using TNFR-1 knockouts
  • Macrophage activation occurs in alveolar space and neutrophil lung migration also occurs
  • DAMP release (commonest for lung are HMGB-1 and RAGE)
  • Cytokines are released e.g. IL-6, 8, IL-1B, IFN-gamma (this is important for viral response and T cell differentiation)
  • Cell death- there is necrosis in lung biopsies, and also apoptotic mediators e.g. FAS, FAS-I and BCl-2
34
Q

Therapeutic intervention for ARDS

A

TREAT UNDERLYING CONDITIONS
Inhaled therapies
Bronchodilators
Pulmonary vasodilators
Steroids
Antibiotics
Anti-virals
Drugs
Pyridostigmine
Plasma exchange
IViG
Rituximab

RESPIRATORY SUPPORT
Physiotherapy
Oxygen
Nebulisers
High flow oxygen
Non- invasive ventilation
Mechanical ventilation
Extra-corporeal support

MULTIPLE ORGAN SUPPORT
Cardiovascular support
Fluids
Vasopressors
Inotropes
Pulmonary vasodilators
Renal support
Haemofiltration
Haemodialysis
Immune therapies
Plasma exchange
Convalescent plasma

35
Q

How does the pressure-volume loop change for ARDS from normal?

A
  • ARDS lung is much stiffer so volume is reduced and more pressure is used at the top to get very little gain in volume increase
  • Lung can drop below lower inflection point leading to lung collapse
  • We try to keep end expiratory pressure so that lung remains open and that we open lung just enough- we don’t push it too hard with too much pressure that would cause damage and inflammation and oedema and alveoli will stop working
36
Q

How most commonly gets lung cancer? (4)

A
  • Age- peak is 75-90
  • Sex- M>F
  • Lower socioeconomic status
  • Smoking history- duration, intensity, when stopped
37
Q

What other than smoking are causes of lung cancers?

A
  • Passive smoking is 15% of these
  • Chronic lung diseases (COPD, fibrosis)
  • Asbestos- exposure increases risk up to x2
  • Radon e.g. silver miners in Germany in 1800s
  • Indoor cooking fumes- wood smoke, frying fats
  • Air pollution
  • Familial/genetic- several loci identified
38
Q

Pathogeneis of lung cancer

A

Inhaled carcinogens interact with the epithelial of the upper and lower airways

This leads to the formation of DNA adducts (pieces of DNA covalentaly bonded to cancer causing chemicals)

Persisting DNA adducts/misrepaired adducts result in a mutation and can cause genomic alterations.

39
Q

What are the 4 main types of lung cancer?

A

Squamous cell carcinoma (~30% of cases).
– originating from bronchial epithelium; centrally located

Adenocarcinoma (~40%)
– most common from 1980s onwards – low tar cigarettes, inhaled more deeply / retained longer
– originating from mucus-producing glandular tissue; more peripherally-locate

Large cell lung cancer (~15%)
heterogenous group, undifferentiated

Small cell lung cancer (~15%)
originate from pulmonary neuroendocrine cells
highly malignant

40
Q

Common oncogenes impacted in lung cancer

A

epidermal growth factor receptor (EGFR) tyrosine kinase
-15-30% of adenocarcinoma
-more so in women, Asian ethnicity, never-smokers

anaplastic lymphoma kinase (ALK) tyrosine kinase
- 2-7% of non-small cell lung cancer
-especially in younger patients and never smokers

c-ROS oncogene 1 (ROS1) receptor tyrosine kinase
1-2% of non-small cell lung cancer
especially in younger patients and never smokers

BRAF (downstream cell-cycle signalling mediator)
1-3% of non-small cell lung cancer
especially in smokers

41
Q

Key symptoms of lung cancer

A

Cough
Weight loss
Breathlessness
Fatigue
Chest pain
Haemoptysis

42
Q

Signs of lung cancer

A

Clubbing, Cachexia, Superior vena cava obstruction (Pemberton’s sign), Horner’s syndrome

43
Q

Imaging in lung cancer

A

Chest X ray
Staging CT ( chest and abdomen)
PET - CT occult metastsis

44
Q

Biopsy in lung cancer

A

Bronchoscopy - central and segmented airway tumours

Endobronchial ultrasound and transbronchial-needle aspiration of mediastinal lymph nodes (EBUS [TBNA])
To stage mediastinum +/- achieve tissue diagnosis

CT-guided lung biopsy
To access peripheral lung tumours

45
Q

Staging and classification of lung cancer

A

T1- T4
<3, 3 -5 , 5- 7 (invading a little a lot) , 7+ ( invading a lot)

N0 - N3
Ipsi Ipsi Contra lung mediatinal lung

M0 - M1c close, far but one, far but more

Could also be staged as
Early vs locally-advanced vs metastatic

46
Q

Determinants of lung cancer treatment

A

Patient fitness
Cancer histology
Cancer stage
Patient preference
Health service factors

47
Q

Patient fitness – WHO performance status

A

0 – Asymptomatic (Fully active, able to carry on all predisease activities without restriction)

1 – Symptomatic but completely ambulatory (Restricted in physically strenuous activity but ambulatory and able to carry out work of a light or sedentary nature. For example, light housework, office work)

2 – Symptomatic, up and about >50% of waking hours(Ambulatory and capable of all self care but unable to carry out any work activities)

3 – Symptomatic, confined to bed or chair >50% of waking hours (Capable of only limited self-care)

4 – Completely disabled (Completely disabled. Cannot carry on any self-care. Totally confined to bed or chair)

5 – Death

48
Q

Which group according to WHO classification of patient fitness is qualified for radical treatment?

A

0 – Asymptomatic (Fully active, able to carry on all predisease activities without restriction)

1 – Symptomatic but completely ambulatory (Restricted in physically strenuous activity but ambulatory and able to carry out work of a light or sedentary nature. For example, light housework, office work)

2 – Symptomatic, up and about >50% of waking hours(Ambulatory and capable of all self but not able to carry out work)

49
Q

What sections of the lung can be taken out and what are they called?

A

Wedge resection- small section of lung tissue and a bit of healthy tissue

Segmental resection - large section of lung tissue but not yet a full lobe

Lobectomy - lung

Pneumonectomy - one out of lung pair

50
Q

What two ways can lung be accessed in surgery?

A

Open thoracotomy
Video assisted thorascopic surgery

51
Q

Radical radiotherapy:
Who is it good for?
How does it work?

A

Alternative to surgery for early stage disease
Particularly if comorbidity
Stereotactic ablative body radiotherapy (SABR)

  • Technique of choice
  • High-precision targeting, multiple convergent beams
52
Q

First line for metastatic NSCLC with mutation

A

Anti- EGFR
Anti- ALK
Anti - ROS1

improvements in progression-free survival, modest overall survival vs standard chemotherapy

Side effects

generally well-tolerated (tablets)
rash, diarrhoea, and (uncommonly) pneumonitis

53
Q

First line for metastatic NSCLC with no mutation (and PDL1 ≥50%)

A

Pembrolizumab

improvements in progression-free survival and overall survival vs standard chemotherapy

generally well-tolerated
Immune-related side-effects in 10-15%

54
Q

First line for metastatic NSCLC with no mutation and PDL1 ≤50% (in combination with immunotherapy)

A

Cytotoxic chemotherapy

Target any rapidly dividing cells
Platiunum-based regimens

Frequent: fatigue, nausea, bone marrow suppression, nephrotoxicity
Quality of life poorly evaluated in trials; no evidence for improvement

55
Q

Management of locally advanced disease (involving thoracic lymph nodes)

A

Surgery + adjuvant chemotherapy

Radiotherapy + chemotherapy +/- immunotherapy

BRS missed out (10 decks)

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