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Cardiorespiratory 2 > Obstructive lung disease > Flashcards

Obstructive lung disease Flashcards

1
Q

what are the 3 major components of asthma

A
  1. Chronic inflammation
  2. Variable (reversible) airflow limitation
  3. Obstructive airflow
  4. History of respiratory systems (e.g. wheeze shortness of breath, chest tightness and cough) vary in length and intensity
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2
Q

what are the risk factors of asthma

A
  • Smoke
  • Chemicals
  • Animals
  • Pollen
  • Air pollution
  • Medicine
  • Exercise
  • Cold air
  • Stress
  • Viruses
  • Dust
  • Mould
  • consequence of gene-environement interactions
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3
Q

what does a heterogeneous condition mean in asthma

A

means that it is in children and adults

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4
Q

name some obstructive lung diseases

A

asthma and COPD

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5
Q

for someone with asthma was does the volume time graph look like

A

The volume that they are over to expire over a given period of time is significantly less than someone who is normal thus asthma has airflow limitation

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6
Q

what does the histopathology look like of asthma

A
  • Thickening of the basement membrane
  • Airway smooth muscle hypertrophy (increase in volume)
  • Leukocyte infiltration
  • Goblet cell hyperplasia (increase in number) and mucus hypersecretion
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7
Q

what are two types of asthma

A

T2-type asthma

non-T2 type asthma

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8
Q

what is T2 type asthma

A
  • allergic asthma and exercise induced asthma
  • tends to start in childhood
  • leads to late onset eosinophilic asthma
  • aspirin exacerbated respiratory disease
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9
Q

what is non T2 type asthma

A
  • obesity associated asthma
  • smoking related neutrophilic asthma
  • smooth muscle mediated paucigranulocytic asthma
  • adult onset asthma
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10
Q

describe the T cell response to asthma

A
  • Dendritic cell causes activation of TH2 cell
  • TH2 cells are activated : there Central role is Release inflammatory mediators:
  • interleukin-4 (IL-4) and IL-13 = Stimulates B cells to synthesize IgE
  • IL-5 = Eosinophil activation
  • ## IL-9 = mast cell proliferation – this causes an increased histamine production and further activation of mast cells
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11
Q

what are the symptoms of asthma in children

A

isolated symptoms of cough, wheeze and shortness of breath are neither sensitive nor specific for asthma

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12
Q

what are the symptoms of asthma in adults

A
  • Almost all children with asthma have intermittent cough, wheeze and/or exercise induced symptoms, but only about a quarter of children with these symptoms have asthma
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13
Q

how can an allergen cause asthma

A
  • Allergens activate sensitized mast cells by crosslinking surface-bound IgE molecules ( which are surface bound mast cells) this leads to degranulation and to release several bronchoconstrictor mediators (e.g. histamine) by mast cells, histamine then leads to bronchoconstriction
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14
Q

what can increase the probability fo asthma from the diagnosis

A
  • Patients/Parents/Guardians: wheeze often used to describe any abnormal respiratory noise
  • Important: distinguish wheezing – a continuous, high pitched musical sound coming from the chest – from other respiratory noises, such as stridor
  • Wheeze heard by a healthcare professional on auscultation is an important sign that increases the probability of asthma
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15
Q

how can you diagnose asthma properly

A

previous and current medical history + lung function tests

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16
Q

what tests do you use in order to work out ofthey have asthma

A
  • PEF charting
  • challenge test
  • skin prick IgE
  • blood eosinophils
  • FEV1
  • spirometry
  • then if you have suspected asthma give medication and treatment and if they have a good response to this then it is likely that they have asthma
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17
Q

what is the volume in a volume time graph

A

this is the volume of air that you can breathe out in a fixed volume mervouver/forced

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18
Q

what is the reduced volume over a period of time in someone with asthma in a volume time graph

A
  • In an individual with asthma due to narrowing with the airways there is airflow limitation due to narrowing of the airways
  • After treatment with a bronchodilator there is significant improvement with an FEV1 there is volume that you can breath out in one second
  • There is improvement in FEV1 and the total volume of air they are able to breath out
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19
Q

describe the pathway of the flow volume graph

A

At the red line someone has taken a deep breath in
The initially expriation is rapid and very fast
Then it slows down as you cant breath out anymore and your hitting residual volume this causes the reduce in the flow rate in the green line

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20
Q

what is the maximum flow rate is a flow volume graph

A

PEF is the maximum flow rate

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21
Q

what happens to the PEF in patients with asthma

A
  • it can be reduced
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22
Q

what does asthma cause in a flow volume graph

A
  • it causes a reduced flow rate
23
Q

normal spirometry in an asymptomatic patient…

A

Normal spirometry in an asymptomatic patient does not rule out the diagnosis of asthma

24
Q

what is the lower limit in spirometry to demonstrate airway obstruction

A

FEV1/FVC <70%
- As you get older the lung function declines, below a certain age if the FEV1/FVC value is 70% you don’t have asthma but take into account age, height, ethnicity taken into account then they have asthma

25
Q

how do you measure the PEF

A
  • PEF is best used to provide an estimate of variability of airflow from multiple measurements made over at least two weeks
  • They have increased likelihood of asthma with greater than or equal to 20% variability
26
Q

how do you manage asthma

A
  • they should have a regular review
  • asthma plan
  • these both monitor current symptom control and the impact asthma is having on daily activities and quality of life as well as to assess future risk
27
Q

what are the ways of reviewing asthma

A
  • royal college of physicians 3 questions (no to all questions consistent with controlled asthma)
  • asthma control questionnaire (well controlled is less than 0.74, poor control is more than 1.5)
  • asthma control test or child asthma control test( poor control is less than 20)
28
Q

what are the risk factors for future exaberations

A
  • history of previous asthma attacks
  • persistent asthma symptoms
  • vitamin D deficiency
  • low income family
  • comorbid atopic/allergic disease
  • suboptimal drug regiment
  • young age
  • exposure to tobacco smoke
  • obesity
  • low parental education
29
Q

what 3 questions are for the royal college of physicians test

A

questions about impact of asthma symptoms on sleep, daytime symptoms and activities

30
Q

what are the asthma management goals

A
  • Control of disease
  • No daytime symptoms
  • No night time awakening due to asthma
  • No need for rescue medication
  • No asthma attacks
  • No limitations on daily activity
  • Normal lung function
  • Minimal drug side effects
31
Q

what is the rescue medication of asthma

A

inhaled short acting beta 2 agonist as short term reliver therpay for all patients with symptomatic asthma

32
Q

what is the first line therpay for asthma

A

Low-dose ICS; smokers/ex-smokers may require higher doses of ICS

33
Q

what is the add-on for th first line therapy for asthma

A

1st choice add-on therapy to ICS in adults is inhaled long-acting β2 agonists

34
Q

what should you consider for asthma patients after the first 2 steps of treatmetn

A

Consider combined maintenance and reliver therapy (SMART/MART) in adult patients who have a history of asthma attacks on medium dose ICS or ICS/LABA – depending if they got good asthma control or worsening asthma

35
Q

what is the difference in use techniques between aerosol and dry powder inhaler

A
  • Aerosol - Inhale slow and steady, dry powder inhaler - inhale quick and deep
36
Q

how do ICS work

A
  • Bound to a receptor in a cytoplasm which is known as the glucocorticoid receptor
  • Once in the cytoplasm they go into the nucleus and bind to GRE
  • These increase anti-inflammatory genes
  • Or they can recruit transcriptional machinery that can downregulate proinflammatory genes
37
Q

how do beta 2 agonist work

A

beta 2 adgrenic receptor agonists bind to beta 2 adrenergic receptor – a cascade of signal transduction events = airway smooth muscle relaxation and this leads to bronchodilation

38
Q

how do LABAs work with ICS and b2 agonists

A
  • LABA increases GR nucleus translation which increases GRE binding and increases anti inflammatory effects
  • they also help cause bronchodilation by increasing b2-receptor expression and b2-receptor coupling plus down regulation of B2 receptor sea prevention of b-agonist tolerance
39
Q

what is the risk factors for COPD

A
  • Long term exposure to noxious environmental particles, genetics, and lung development
  • Smoking – passive smoking and smoke from crackers
  • Genetic response (alpha-1 antitrypsin deficiency)
  • Occupational dust and chemicals
  • Indoor smoke from wood, coal, cow dungs, crop residues used from cooking
  • Frequent lung infections as a child
40
Q

what is the histopathology of COPD

A
  • Excess mucus
  • chronic inflammation
  • small airway disorders
  • Destruction to the alveoli – emphysema
  • Bronchoconstriction
  • fibrosis
41
Q

what is the difference between COPD and asthma

A
  1. COPD is persistent airflow limitation whereas asthma is variable airflow limitation
  2. asthma has a good steroid response whereas COPD has a poor steroid response
  3. asthma has atopy in the majority whereas COPD has no increased atopy
  4. in asthma eosinophils mast cells and CD4(TH2) cells response in CODP neutrophils, macrophages and CD8 (TC1) Cells response
42
Q

how is COPD caused

A
  • Cigarette smoke (major risk factor) = irritates & activates epithelial cells & macrophages → inflammatory mediators

Macrophages release CXCL8
= chemokine = attracts neutrophils

Epithelial cells release CXCL9 & CXCL10 = chemokine = attracts T helper 1 (TH1) cells and type 1 cytotoxic T (TC1) cells

TC1 & neutrophils → Proteases (e.g. metalloproteinase 9 (MMP9)leads to = elastin degradation

Neutrophil elastase leads to = mucus hypersecretion.

Epithelial cells & macrophages → transforming growth factor-β (TGFβ) = stimulates fibroblast proliferation = fibrosis in the small airways

43
Q

what are the clinical signs of COPD

A
  • Shortness of breath
  • Chronic cough
  • Phlegm
  • Wheezing
  • Chest tightness
  • Respiratory infection
44
Q

how do you diagnose COPD

A

current medical history and lung function test

45
Q

what assessment tool do you use in COPD

A

ABCD assessment tool

46
Q

what factors does the ABCD assessment tool use

A
  • Severity of symptoms
  • Extent of lung function decline
  • Exacerbations
47
Q

what is the COPD management goals

A
  • Reduce symptoms
  • Reduce frequency and severity exacerbations
  • Improve health status and quality of life
  • Improve exercise tolerance
48
Q

the greater the delicate of FEV1 ….

A
  • The greater the decline of FEV1 the greater the severity of lung function
49
Q

describe the ABCD assessment tool

A

group A - mMRC 0-1 or CAT greater than 10, 0 to 1 moderate exacerbations but don’t lead to hospital admission

Group b

  • MmRC greater or equal to 2 or a CAT greater than equal to 10
  • 0 to 1 moderate exacerbations but don’t lead to hospital admission

Group C

  • mMRC 0-1 or CAT greater than 10, 0 to 1
  • greater than or equal to 2 moderate exacerbations or greater than and equal to 1 leading to hospitalisation

Group D

  • MmRC greater or equal to 2 or a CAT greater than equal to 10
  • greater than or equal to 2 moderate exacerbations or greater than and equal to 1 leading to hospitalisation
50
Q

describe the treatment of groups ABCD

A

group A - bronchodilator
group B. LABA or LAMA
Group C - LAMA
Groups D - LAMA or LAMA and LABA or ICA and LABA

51
Q

what is the first line treatment in COPD

A
  • Bronchodilators is the first line treatment – LAMA and LABA
52
Q

what is a LAMA

A

long acting muscarinic antagonists M3 muscarinic receptor antagonists
- Muscarinic antagosnist block the binding of acetylcholine to M3 muscarinic receptor thereby inhibiting smooth muscle cell contraction

53
Q

What is a LABA

A

LABA long acting beta 2 agonists beta 2 receptor agonists

Cardiorespiratory 2 (43 decks)

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