obstructive disease overview Flashcards

1
Q

what is the asthma triad?

A

airway hyper-responsiveness, airway inflammation and reversible bronchospasm

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2
Q

what is the progression of uncontrolled asthma?

A

airway hyper-responsiveness (bronchospasms) –> chronic airway inflammation –> irreversible airway remodelling

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3
Q

describe the inflammatory cascade

A

genetic predisposition & trigger factor –> airway inflammation –> mediators/TH2 cytokines –> airway hyper reactivity

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4
Q

what is the treatment at each stage of the cascade?

A

avoidance –> corticosteroids –> anti-leukotriene, anti-IgE, anti-IL4/5 –> bronchodilators

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5
Q

what are some common triggers of asthma?

A

animal dander, dust mites, pollens, fungi, exercise, infection smoke, cold, NSAIDs & b-blockers

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6
Q

what is the general presentation of asthma?

A

episodic breathlessness, diurinal variability, non-productive cough, wheeze, triggers, associated atopy, family history,

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7
Q

how is asthma diagnosed?

A

peak flow diary, spirometry, reversibility testing (b2-agonists), provocation testing (histamine, exercise, allergen)

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8
Q

in terms of diurnal variability, when is asthma worst?

A

morning

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9
Q

what causes COPD?

A

noxious particles/gases from either smoking or environmental exposure

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10
Q

what are the characteristic pathological changes in COPD?

A

inflammation, mucocilliary dysfunction and tissue damage

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11
Q

what are the characteristics and symptoms of COPD?

A

late onset, frequent infective exacerbations, productive cough, progressive breathlessness, wheezing, non-atopic, reduced breath sounds

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12
Q

what are the alveolar changes that occur in COPD?

A

collapse, mucosal and peribronchial inflammation and fibrosis, mucus hypersecretion

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13
Q

what is the pathogenesis of COPD?

A

activation of alveolar macrophages but CD8 lymphocytes causing the release of inflammatory cytokines and chemotaxis which attract neutrophils. neutrophils release proteases which destroy the alveolar wall and cause mucus hyper secretion

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14
Q

what is chronic bronchitis?

A

chronic neutrophilic inflammation causing mucus hypersecretion and partially reversible smooth muscle spasm & hypertrophy

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15
Q

what is emphysema?

A

alveolar destruction causing impaired gas exchange and a loss of bronchial support (IRREVERSIBLE)

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16
Q

what is the protease-antiprotease imbalance in COPD?

A

an increase in protease activity (neutrophil elastase, matrix metalloproteinases, etc) and corresponding decrease in anti - protease activity (a1AT deficiency, etc) which favours alveolar destruction

17
Q

when would a COPD patient be classified as high risk for exacerbations?

A

two exacerbations or more within the last year and/or an FEV1

18
Q

what is the chronic cascade?

A

progressive irreversible airflow obstruction –> impaired alveolar gas exchange –> respiratory failure –> pulmonary hypertension –> cor pulmonale –> death

19
Q

how is COPD management decided?

A

GOLD stage

20
Q

how do we manage COPD?

A

non-pharmalogical: smoking cessation, immunisation, exercise, oxygen (domiciliary), venesection, lung volume reduction, stenting

pharmalogical: LAMA, LABA, LAMA-LABA, LABA-ICS, PDE4I (roflumilast), antibiotics

21
Q

what type of inflammatory cell is involved in A) asthma and B) COPD

A

A) eosinophils

B) neutrophils

22
Q

how do we diagnose COPD?

A

spirometry, peak flow, symptom severity (mMRC/CAT), DLCO test (TLCO reduced)