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Supporting Life > Asthma > Flashcards

Asthma Flashcards

1
Q

What is asthma

A

Airways smooth muscle hyper responsiveness leading to periodic, at least partly reversible obstruction of the airways

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2
Q

What is the obstruction caused by

A

Inflammation/swelling of the mucosal lining.

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3
Q

What does the obstruction cause

A

Turbulent airflow - audible wheeze. Should hear in all lung fields

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4
Q

What are signs of pneumothorax

A

Hyper resonant and no breath sounds

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5
Q

What are signs of pneumonia

A

Bacterial infection of one lobe - dull percussion

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6
Q

What are signs of lung collapse

A

Blockage in proximal airway, dull percussion everywhere

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7
Q

How is asthma severity assessed

A

PEFR/FEV1 and response to bronchodilator (nebulised salbutamol 5mg given with pure O2)
Blood gases: oximetry <92%

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8
Q

Who are high risk asthma px

A

Poor compliance, psychosis, depression, denial, alcohol or drug abuse, obesity, social problems, severe stress from any source

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9
Q

What is cyanosis a sign of

A

Terminal sign of asthma (pO2 has to be around 50)

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10
Q

What does hypercapnia cause in the brain

A

Hypercapnia is a potent vasodilator - causes cerebral oedema

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11
Q

When should an asthma px be admitted

A

FEV1/PERF less than 50%, predicted 15-30 minutes after bronchodilator

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12
Q

What is the management for admitted severe asthma

A

Oxygen - high conc up to 100%
Hypercapnia is asthma reflects alveolar hypoventilation and not lung disease

Inhaled beta2-agonits (prevents bronchospasm)
Nebulised
Give continuously if necessary
Always nebulise with O2: may acute aggravate hypoxia in severe asthma; hypoxia and hypercapnia alter cardiac response to beta2-agonist
If px does not have access to nebuliser, breath in Ventolin through spacer

Ipatropium bromide 0.5 mg 4-6hourly added to beta2-agonist if acute severe or life threatening asthma

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13
Q

What is given IV in severe asthma

A

Single bolus of IV magnesium sulphate if PEF<50%

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14
Q

What is the role of steroids in acute asthma

A

Glucocorticoids: given orally
Reduction in airflow obstruction begins 1-3 hours, peaks 5-9 hours after single dose
Probably no need to give 0.6 mg/kg prednisolone in 24 hours; typical emergency regimens are 2-3 mg/kg hydrocortisone 4 hourly

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15
Q

What to do with acute asthma px with a good response to management

A

Continue oxygen, nebulised beta2-agonsits 4 hourly, glucocorticoids
Do not discontinue any existing inhaled glucocorticoid therapy

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16
Q

What to do with acute asthma px with a poor response to management

A 
Continuous high flow oxygen
Nebulised beta2-agonist every 15-30 mins
Consider complications
Hypokalaemia (beta agonists cause migration of potassium ions intracellularly) 
Coexisting problems
Admit to intensive care
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17
Q

How is vent support given with asthma

A

Benzodiazepine and pancuronium sedation

Aim to correct hypoxaemia with permissive hypercapnia

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18
Q

What is allergic asthma

A

most easily recognised, usually commences in childhood. Associated with Fx. Usually presents eosinophilic airway inflammation. Good responses to ICS

19
Q

What is non allergic asthma

A

sputum may be neutrophilic, eosinophilic or with few inflammatory cells. Less response to ICS

20
Q

What is late onset asthma

A

more common in women. Tendency to non-allergic, higher doses of ICS

21
Q

What is asthma with fixed airflow limitation

A

long standing asthma, airflow limitation thought to be due to airway wall remodelling

22
Q

What is asthma with obesity

A

prominent resp symptoms, little eosinophilia

23
Q

What are the inflammatory pathologies of asthma

A

Inflammatory infiltrate (Th2, mast cells and eosinophils)
Mucosal oedema:
Bronchial microvascular leak
Mucus hypersecretion: Blockage of airways
Bronchial smooth muscle contraction:
Action of inflammatory mediators

24
Q

What are the remodelling pathologies of asthma

A

Reticular BM thickening
Airway smooth muscle thickening
Submucosal mucus gland hypertrophy

25
Q

What drugs target b2 adrenoceptor?

A

Selective b2 adrenoceptor agonists:
Inhaled
Short acting: salbutamol
Long-acting: formoterol, salmeterol, vilanterol

26
Q

What drugs target muscarinic receptors (M3)

A

Inhaled
Short-acting: Ipratropium
Long-acting: Tiotropium, Umeclidinium

27
Q

What is the mechanism of muscarinic receptor antagonists

A

Anticholinergic: block effects of Ach released from cholinergic parasympathetic nerve fibres to smooth muscle and mucus glands
Prevents airway smooth muscle contraction
Prevents mucus hypersecretion
Less effects

28
Q

What are the side effects of muscarinic receptor antagonists

A

dry mouth, palpitations, headache, dizziness, blurred vision

29
Q

What is the mechanism of action of b2 agonists

A

High levels of cAMP relaxes bronchial smooth muscle and also inhibits release of bronchoconstriction mediators such as histamine
After inhalation, salbutamol reaches the lungs directly - acts within 3-5 minutes

30
Q

What is vilanterol

A

long acting B2 agonist with bronchodilation up to 72 hours

31
Q

What does tiotropium do

A

attenuates IL-13-induced goblet cell metaplasia

32
Q

What does ICS therpay acheive

A

Reduces asthma symptoms
Increases lung function
Improve QoL
Reduces the risk of exacerbations, hospitalisations and death

33
Q

How do corticosteroids work

A

Suppress Th2

Reduce the infiltration and activation of eosinophils, Th2 cells, and other inflammatory cells

34
Q

What is Fluticasone Furoate

A

Long-acting ICS
Results in a longer duration of action and prolonged retention in the lung; enables it use as a once-daily ICS
Longer duration of action enables once-daily dosing: potential to improve px convenience and enhance compliance

35
Q

What is Montelukast

A

Leukotriene Receptor Antagonist
Potent arachidonic acid-derived inflammatory mediators
CysLT1 receptor mediates the broncho constrictive and proinflammatory effects of cysteinyl-leukotrienes
Montelukast is a competitive antagonist of the CysLT1 receptor
Once daily oral administration

36
Q

Who is montelukast best suited for

A

Asthma px with aspirin exacerbated resp disease (increased production of cysteinyl-leukotrienes)

37
Q

What is T2 inflammation in asthma

A

Airway epithelium interacts with environment (allergens, viruses, smoke etc.)
Releases cytokines once activated
IL-33, IL-25 released
Signals to downstream cells to innate and adaptive
IL-C2 on innate
Th2 cell on adaptive ->product of naiive t cells
These produce Il-4 (tells B cells to make IgE), Il-5 (eosinophil maturation and migration from bone marrow), Il-13 (airway hyper responsiveness and remodelling)

38
Q

How does anti-IL-5 work

A

inhibits eosinophils in airways - given 4 weekly
Mepolizumab (sc)
Reslizumab (iv)
Eosinophils central effector cell in asthma. Critically involved in the synthesis, maturation, homing and activation of eosinophils

39
Q

How does anti-IgE work

A

Depletes IgE, reduces allergen induced mast cell activation and decrease expression of IgE high affinity receptors on amst cells, blocks effects of IgE on DCs
Decreases exacerbation rates

40
Q

What is Tezepelumab

A

Anti-TLSP, anti-IL-33: dampens down entire airway. Blood eosinophil, exhaled NO and total IgE levels all fallen

41
Q

What is the dominant cuase of asthma exacerabtion

A

Viruses - Rhinovirus most frequent trigger

42
Q

What are the 3 families of antiviral cytokine interferon

A

T1 (IFN-alpha and beta) and Type 3 (IFN-lambda)

43
Q

What do antiviral cytokines do

A

Block viral entry into cells
Control viral replication inside the cell
Induce apoptosis
Induce other cytokine’s -> recruitment of NK, CD4, CD8

44
Q

How does Omalizumab work

A

DCs produce T1 IFN in response to viruses

DCs express IgE receptor - crosslinking this receptor impairs production of IFN

Supporting Life (14 decks)

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