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
What drugs target b2 adrenoceptor?
Selective b2 adrenoceptor agonists: Inhaled Short acting: salbutamol Long-acting: formoterol, salmeterol, vilanterol
26
What drugs target muscarinic receptors (M3)
Inhaled Short-acting: Ipratropium Long-acting: Tiotropium, Umeclidinium
27
What is the mechanism of muscarinic receptor antagonists
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
What are the side effects of muscarinic receptor antagonists
dry mouth, palpitations, headache, dizziness, blurred vision
29
What is the mechanism of action of b2 agonists
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
What is vilanterol
long acting B2 agonist with bronchodilation up to 72 hours
31
What does tiotropium do
attenuates IL-13-induced goblet cell metaplasia
32
What does ICS therpay acheive
Reduces asthma symptoms Increases lung function Improve QoL Reduces the risk of exacerbations, hospitalisations and death
33
How do corticosteroids work
Suppress Th2 | Reduce the infiltration and activation of eosinophils, Th2 cells, and other inflammatory cells
34
What is Fluticasone Furoate
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
What is Montelukast
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
Who is montelukast best suited for
Asthma px with aspirin exacerbated resp disease (increased production of cysteinyl-leukotrienes)
37
What is T2 inflammation in asthma
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
How does anti-IL-5 work
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
How does anti-IgE work
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
What is Tezepelumab
Anti-TLSP, anti-IL-33: dampens down entire airway. Blood eosinophil, exhaled NO and total IgE levels all fallen
41
What is the dominant cuase of asthma exacerabtion
Viruses - Rhinovirus most frequent trigger
42
What are the 3 families of antiviral cytokine interferon
T1 (IFN-alpha and beta) and Type 3 (IFN-lambda)
43
What do antiviral cytokines do
Block viral entry into cells Control viral replication inside the cell Induce apoptosis Induce other cytokine's -> recruitment of NK, CD4, CD8
44
How does Omalizumab work
DCs produce T1 IFN in response to viruses | DCs express IgE receptor - crosslinking this receptor impairs production of IFN