Asthma Flashcards by S Als

Asthma

Reversible increases in airway resistance, involving bronchoconstriction and inflammation

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What ratio can be used to characterise asthma; what values

reversible decreases in FEV1:FVC

forced expiratory volume in one second : Forced vital capacity

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Can Asthma be Lethal

Yes

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What variations can be used to diagnose asthma

Variations in PEF (peak expiratory flow) which improve with a B2 agonist indicate asthma

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Symptoms of Chronic Bronchitis

Increased mucous, airway obstruction, intercurrent infection

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COPD, most common cause, quantitative value used to indicate it

Chronic Obstructive Pulmonary Disease

Some combination of chronic bronchitis and emphysema

> 90% smoking related

FEV1 reduced

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Sympathetic control of bronchial calibre

Circulating adrenaline acts on β2 adrenoceptors on bronchial smooth muscles to cause relaxation

(top most important)

sympathetic respose reduces parasympathetic involvement by releasing noradrenaline, inhibitng their transmission

additionally act on β2 adrenoceptors on mucous glands to inhibit secretion

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Parasympathetic control of bronchial calibre

Acetyl choline acts on the muscarinic M3-receptors to cause bronchoconstriction and increasing mucous productoin

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Factors that predispose asthma attacks

Allergens
Cold air
Viral infections
Smoking
Exercise

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Clinical features of asthma

Wheezing
Acute onset of Breathlessness
Tight Chest
Cough (worse at night/exercise) (Nocturnal in kids)
Decreases in FEV1 reversed by a B2 agonist

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Lung Function Test results (FEV1 vs FVC) graph for normal vs asthamtic patient

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Biological response during asthmatic attack

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How does PEF Change during an asthmatic attack (Early and late phase)

**This can vary a lot in clinical presentation with both phases simultaenously or only one occurring

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What are the 3 Spasmogens

Histamine
Prostaglantin D2
Leukotrienes

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How are spasmogens made

Arachidonic acid is present in cell membranes and is chopped out by phosphospholipase A2 (PLA2)

A. Acid is released which is the substrate for the lipooxygenase (LOX) pathway which produces leukotrienes or is the substrate for the cyclooxygenase (COX) pathway which produces prostaglandins

(Also platelets releasing platelet activating factor PAF)

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Chemotaxins

Leukotriene B4, PAF (Platelet Activating Factors)

Attract leukocytes to airways and exacerbate asthamtic attack and inflammation

Spasmogens

Chemicals that cause the airways to go into spasm or constriction

Why are anti-histamines not that effective for asthma

Because there are more mediators than just histamine

Pharmacological basis of Asthmatic therapy

Bronchodilators
Reverse bronchospasm and causing rapid relief
(relievers)

Preventors
Used to prevent an attack; may be anti-inflammatory

B2-adrenoceptor agonists

Salbutamol (blue inhaler)
Selective for B2 receptors
Trade name is ventolin
Asthma drug of first choice

Causes brochodilation by acting on b2-adrenoceptors on smooth muscle to increase cAMP; increases FEV1

Mechanism of Salbutamol

Salbutamol (blue inhaler)
Selective for B2 receptors
Trade name is ventolin
Asthma drug of first choice

Causes brochodilation by acting on b2-adrenoceptors on smooth muscle to activate adenylyl cyclase to increase cAMP which increases FEV1 and relaxes lungs

How do B2-Agonists work in terms of para-/sympathetic activity and what is the effect of its overuse

Reduces parasympathetic activity

Prolonged use may lead to receptor down-regulation (desensitisation)

Long Acting Beta Agonists (LABA)

Anti asthma medication used twice a day (e.g. salmeterol) given for long-term control and prevention

Xanthines

e.g. Theophylline

Bronchodilators; not as good as salbutamol (2nd line use); used orally or iv in emergency

Adenosine receptor antagonists
Phosphodiesterase inhibitors (thus increasing cAMP)

This is good in emergencies because youre using everything but the kitchen sink to try open the airways

Inhalers and Climate Change

Metered Dose Inhalers (most inhalers) release excessive amounts of hydrofluorocarbons (GHGs) into the atmosphere (equivalent to a drive from london to sheffield per inhaler) Instead dry powder inhalers are much more sustainable Inhalers are 4% of NHS GHG emmissions

What is the equivalent lifestyle change of shifting from MDIs to Dry Powder Inhalers on the planet

Equivalent lifestyle change as becoming a vegetarian

PDE IV Inhibitor

Roflumilast - Selective PDE IV inhibitor licensed for COPD

Muscarinic M-receptor antagonists and how is it taken (and why)

Iptratropium/*Tiotropium* Blocks parasympathetic bronchoconstriction; little use in asthma but used in COPD It is inhaled because inhalation prevents antimuscarinic side effects as opposed to tablets that have more undesired systemic effects

Anti-inflammatory Agents (Corticosteroids) for asthma

Preventative - Do not reverse an attack (use inhaled to avoid systemic effect from pills) Cotricosteroid binds to intracellular receptor, affects nucleus gene expression, cell is told to produce mRNA that codes for a protein with two names Lipocrortin/Annexin A1; also reduces cytokine production

Function of Lipocortin/Annexin A1

Inhibits synthesis of PGs and LTs by antagonising the magic protein PLA2 PLA2 is responsible for taking the A. Acid out of membranes to produce PGs and LTs

Steroids

Given with B2-agonists to reduce receptor down-regulation (enhances effect of the agonist) Side effects - throat infections/hoarseness due to myopathy in throat muscles (inhalation) Tell patient to rinse mouth out after inhalation Adrenal suppression (oral) (Used for very short period of time)

Leukotriene Receptor Antagonists (LTRA)

Montelukast Increased role as add on therapy when initial treatment is insufficient Preventative and a little Bronchodilators Antagonise actions of LTs by antagonising their receptors

Omalizumab

Used in difficult to treat asthma Monoclonal antibody (MAB) against free IgE but not bound IgE Prevents IgE from binding to immune cells which leads to allergen induced mediator release in allergic asthma

Steps of drugs given to asthmatics

Start with short acting B2-agonist plus regular inhaled steroid --> Trial of LABA (or LTRA/Xanthine if this fails) --> Increase dose of inhaled steroid --> Add oral steroid

Guidlines for asthma medication

If salbutamol is used >2 times a week, step up Spacer device used when technique is poor/reducing steroid impactation Bronchodilator before steroid Rinse mouth out after steroid

COPD Treatment

STOP SMOKING FFS Receiving appropriate vaccinations against stuff like the flu Bronchodilators (B2-agonist/salbutamol + ipratropium) Inhaled steroids? Antibiotics for intercurrent infections Oxygen therapy **Ipratropium blocks PS broconstriction

NSAIDs and asthma

Non-steroidal anti-inflammatory drugs 15% of asthmatics are sensitive to such drugs e.g. aspirin, ibuprofen They stop PG production (which is good) but increases leukotriene productions

Beta-blockers and asthma

Contraindicated in those with asthma | Think of it like a reverse beta2 agonist