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Medicine 2 Weeks 1 - 6 COPY > Asthma > Flashcards

Asthma Flashcards

1
Q

Asthma

A

Reversible increases in airway resistance, involving bronchoconstriction and inflammation

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2
Q

What ratio can be used to characterise asthma; what values

A

reversible decreases in FEV1:FVC

forced expiratory volume in one second : Forced vital capacity

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3
Q

Can Asthma be Lethal

A

Yes

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4
Q

What variations can be used to diagnose asthma

A

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

**OR FEV1:FVC

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5
Q

Symptoms of Chronic Bronchitis

A

Increased mucous, airway obstruction, intercurrent infection

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6
Q

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

A

Chronic Obstructive Pulmonary Disease

Some combination of chronic bronchitis and emphysema

> 90% smoking related

FEV1 reduced

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7
Q

Sympathetic control of bronchial calibre

A

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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8
Q

Parasympathetic control of bronchial calibre

A

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

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9
Q

Factors that predispose asthma attacks

A 
Allergens
Cold air
Viral infections
Smoking
Exercise
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10
Q

Clinical features of asthma

A

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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11
Q

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

A

**Like a competitive inhibitor

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12
Q

Biological response during asthmatic attack

A
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13
Q

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

A

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

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14
Q

What are the 3 Spasmogens

A

Histamine
Prostaglantin D2
Leukotrienes

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15
Q

How are spasmogens made

A

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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16
Q

Chemotaxins

A

Leukotriene B4, PAF (Platelet Activating Factors)

Attract leukocytes to airways and exacerbate asthamtic attack and inflammation

17
Q

Spasmogens

A

Chemicals that cause the airways to go into spasm or constriction

18
Q

Why are anti-histamines not that effective for asthma

A

Because there are more mediators than just histamine

19
Q

Pharmacological basis of Asthmatic therapy

A

Bronchodilators
Reverse bronchospasm and causing rapid relief
(relievers)

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

20
Q

B2-adrenoceptor agonists

A

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

21
Q

Mechanism of Salbutamol

A

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

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

22
Q

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

A

Reduces parasympathetic activity

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

23
Q

Long Acting Beta Agonists (LABA)

A

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

24
Q

Xanthines

A

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

25
Q

Inhalers and Climate Change

A

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

26
Q

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

A

Equivalent lifestyle change as becoming a vegetarian

27
Q

PDE IV Inhibitor

A

Roflumilast - Selective PDE IV inhibitor licensed for COPD

28
Q

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

A

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

29
Q

Anti-inflammatory Agents (Corticosteroids) for asthma

A

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 Lipocrortin/Annexin A1; also reduces cytokine production

30
Q

Function of Lipocortin/Annexin A1

A

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

31
Q

Steroids for Asthma

A

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)

32
Q

Leukotriene Receptor Antagonists (LTRA)

A

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

33
Q

Omalizumab

A

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

34
Q

Steps of drugs given to asthmatics

A

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

35
Q

Guidlines for asthma medication

A

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

36
Q

COPD Treatment

A

STOP SMOKING FFS

Receiving appropriate vaccinations against stuff like the flu

Bronchodilators (B2-agonist/salbutamol + ipratropium (muscarinic M3 receptor))

Inhaled steroids?

Antibiotics for intercurrent infections

Oxygen therapy

**Ipratropium blocks PS NS broconstriction

37
Q

NSAIDs and asthma

A

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

38
Q

Beta-blockers and asthma

A

Contraindicated in those with asthma

Think of it like a reverse beta2 agonist

Medicine 2 Weeks 1 - 6 COPY (54 decks)

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