L17: Drugs & the Respiratory System Flashcards

1
Q

Location of asthma in the lungs

A

Trachea

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2
Q

Location of bronchitis

A

Bronchi- Bronchioles

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3
Q

2 zones in the lungs

A

1) Conducting Zone
2) Transitional & Respiratory Zones

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4
Q

Location of COPD

A

Respiratory bronchioles

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5
Q

Location of small airways disease

A

Respiratory bronchioles- alveolar ducts

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6
Q

Location of emphysema

A

Alveolar sacs

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7
Q

Where does tuberculosis tend to occur in?

A

Upper lung lobes

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8
Q

How does the body respond to allergens into the body?

A

Releasing an antibody called immunoglobin, too much IgE can cause inflammation of lungs

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9
Q

3 phases in lung function after allergen exposure

A

1) Immediate asthmatic phase
2) Delayed phase
3) Airway/bronchial hyperresponsiveness

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10
Q

What is the immediate phase after allergen exposure?

A

Due to bronchospasm released from allergen-triggered mast cells acting on bronchiolar smooth muscle

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11
Q

What is the delayed phase after allergen exposure?

A

Airway narrowing due mainly to mucosal swelling as a result of mediators released from inflammatory cells

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12
Q

What is the AHR phase after allergen exposure?

A

Combined effects of bronchospasm on an inflamed aiway sensitive to any inhaled irritant

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13
Q

Drugs used in a pharmacological treatment of asthma 1

A

1) bronchodilators
2) anti-inflammatory agens

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14
Q

2 agonists in current treatment of symptoms

A

1) short acting beta-2 agonists
2) long acting beta-2 agonists
3) theorphylline

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15
Q

What do muscarinic antagonists prevent?

A

Prevent smooth muscle contraction & mucus secretion induced by activation of parasympathetic nerves

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16
Q

What are muscarinic antagonists used in the treatment of?

A

COPD

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17
Q

What bromides are bronchoconstriction inhibited by?

A

1) ipratropium bromide
2) tiotropium bromide

18
Q

Actions of glucocorticosteroids in asthma

A
  • Inhibition of leukotriene & cytokine synthesis/release
  • Inhibition recruitment of inflammatory cells
  • Increases beta-adrenoceptor function
19
Q

Role of inhaled corticosteroids in asthma therapy

A
  • Prevents infiltration & activation of inflammatory cells
  • Improves airflow
  • Decrease airway
  • Reduce symptoms
20
Q

Side effects of glucocorticosteroids

A

Inhaled route
Oral/prolonged high dose

21
Q

What do xanthines inhibit?

A

phosphodiesterase (PDE)

22
Q

Treatment options for COPD

A

quit smoking
anti-inflammatory drugs

23
Q

Mechanism of action of muscarinic antagonists

A

Blocks M3 receptors on aiway smooth muscle- preventing bronchoconstriction & reduce mucus secretion

24
Q

One type of steroids used in anti-inflammatory therapy

A

Glucocorticosteroids

25
Q

How does glucocorticosteroids work on asthma ?

A

Suppress multiple inflammation by:
1) Suppressing cytokine production
2) Reducing leukotriene & prostaglandin synthesis
3) Block recruitment of inflammatory cells
4) Increase b-adrenoceptor function

26
Q

Role of inhaled corticosteroids (ICS) in asthma therapy

A

1) Prevents infiltration
2) Reduce mucosal oedema
3) Improves airflow

27
Q

Role of PLA2 in the action of inhaled GCS

A

Convert membrane bound phospholipids into arachidonic acid

28
Q

What does leukotriene antagonists inhibit?

A

Bronchoconstriction, oedema, mucus production

29
Q

Mechanisms of xanthines

A

Inhibit phosphodiesterase (PDE), enzyme that degrades cAMP, causing bronchodilation- leading to relaxation

30
Q

Function of cromones

A

Prevents mast cell degranulation, reducing inflammation

31
Q

Mechanism of Anti-IgE therapy

A

Binds free IgE, preventing mast cell activation

32
Q

Pathophysiology of chronic obstructive pulmonary disease

A

1) chronic inflammation of drugs
2) progressive breathlessness

33
Q

Treatments of chronic obstructive pulmonary disease

A

1) bronchodilators- muscarinic antagonists & beta-2 antagonists

2) anti-inflammatory drugs- ICS

3) Anti-tussives (cough)

34
Q

What does pro-inflammatory ligands bind to whcih activates G-protein signalling & adenylyl cyclase?

A

Pro-inflammatory receptors

35
Q

What is PDE4?

A

Phosphodiesterase

36
Q

What does PDE4 break down in the cAMP signalling pathway?

A

cAMP into AMP, reducing signalling effects

37
Q

What do PDE4 inhibitors prevent?

A

cAMP breakdown

38
Q

What does cAMP activate to influence downstream signalling?

A

pKa, Epac 1/2

39
Q

Effects of Epac 1/2,

A

Inhibits Rap1 to decrease cell proliferation

40
Q

What does pKa activate & inhibit?

A

Activate: Creb, increasing anti-inflammatory cytokine production

Inhibit: NF-kB & Bcl6, decrease pro-inflammatory cytokines & cell proliferation