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Pharmacy Stage 2 > Asthma Pharmacology > Flashcards

Asthma Pharmacology Flashcards

1
Q

what is asthma?

A

a recurrent and reversible obstruction to the airways in response to substance (stimuli).

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2
Q

6 examples of things that can cause asthma?

A
  1. allergens
  2. exercise (cold, dry air)
  3. respiratory infections
  4. smoke
  5. dust
  6. environmental pollutants
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3
Q

what does intermittent attacks of bronchoconstriction (asthma) cause?

A
  1. coughing
  2. wheezing
  3. breathing difficulties
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4
Q

What are the pathological changes to the bronchioles from long standing inflammation?

A
  1. smooth muscle mass increases in the bronchus
  2. interstitial fluid accumulates forming an oedema
  3. more mucus is secreted
  4. epithelial lining is damaged which exposes nerve endings
  5. lumen of airways is narrowed due to this inflammation
    (look at image on slide 4)
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5
Q

Two phases of an asthma attack?

A
  1. immediate phase

2. delayed phase

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6
Q

What happens during the delayed phase of an asthma attack?

A

an inflammatory reaction

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7
Q

What happens during the immediate phase of an asthma attack?

A

a bronchospasm

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8
Q

What happens during the early phase of an asthma attack (bronchospasm)?

A
  1. Bronchoconstriction
  2. Increased mucus production
  3. Vasodilation/increased vascular permeability
  4. Release of mediators of inflammation
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9
Q

What happens during the late phase of an asthma attack (inflammation)?

A
  1. Recruitment of leukocytes and T cells by cytokines and chemokines produced by resident mast cells and epithelial cells
  2. Further release of mediators of inflammation
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10
Q

Explain the process of sensitization to asthma?

A
  1. stimuli (e.g. allergen) antigen binds to denderitic cells on cell surface.
  2. TH2 cells have receptors which bind to this antigen (antigen presenting cells)
  3. This activates B cells.
  4. IL-4, a cytokine, stimulates the production of IgE antibodies from B cells.
  5. IgE activate mast cells
  6. IL-5, cytokine, then activate eosinophils to release granules and mediators.
    (image on slide 7)
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11
Q

What does TH2 cells release and what do they do?

A
  1. IL-4: stimulates the production of IgE by B cells and activate mast cells
  2. IL-5: activates locally recruited eosinophils
  3. IL-13: stimulate mucus secretion from bronchial submucosal glands and also stimulate IgE production by B cells and activate mast cells
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12
Q

What is the immediate response mechanism upon re-exposure to the asthma causing antigen?

A
  1. antigen binds to IgE-IgE receptor complex
  2. the antigen causes a cross-link between the IgE receptors so 2 complexes required for 1 antigen.
  3. this stimulates Ca2+ entry into mast cells.
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13
Q

What happens once calcium enters the mast cell during the immediate response to re-exposure to the antigen?

A
  1. release of secretory granules containing histamine production and release of other agents (LTC4 and LTD4) which all cause airway, smooth muscle contraction.
  2. release of substances (LTB4) , which attract cells into the area, hence causing inflammation (e.g. eosinophils)
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14
Q

What is the effect of mast cells in the immediate phase of an asthma attack (bronchospam)?

A
  1. bronchospasm
  2. increased vascular permeability
  3. mucus production
  4. recruitment of additional mediator-releasing cells from blood
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15
Q

During the late phase of asthma, what cells arrive at the site?

A

basophils
eosinophils
neutrophils
lymphocites

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16
Q

What mediators are released during the late phase of an asthma attack?

A
  1. Eotaxin
  2. Major basic protein
  3. IL1, IL6, TNF
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17
Q

What are eotaxins?

A

they are chemoattractants and they activate eosinophils.

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18
Q

What do major basic proteins do?

A

cause epithelial damage and more airway constriction

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19
Q

What do IL1, IL6 and TNF’s do?

A

Contribute to amplify inflammation

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20
Q

Where is the respiratory centre?

A

in the medulla oblongata

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21
Q

How is respiration regulated?

A
  • it is a spontaneous rhythmic discharge of signals from the medulla oblongata
  • it is an autonomic regulation
22
Q

What modulates the respiratory centre?

A

PCO2, PO2, afferents from the lungs (nerve-fibres that carry signals towards the respiratory centre from the lungs)

23
Q

Explain how the autonomic regulation of respiration works from the parasympathetic innervation.

A
  • Signal travels from the spinal cord to the M3 cholinergic receptors in the bronchial and vascular smooth muscles and the glands.
  • this increases IP3 levels
  • hence stimulating bronchoconstriction and increased mucus secretion
24
Q

Explain how the autonomic regulation of respiration works from the sympathetic innervation (in relation to adrenaline).

A
  • signal from the spinal cord is transmitted to the adrenal medulla
  • adrenaline is secreted into the blood
  • adrenaline acts on β2 receptors on bronchial smooth muscle
  • cAMP concentration increases
  • bronchodilation occurs
25
Q

Explain how the autonomic regulation of respiration works from the sympathetic innervation (in relation to noradrenaline).

A
  • signal from spinal cord transmitted to lungs.
  • neuronal noradrenaline acts on β2 receptors
  • mucus secretion decreases
26
Q

What is given to treat immediate phase bronchospasm?

A

bronchodilators e.g.:

  1. β2 agonists
  2. muscarinic antagonists
  3. xanthines
27
Q

What sympathetic effects do β2 receptors mediate?

A
  1. pupil dilation
  2. ciliary muscles relax (adjusted for far vision)
  3. airways dilate (bronchodilation)
  4. heart rate increases
  5. blood vessels in limb muscles dilate
  6. Blood vessels to visceral organs & skin constrict
  7. Brain activity general alertness
28
Q

How do β2 adrenergic agonists work?

A

Dilate the bronchi by:

  1. Direct action on the β2 receptors on bronchial smooth muscle (mimic circulating adrenaline)
  2. Decrease mucus secretion (mimicking noradrenaline)
  3. Possibly also inhibits mediator release from mast cells
29
Q

Give 2 examples of β2 adrenergic agonists and how long they act for.

A

Short acting-Salbutamol 4-6 hrs
Long acting Salmeterol 12 hrs
(both given as an inhaler)

30
Q

What are side effects to β2 adrenergic agonists?

A
  • Low tolerance

- Tremor

31
Q

What is the action of salbutamol and salmeterol on β2 adrenoreceptors?

A
  • they stimulate these receptors, which are coupled to G-proteins.
  • this activates adenylyl cyclase
  • this increases cAMP levels
  • resulting in smooth muscle relaxation
  • hence bronchodilation and decreased mucus secretion
32
Q

what 7 things does the parasympathetic innervation mediate?

A
  1. pupils constrict
  2. Lens of eye readjust for closer vision
  3. Airways in lungs constrict
  4. Heart rate decrease
  5. Blood vessels to limb muscles constrict
  6. Blood vessels to visceral organs more dilated
  7. Salivary secretions normalise
33
Q

What 6 things dose the muscarinic antagonist do?

A
  1. pupil dilate (relaxation of constrictor pupillary muscle) (blurred vision)
  2. increased focal length of the lens (relaxation of ciliary muscle)
  3. Bronchodilation
  4. decreased GI motility
  5. increased cardiac output, (rate & force)
  6. decreased exocrine gland secretion (dry mouth decreased sweating)
34
Q

what do muscarinic antagonists do?

A
  1. dilate the bronchi by blocking the M3 mediated bronchoconstriction
  2. decrease mucus secretion by blocking M3 mediated smooth muscle contraction
35
Q

Give an example of a muscarinic antagonist?

A

Ipratropium (given by inhalation)

36
Q

Although Ipratropium isn’t selective, it isn’t well absorbed into the circulatory system. Outline a benefit of this?

A
  • Ipratropium blocks M3 receptors to prevent muscle contraction.
  • If it got into the system, it could inhibit other muscles from contracting resulting in muscle spasms and other muscle related side effects e.g. stomach may not be able to churn food etc.
37
Q

What is Xanthine?

A

a derivative of caffeine and theobromine

38
Q

What does Xanthine do?

A
  • stimulates bronchodilation by blocking phosphodiesterase III and IV, hence increasing cAMP resulting in bronchodilation.
  • Inhibition of phosphodiesterases, which are associated with the inflammatory process, means Xanthine has good anti-inflammatory properties
39
Q

Give an example of a Xanthine?

A

Theophylline

40
Q

What side effects are associated with Theophylline?

A
  • chronotropic (modifying heart rate/rhythm) and inotropic (modifying speed/force of muscle contraction) stimulation
  • CNS stimulation
  • GI disturbances
41
Q

How do glucocorticoids work?

A

By suppressing the inflammatory response. Does this by inducing the synthesis of lipocortin which inhibits phospholipase A2, hence decreases the production of inflammatory mediators: LTD4, LTC4, LTB4, PGE2, PGI2

42
Q

What are LTC4 and LTD4

A

Spasmogens

43
Q

What are PGE2 and PGI2?

A

Vasodilators and cytokines (which stimulate lymphocytes)

44
Q

What are LTB4?

A

Chemotaxins

45
Q

Give examples of glucocorticoids and state their route of admin?

A

Beclomethasone-inhaled
Prednisolone-orally
Hydrocortisone-injected

46
Q

What phase of asthmatic shock are glucocorticoids useful for?

A

The delayed phase

47
Q

What is the role of sodium cromolyn?

A
  1. A mast cell stabiliser

2. Inhibits hyper-responsivity

48
Q

How does sodium cromolyn stabilise mast cells?

A

By inhibiting histamine and inflammatory mediators release

49
Q

How does sodium cromolyn inhibit hyper-responsivity?

A

By depressing neuronal reflexes triggered by irritant receptors

50
Q

What is used to target both phases of an asthmatic shock and persistent asthma?

A

Cysteinyl-leukotriene (Cys-LT1) receptor antagonist

51
Q

What drugs cause adverse effects in patients with respiratory diseases?

A
  1. Beta-adrenoreceptor antagonists can cause severe fatal asthma
  2. ACE inhibitors can cause cough
  3. NSAID precipitate asthma

Pharmacy Stage 2 (85 decks)

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