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Medicine Phase 2a Respiratory > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What type of drug is Reslizumab

A

…mab = Monoclonal AntiBody

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2
Q

What type of drug is Dexamethasone

A

…sone = corticosteroid

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3
Q

What type of drug is Prednisolone

A

…lone = corticosteroid

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4
Q

What type of drug is Salmeterol

A

…terol = bronchodilators

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5
Q

What type of drug is Nintedanib

A

…nib = kinase iNhIBitor

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6
Q

What are the 2 vital regions of the respiratory system

A

Conducting airways

Respiratory region

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7
Q

What does the respiratory region consist of

A

Respiratory bronchioles
Alveolar ducts
Alveolar sacs

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8
Q

What is most common device used to inhaled respiratory drugs

A

Inhaler

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9
Q

What device delivers medication in form of an aerosol

A

Nebuliser

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10
Q

Describe differences in blood flow between conducting airways and respiratory region

A

Conducting airways - smaller surface area and lower regional blood flow
Respiratory region - accounts for >95% of lungs surface area and is directly connected to the systemic circulation via the pulmonary circulation

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11
Q

Deliver systems for inhaled drugs

A

Pressurised metered-dose inhalers (pMDIs)
Spacer devices
Dry powder inhalers (DPIs)
Nebulisers

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12
Q

What causes bronchoconstriction of airways

A

Tightening of airway smooth muscle (ASM)
Lumenal occlusion by mucus and plasma
airway wall thickening

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13
Q

In what diseases would you most commonly see bronchoconstriction

A

Asthma

COPD

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14
Q

2 main categories of treating bronchoconstriction

A

Bronchodilation - adrenergic (sympathetic)

Block bronchoconstriction - anti-cholinergic (parasympathetic)

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15
Q

Examples of bronchodilators

A

Beta 2 Adrenoreceptor Agonists

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16
Q

How do Beta 2 Adrenoreceptor Agonists work

A

Act on B2-adenoreceptors to cause smooth muscle relaxation and bronchodilation
Also inhibits histamine release from lung mast cells

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17
Q

Examples of Beta 2 Adrenoreceptor Agonists

A

SABA/Short acting B2-adrenoreceptor agonists
LABA/Long acting B2-adrenoreceptor agonists
ultra-LABA (E.g. Indacaterol - allow once daily dosing)

18
Q

Example of SABA

A

Salbutamol

19
Q

Example of LABA

A

Formoterol and Salmeterol

20
Q

What LABAs combined with in treatment of asthma

A

Inhaled cortiosteroids

21
Q

What are LABAs combined with in treatment of COPD

A

Inhaled Long-acting Anti-Muscarinic Agent (LAMA)

22
Q

What is effect of acetylcholine on airway smooth muscle

A

Contracts ASM by activating muscarinic receptors on smooth muscle cells

23
Q

What is effect of anticholinergics on muscarinic receptors

A

Block ACh binding

24
Q

What is Atropine

A

Naturally occuring anticholinergic found in deadly nightshade
Reverses bronchoconstriction caused by parasympathetic nerve stimulation

25
Q

What is the most effective anti-inflammatory drug for asthma

A

Glucocorticoids

26
Q

Effects of inhaled corticosteroids on asthma

A

improve the quality of life of patients with asthma
improve lung function
reduce frequency of exacerbations
Can prevent irreversible airway changes

27
Q

Examples of Inhaled Corticosteroids

A 
Beclomethasone dipropionate (pMDI and DPI)
Budesenide
28
Q

How do inhaled corticosteroids reduce inflammation

A

Reduce numbers of inflammatory cells in airways:
Suppress the production of chemotactic mediators
Reduce adhesion molecule expression
Inhibit inflammatory cell survival in the airway
Suppress inflammatory gene expression in airway epithelial cells

29
Q

Side effects of ICS

A 
Reduce SEs by giving at lowest effective dose
Overuse in long-term can cause:
Loss of bone density
Adrenal suppression
Cataracts, glaucoma
30
Q

Corticosteroid resistance in asthma and COPD

A

(Non-eosinophilic) Asthma - approx 10% patients require maximal dose and 1% require regular oral corticosteroids. Small no. patients are completely unresponsive to ICS.

COPD - most patients are resistant to ics

31
Q

Mechanisms of corticosteroid resistance

A

Possible genetic causes – could this allow us to predict which patients will be resistant?
Poor GR binding and nuclear translocation
Reduced downstream cellular signalling following corticosteroid:GR binding

32
Q

*Interactions between B2 agonists and ICS

A

Glucocorticoids increase the transcription of the b2-receptor gene, resulting in increased expression of cell surface receptors.
Long-acting b2-Agonists increase the translocation of GR from cytoplasm to the nucleus after activation by glucocorticoids

This all leads to an overall greater efficacy and need for lower doses

33
Q

What cells largely drive inflammation in allergic asthma

A

Eosinophils

Lymphocytes

34
Q

What is Bronchiectasis

A

Obstructive lung disease
Abnormal dilation of the bronchi - excessive sputum production and chest pain
Associated with cystic fibrosis (but can have non CF bronchiectasis)

35
Q

Treating Bronchiectasis

A

Antibiotics - infective elements
Physical therapy clears airways
Surgery and transplantation in severe cases
Medication

36
Q

Medical treatment bronchiectasis

A

Mucolytics treat hypersecretion
B2 agonists most useful in COPD/asthma/Bronchiectasis overlap syndromes
Anticholinergics and ICS have limited effect

37
Q

Complications of excessive fibrosis

A

excessive fibrous connective tissue leads to permanent scarring, airway wall thickening and breathing difficulties

38
Q

Fibrosis medical treatment

A

Some forms respond to corticosteroids
PIRFENIDONE and NINTEDANIB are new drugs that significantly slow the rate of disease progression in Idiopathic Pulmonary Fibrosis

39
Q

What is Pirfenidone

A

Commonly used antifibrotic in IPF
Anti-fibrotic, Anti-inflammatory and Anti-oxidant properties
Oral

40
Q

Effects of pirfenidone

A

Reduces:
fibroblastproliferation
collagenproduction
production of fibrogenic mediators

41
Q

What is Nintendanib

A

Tyrosine Kinase Inhibitor

42
Q

How does Nintendanib work

A 
Tyrosine kinase inhibitor
Inhibits VEGFR (Vascular endothelial growth factor receptor) and other growth factor receptors, which are some of the drivers of the fibrotic process

Medicine Phase 2a Respiratory (22 decks)

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