respiratory pharmacology Flashcards

1
Q

what drugs end in mab?

A

monocolonal antibodies e.g. reslizumab

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2
Q

what drugs end in sone?

A

corticosteroids e.g. dexamethasone

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3
Q

what drugs end in terol?

A

bronchodilators e.g. salmeterol

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4
Q

what drugs end in lone?

A

corticosterids e.g. prednisolone

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5
Q

what drugs end in nib?

A

kinase inhibitor

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6
Q

what are respiratory drugs targeted at?

A

respiratory regions of conducting pathways

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7
Q

what is the pathophysiology of bronchoconstriction?

A
Constriction of the airways due to
tightening of airway smooth muscle (ASM)
luminal occlusion by mucus and plasma
airway wall thickening
Leads to airflow obstruction.
Most commonly seen in asthma & COPD
Reversible vs non-reversible
In asthma, ASM is both primed to contract and is resistant to relaxation
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8
Q

how is bronchoconstriction treated?

A

Bronchodilators:
Adrenergic (sympathetic) - bronchodilation
Antoi-cholinergic (parasympathetic) - block bronchoconstriction
B-adrenoceptor agonist - smooth muscle relaxants, inhibit histamine for lung mast cells
SABA, LABA, ultra-LABAs, LABAs are often combined with inhaled corticosteroids for the
treatment of asthma and with an inhaled long-acting antimuscarinic
agent (LAMA) for treating COPD patients.
Atropine - naturally occuring anticholinergic found in deadly nightshade, block receptor M1-M5 on airway smooth muscle
Ipratropium bromide and tiotropium bromide

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9
Q

what is the pathophysiology of inflammation in the lungs?

A

Neutrophils and eosinophils, lead to direct lung damage and perpetuation of inflammation
Can be acute or chronic

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10
Q

how is inflammation treated?

A

Glucocorticoids:
Improve quality of life for asthma patients, reduce frequency of attacks, prevents irreversible damage to lungs
Reduce number of inflammatory cells in airways, suppresses inflammatory gene expression in airway epithelial cells
Side effects - loss of bone density, adrenal suppression, cataracts, glaucoma
Can become resistant (more common in COPD)
Most inhaled (ICS)

ICS - beclomethasone dipropionate, budesonide, ciclesonide, fluticasone propionate, mometasone furoate

Beta agonists and ICS often prescribed together:
ICS increase transcription of B2 receptor gene = increased expression on cell surface
LABA increase translocation of GR from cytoplasm to the nucleus after activation by ICS

MCA - low half life, delivered subcutaneous, expensive, highly specific, used for people who don’t respond to other medications

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11
Q

ho wis bronchiectaisis treated?

A
Associated with CF and others 
Obstructive
Permits infection 
Inflammatory cells into airways  
Antibiotics, PT, surgery, transplant for severe disease
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12
Q

how is fibrosis treated?

A

Fibrous connective tissue leads to permanent scarring and airway thickening, interstitial lung disease
Transplants, corticosteroids, pirfenidone and nintedanib = slow rate of disease in IPF, reduced fibroblast, collagen production, and mediators

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