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BLOCK 9; Week 4-M > Bronchodilator Therapy-Singer > Flashcards

Bronchodilator Therapy-Singer Flashcards

1
Q

What are the cellular mechanisms of asthma?

A
  1. allergen goes to dendritic & mast cells
    dendritic cells activate th2 cells & mast cells activate eosinophils
    eosinophilia
    get some neutrophils too
  2. smooth muscle hypertrophy & hyperplasia
  3. mucus plugs from goblet cell hyperplasia
  4. nerve activation–>epithelial shredding & bronchoconstriction
    epithelial leakiness & edema in lungs.
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2
Q

What is the FEV1 like for the following asthma patients?
mild
moderate
severe

A

mild: FEV1 greater b/c a little smooth muscle hypertrophy w/o all the other complications yet
moderate: FEV1 lower, fibrosis begins
severe: FEV1 very low

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3
Q

Which levels of asthma are bronchodilators & corticosteroids most helpful for?

A

mild-moderate

hard to help severe asthmatics

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4
Q

T/F Smooth muscle is a distinct part of the asthma, completely separate from the immune process.

A

False. It is a part of the immune process.

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5
Q

Describe the basics of COPD.

A

Emphysema & Chronic Bronchitis
bronchioles disintegrate & alveolar walls are destroyed
clogged with mucus, but no inflammatory component

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6
Q

T/F First line treatment for COPD is corticosteroids.

A

False. no inflammatory component to this disease, so it doesn’t really help.

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7
Q

HOw do epigenetics play a role in asthma?

A

environmental exposure of parent can lead to epigenetic modification that is inherited by child & causes asthma

including: covalent modification of cytosine in CpG dinucleotides
* **maternal alleles appear to matter more.

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8
Q

What must you keep in mind when you decide on doses of inhaled drugs for asthma?

A

80% of the drug will be ingested instead of inhaled–>potential systemic effects

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9
Q

What were the first drugs used in asthma pre-1900?

A

beta agonists: ephedrine
anticholinergics
black coffee (caffeine similar to theophylline)

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10
Q

When did corticosteroids begin being used for asthma treatment?

A

around the 1950s

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11
Q

WHat are methylxanthines & where are they used in the world for asthma treatment?

A

theophylline
aminophylline
these are cheap & are used in other countries b/c of risk for seizures

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12
Q

What are some important examples of beta 2 adrenergic agonists? What are they all derivatives of?

A

albuterol
formoterol
salmeterol
**all derivatives of NE or epi

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13
Q

WHat is the MOA of beta 2 adrenergic agonists?

A

activates beta 2 receptor on muscle cells of lung
G-protein coupled receptor, activates adenylyl cyclase
increase in cAMP
activates PKA
lowers intracellular calcium
vasodilation

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14
Q

What are some other good effects of beta adrenergic agonists?

A

Prevention of mediator release from mast cells.

Prevention of microvascular leakage and edema.

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15
Q

What are some maybe not so good effects of beta adrenergic agonists?

A

Increase in mucus secretion from submucosal glands and ion transport across airway epithelium.

Reduction in neurotransmission in human airway cholinergic nerves by an action at presynaptic b2 receptors to inhibit acetylcholine release.

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16
Q

What are some short acting bronchodilators (SABA)? How long do they work for? How should they be used?

A

albuterol
3-4 hours
can be used 4-6X/day
used for acute attacks

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17
Q

What are some long acting bronchodilators (LABA)? How long do they work for How should they be used?

A

salmaterol
formoterol
last more than 12 hours
taken BID w/ inhaled corticosteroid

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18
Q

Can a LABA ever be used w/o ICS?

A

Yes, for COPD.

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19
Q

What are some important side effects for beta 2 agonists?

A 
Muscle tremor
Tachycardia 
Hypokalemia
Restlessness
Hypoxemia

Increased mortality with LABA

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20
Q

What is an important potential side effect of theophylline?

A

seizures refractory to AEDs

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21
Q

What are some examples of methylxanthines, still in the category of bronchodilators?

A

xanthine
theobromine
theophylline
caffeine

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22
Q

What is the MOA of theophylline?

A

inhibits phosphodiesterases
keeps cAMP levels high for activation of PKA
If PKA is active–decreased intracellular calcium & bronchodilation

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23
Q

What is an additional function of theophylline?

A

acts on adenosine receptors

24
Q

We’ve talked about how awesome theophylline is in bronchodilation. What are other cool effects it has in the lung?

A

decreases endothelial cell leakage
increases respiratory skeletal muscle strength
decreases eosinophils, T lymphocytes, mast cells, macrophages

25
Q

What are the effects of methylxanthines on CNS, cardiac, metabolic systems?

A

Think of side effects of coffee!
CNS – increased alertness, reduced fatigue, tremor, insomnia, anxiety

Cardiovascular – increased cardiac contractility, reduced peripheral vascular resistance

Metabolic –diuresis, increased basal metabolic rate

26
Q

Which types of asthma patients benefit from methylxanthines? How is it administered?

A

oral or IV
more severe patients
given w/ ICS

27
Q

What can methylxanthines do in patients with COPD?

A

can decrease corticosteroid resistance thru HDAC activation (histone deacetylase)

28
Q

Why might you need to increase the dose of theophylline in some patients?

A

b/c it has increased clearance in marijuana smokers & kids

induction of CYP12

29
Q

When might you see decreased clearance of theophylline?

A

Reduced clearance in liver disease, heart failure, pneumonia

Reduced clearance with co-administration of

- erythromycin
- ciprofloxacin
- cimetidine
30
Q

There are some weird side effects specific to theophylline based off of its A1 receptor antagonism, PDE4 inhibition, and PDE3 inhibition. What are they?

A

A1 receptor antagonism: Diuresis
PDE4 inhibition: N/V, HA, gastric discomfort
PDE3 inhibition & A1 receptor antagonism: cardiac arrhythmias & epileptic seizures

31
Q

What are the different types of muscarinic receptors in the airway?

A

M1: pregang
M2: postgang, affects Ach release onto muscle
M2 & M3 on muscle:
M2-counteract relaxation, M3-contraction

32
Q

What are some examples of anticholinergics used in bronchodilation in asthma?

A

atropine
ipratropium
tiotropium

33
Q

Which of the anticholinergics used to treat asthma are nonselective?

A

atropine & ipratropium both nonselective

tiotropium acts on M1-M3, but dissociates quickly from M2, & is thus the most selective.

34
Q

Which anticholinergics are tertiary & which are quarternary ammonium derivatives?

A

tertiary: atropine
quaternary: ipratropium, tiotropium

35
Q

Which of the anticholinergics has a short half life–needing to be taken 4-6X/day?

A

ipratropium

36
Q

T/F Anticholinergics will really open up the airways of patients w/o asthma or COPD.

A

False. Only does anything if there is a problem already.

37
Q

What are some side effects of ipratropium?

A

bitter taste

can cause glaucoma if used in an elderly patient’s face mask

38
Q

What is a side effect of tiotropium?

A

dry mouth

39
Q

How can we summarize the mechanisms of the bronchodilators?

A

Beta 2 receptors on smooth muscle cells stimulate AC to make cAMP (beta 2 agonists). Phosphodiesterase tries to break it down (theophylline).
cAMP activates PKA & promotes bronchodilation.
Adenosine promotes bronchoconstriction (theophylline).
Acetylcholine promotes bronchoconstriction (anticholinergics).

40
Q

What are some important examples of inhaled corticosteroids?

A

budesonide
fluticasone
beclomethasone

41
Q

What is the MOA of ICS?

A

repress gene transcription via glucocorticoid receptor
less inflammatory cell transcription
**also decreases endothelial cell leakage, mucus secretion

42
Q

How are ICS usu taken?

A

BID

43
Q

What is something special about beclomethasone?

A

taken as prodrug

cleaved by esterases in lung-then an active steroid

44
Q

Which ICS have a lot of 1st pass metabolism in the liver & therefore have fewer systemic & adverse SE?

A

fluticasone

budesonide

45
Q

Which drug combos make up advair?

A

Fluticasone/salmeterol

46
Q

Which drug combo makes up symbicort?

A

Budesonide/formoterol

47
Q

What are some local side effects of ICS?

A

Local side effects
Dysphonia
Oropharyngeal candidiasis
Cough

48
Q

What are some potential systemic side effects of ICS?

A 
Adrenal suppression and insufficiency	
Growth suppression	
Bruising	
Osteoporosis	
Cataracts	
Glaucoma	
Metabolic abnormalities (glucose, insulin, triglycerides)
Psychiatric disturbances (euphoria, depression)	
Pneumonia
49
Q

What is the MOA of leukotriene antagonists? Give an example.

A

Trigger causes rise in mast cells & eosinophils. These form arachidonic acid + 5-lipoxygenase→leukotrienes. Bind leukotriene receptors & form plasma exudation, mucus secretion, bronchoconstriction, eosinophil recruitment.
LT antagonists act on leukotrienes so that they can’t bind receptors.
Ex: montelukast

50
Q

What is an example of a 5-lipoxygenase inhibitor that prevents the formation of leukotrienes in the first place?

A

zileuton

51
Q

What is the clinical use of montelukast?

A

Orally administered
Widely used to treat children
Avoid ‘steroid phobia’
Significant improvement in mild-moderate asthma
Benefit aspirin-sensitive asthma
Indicated as an add-on therapy in patients not responding to an ICS

52
Q

What are possible side effects of montelukast?

A

Rare cases of hepatic dysfunction

Churg-Strauss syndrome

53
Q

What is an anti-IgE therapy option for asthmatics?

A

omalizumab binds up IgE, decreases chronic inflammation

54
Q

When should omalizumab be used?

A

only severe asthmatics
subcu injections 2-4 weeks
need to take titers a lot too.

55
Q

Give steps 1-5 for management of asthma patients.

A
  1. albuterol, beta agonist as needed
  2. Low-dose ICS, leukotriene antagonist
  3. ICS + LABA, maybe some theophylline
  4. High dose ICS + LABA, maybe + theophylline or leukotriene antagonist, start to consider omalizumab
  5. omalizumab OR long term oral corticosteroid

BLOCK 9; Week 4-M (8 decks)

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