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fpc2 exam 7 > Asthma + COPD > Flashcards

Asthma + COPD Flashcards

1
Q

How much medication is needed for effective delivery through inhalation vs swallowing

A

10-20% inhaled
80-90% swallowed

(inhalation is more effective)

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2
Q

______ is the preferred method of delivery of most medications used in asthma and COPD

A

inhalation.

medication are needed acutely so it can work quickly

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3
Q

Pressurized metered dose inhalers: drugs are ___ from a canister with aid of propellant. most need to be ____ before use

A

propelled

shaken

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4
Q

What do space chambers do?

A

reduce the volume of velocity of particles-> less swallowing and more inhaled.

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5
Q

Why does the inhaler need to be shaken?

A

Medication is a suspension. if it sits there, it clumps and not effective

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6
Q

Dry Powder inhalers: devices scatter a ____ _____ by air turbulence on inhalation. Need to take __________ inspiurations

A

fine powder

quick and deep (forceful)

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7
Q

Nebulizers: turn liquid to _____ and is driven by _____. Administration though _____. What population is this good for?

A

fine mist
stream of gas.
mask
cognitive impairment/altered mentation

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8
Q

Some differences between MDIs and DPIs?

A

liquid vs fine powder
propellant vs none
shake vs don’t shake
slow inhale vs quick + forceful

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9
Q

Soft mist inhalers (respimat): propels a ____ of medication without help of propellant. Contains ____ per use than MDI/DPI.

A

cloud
more particules

might be hard to use for cog impaired patients

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10
Q

up to ___ of patients cannot use their inhalers corrects

A

80%. counseling is crucial

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11
Q

Patients should wait ____ seconds between puffs

A

60 seconds

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12
Q

Which should be used first if Both are prescribed: bronchodilator + corticosteroid

A

bronchodilator first.

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13
Q

Combination inhalers combine __________ in one devide

A

multiple active ingredients. this is more convenient for patients and improves compliants

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14
Q

Short acting inhalers (rescue inhalers) active ingredients include:

A

short acting β agonists (SABA)- albuterol
short acting muscarinic antagonists (SAMA)- ipratropium
too much use- poorly controlled asthma/COPD

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15
Q

How fast do short acting inhalers work?

A

1-2 minutes- quickly reverse bronchoconstriction.

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16
Q

Long acting inhalers (maintenance inhalers) are taken _______ to prevent symptoms of asthma and COPD. They open airways and reduce swelling for ___ hours

A

daily or multiple times per day.
12 hours.
These are the LABAS, LAMAS, ICS

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17
Q

Mechansim of bronchodilators:

A

constrict airway smooth muscle, reverse symptoms, prevent bronchoconstriction.

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18
Q

What are the medication classes of bronchodilators

A 
β 2 adrenergic agonists 
anticholinergic agents (muscarinic)
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19
Q

What are SABAs and LABAs that are on the market? (what do they end in)

A

“terol”
SABA: albuterol, levalbuterol
LABA: formoterol, salmeterol, vilanterol, indacaterol, olodaterol

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20
Q

What is the molecular structure difference between SABAs and LABAs?

A

large side chains on molecular structure. (more lipid-> retention in lipid layer of cell membrane)

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21
Q

What is the difference between albuterol and levalbuterol

A

albuterol is a racemic mix. leva is only R-albuterol.

IS leva better? clinical trial say unclear.

22
Q

What are some side effects of Β2 agonists?

A 
muscle tremor (B2 on skeletal- elderly)
Tachycardia + heart palpitations (peripheral ZVD from atrial β2 receptors)
hypokalemia (β2 stim K entry into skeletal muscle)
23
Q

What are SAMA and LAMA that are on the market? (what do they end in)

A

“ium” (mostly)
SAMA: ipratropium
LAMA: tiotropium, umeclidinium, aclidinium, glycopyrrolate

24
Q

Muscarinic antagonists have a higher selectivity for ___ receptors. These are in _____ and ____

A

M3 receptors

airway smooth muscle (Smooth muscle contraction) and submucosal cells (mucus secretion)

25
Q

MOA of muscarinic antagonists

A

block the action of acetylcholine at parasympathetic sites in bronchial smooth muscle-> bronchodilation

26
Q

Where are M1 muscarinic receptors?

A

epithelial cells + ganglia

27
Q

Where are M2 muscarinic receptors?

A

neurons (augment acetylcholine release)

28
Q

What are the effects of the muscarinic antagonists?

A

bronchodilator (at M3)

decreased mucus production (blockade of M3 receptor. M1 blockage will also help this)

29
Q

What are muscarinic antagonist side effects?

A

anticholinergic: dry mouth (xerostomia), headache, dizziness
other: URIs, bitter taste, cough

30
Q

What are inhaled corticosteroids that are on the market? (what do they end in)

A

“one” and “onide”

beclomthasone, budesonide, ciclesonide, flunisolide, fluticasone, mometasone

31
Q

What is the mechanism of ICS?

A

inhibit the inflammatory response, depression migration of polymorphonuclear leukocytes, reverse capillary permeability

32
Q

What is the downstream effects of inhaled corticosteroids?

A

increase β receptors on SM + improve them
reduce mucus + hyper secretion
reduce bronchial hyper responsiveness
reduce airway edema + exudation

33
Q

_____ are more effective in asthma than COPD. Why?

A

Inhaled corticosteroids

eosinophilic is more sensitive than neutrophilic

34
Q

What inflammatory cells do corticosteroids hit?

A

eosinophils, T cells, mast, Macs, DCs (everything)

cytokines are down as well as sheer numbers of inflammatory cells

35
Q

what cells do corticosteroids hit?

A

epithelial, endothelial, airway SM, mucus

36
Q

What are local side effects of ICS?

A

oral candidiasis, dysphonia (hoarse), cough

37
Q

are there any short acting inhaled corticosteroids?

A

no

38
Q

Systemic side effects of ICs includes?

A

pneumonia, growth suppression, osteoporosis, dermal thinning, adrenal insufficiency
(still less AEs than oral steroids)

39
Q

Why should high does of ICS be avoided in COPD?

A

risk of pneumonia

40
Q

How to prevent oral candidiasis in ICS?

A

rinse mouth and throat with warm water and spit out after inhaler use

41
Q

Short acting agents (can/cannot) be used as long term controllers
some long acting agents need to be taken _____

A

cannot

multiple times a day

42
Q

What are two leukotriene receptor antagonists? How are these delivered?

A

montelukast (Singulair) and safirlukast (accolade)

Tablets

43
Q

What is the MOA of leukotriene receptor antagonists?

A

inhibit cysteine leukotriene receptor resulting in reduced intracellular calcium + inactive phosphokinase C

44
Q

What are the results of leukotriene receptor antagonists?

A

decreased airway edema, SM relax, decreased inflammation

45
Q

What is the FDA boxed warning with Singulair?

A

serious neuropsychiatric events

46
Q

Severe asthma can use ____.

A

Monoclonal antibodies

47
Q

MOA of Omalizumab? MOA for Mepolizumab and resilizumab? MOA for Dupilimumab? what type are each indicated for?

A

Omal: Anti IgE (uncontrolled asthma step 4-5 therapy)
Mepol + resil: Anti IL5/5R (eosinophilic asthma step 4-5)
Dupil: anti IL4 (type 2 asthma allergic or require OCS )

48
Q

Why is Azithromycin used in late COPD?

A

anti-inflammatory properties.

reduce risk of exacerbation, but less effective in active smokers

49
Q

Why is Roflumilast (Daliresp) used in late COPD?

A

Oral PDE4 inhibitor -> inhibit breakdown cAMP-> reduce inflammation
reduce exacerbations in chronic bronchitis, severe COPD, hx of exacerbations (hospitalizations)

50
Q

What are the 4 intervention that all COPD patients will get?

A

smoking cessation
influenza, pneumonococcal + pertussis vaccines
physical activity
SABA (albuterol) and SAMA (ipratropium)

51
Q

How to classify groups A-D in COPD?

A

A: 0-1 exacerbations, low symptoms
b: 0-1 exacerbation, high symptoms
C: >1 exacerbations, low symp
D: >1 exacerbations, high symptoms

52
Q

Which treatment do each

A

fpc2 exam 7 (4 decks)

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