Asthma/ COPD Flashcards

1
Q

therapy for Asthma/ COPD affects the physiology by doing what? (2 things)

A

1) decreasing airway resistance: (1/radius^4)

2) decreasing airway response to irritants (allergen, cold air, exercise)

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2
Q

Methylprednisolone

A

systemic corticosteroid (along with prednisone)

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3
Q

Flucasone

A

Aerosol corticosteroid (local acting)

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4
Q

Albuterol

A

Short acting Beta2 adrenergic agonists

(SABA), along with levabuterol

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5
Q

Salmeterol

A

long acting Beta2 agonist (LABA), along with formoterol

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6
Q

Ipatropium Bromide

A

Short acting Muscarinic antagonist (SAMA)

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7
Q

Tiotroipum

A

Long acting muscarinic antagonist (LAMA)

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8
Q

Theophylline

A

Phosphodiesterase inhibitor which is non-selective aka
Methylxanthine drug

(selective is ODE4 inhibitor: roflumilast (don’t need to know)

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9
Q

Montelukast

A

leukotriene pathway inhibitor (also zileuton* don’t need to know)

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10
Q

Omalizumab

A

IgE inhibitor (“alergEEEE” inhibitor)

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11
Q

asthma’s two mechanisms for decreased radius

A

1) increased constriction of airway,

2) increased mucus production (disabling epithelial cilia)

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12
Q

asthma acts on CNS by

A

inflammatory response that constricts the bronchioles.

…inflammatory response also increases plasma leak and epithelial shedding via TH2 cells,,dendrites, eosinophils, and sensory nerves)

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13
Q

6 asthma stimuli

A
allergens
viral infections ^
pollutants^
cold air*
exercise*
stress*

^ mucosal inflammation
*non-specific hyperreactivity

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14
Q

Process of allergenic asthma

A

Early response

1) Mast cell captures Allergen
2) Mast cell degranulates and releases histamine (etc other mediators).
3) Histamine contracts airway by acting on smooth muscle.
4) –> forced expiration volume is restricted.

Late response
5) Mast cells also recruit T-lympthocytes, which releaes ILs etc. to call Eosinophils, which increase inflammation and increases Neutrophils (hallmark of asthma)

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15
Q

Which stage (early or late) do maintainace drugs work on?

A

Late stage. Affect airway responsiveness to allergens.

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16
Q

What affects early stage?

A

Bronchidilators (rescue drugs, “SA-“ drugs) IV corticosteroids

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17
Q

most asthma drugs are IV

A

most are inhaled, so they don’t target the GI, can be IV in hospital

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18
Q

tone of airways is mostly maintained by which part of NS, so we use anti-_______

A
parasympathetic mediated (vagus)
use anti-muscarinic to block and relax
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19
Q

optimal particle size for asthma meds

A

2-5ums 10-20%inhaled to lungs (less than 2.5um stays in mouth, more goes to GI, liver, systemic)

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20
Q

Asthma meds target

A

1) corticosteroids, leukotriene inhibitors and IgE antibodies target the inflammatory immune cascade
2) Muscarinic antagonists target muscarinic receptors
3) Beta2 adrenergic receptors and methylxanthines target bronchoconstriction

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21
Q

what drug is a methylxanthine?

A

Theophilline

target B2 adrenergic agonists

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22
Q

2 pneumonic for Beta1 and Beta2 sites

A

One heart
two lungs
(and “Be” my “#1” <3 valentine)

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23
Q

Most effective treatment for preventing asthma attack according to Ceriak

A

Inhaled Corticosteroids (ICS) For example Fluticasone.
decrease exacerbations
Fast anti-inflammatory effect (hrs), but max benefit is wks-mths after daily use.

Adding a LABA even more effective (better than increasing steroid dose)

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24
Q

inflammation in cell starts when…

A

NF-kappa-B activated

with a captivator, it binds in nucleus to acetylate (enhances gene transcription)

25
Q

Good Corticosteroid effects

A

1) suppress inflammatory gene transcription
2) 17a substitution increases topical activity of ICS
3) no effect on mediator release, but increase B2 receptors in lung structual cells

26
Q

Adverse Effects:

A

1) thrush (oral candidiasis) (gargle to prevent)
2) suppresses hypothalamic pituitary axis–> bone resorption, skin thinning, growth retardation (mostly for high dose ICS/systemic effects)
3) doesn’t help with COPD because it COPD is not about inflammation

27
Q

dx of COPD means they have…

A

FEV1<50% with exacerbations

28
Q

MC asthma control is a combo of

A

ICS + SABA

29
Q

1st pass metabolism of ICS

A

1st pass metabolism in liver once in systemic circulation (80-90% swallowed to GI tract)
10-20% to lungs.

30
Q

COPD is reversible True or false?

A

false… includes emphysema and/or chronic bronchitis, usually a combo

31
Q

Astha is reversible True or False?

A

true. chronic inflammatory disease increasing airway resistance is temporarily reversible (avoiding triggers, and through medication,) but not curable

32
Q

types of inhalers

A

1) metered dose inhalers (MDI) pressurized cannister
2) MDI with spacer (decreases amt to GI/ posterior pharynx)
3) Dry powder (released by fast deep breath)
4) MDI with facemask (infant kids)
5) Nebulizer with mouthpiece/mask (mist for infants, kids, people who can’t use inhaler)

33
Q

Methylprednisolone category

A

systemic corticosteroid

34
Q

adverse effect of methylprednisolone

A

bone resorption, skin thinning, growth retardation

35
Q

indications for methylprednisolone

A

asthma exacerbation
SHORT TERM 3-10days then switch to ICS.
IV use for status asthmaticus

36
Q

Flucanisone

A

aerosol corticosteroid

37
Q

indications for flucanisone

A

controversial use in COPD
only used if FEV1 is <50% with exacerbations
No anti-inflammatory effect

38
Q

contraindications for flucasone

A

oropharyngeal andidaisis, dysphonia (gargle and spit to prevent)
high dose the same as methyl prednisolone (bone resorption, skin thinning, growth retardation)

39
Q

Albuterol

A

SABA used for rescue

bronchodilation (use less than 2x/wk or step up drugs)

40
Q

timing of SABA

A

albuterol works in 3-5min, peaks at 30min, lasts for 3-6 hours

41
Q

timing of LABA

A

12 hours (salmeterol)

ultra LABA used for COPD 36hrs

42
Q

Methylanthines mechanism of action

which drug is associated

A

work though preventing C-AMP –> 5AMP and PKA (downstream targets to relax smooth muscle, by decreasing Ca into cell via K-channel de-activation to prevent depolarization)

Basically do opposite of phosphodiesterase which changes C-AMP –> 5amp

Theophylline is a phosphodiesterase inhibitor

43
Q

contraindications for LABA and SABA

A

SABA: tolerance, rarely:tachycardia
LABA: tremor, tachycardia, hypokalemia
(need to also take ICS if asthma but can be alone in COPD)

44
Q

Ipatropium Bromide

A

Muscarinic antagonist which blocks effect of Ach release from vagus nerve to M3 receptors to stop muscle contraction: i.e. they bronchodilate, AND they reduce mucus secretion.
Ipa is Short acting SAMA

45
Q

pneumonic for remembering which is LAMA and which is SAMA

A

SAMA: sam is an IPA rat (IPrAtropium) (ipRATropium)

LAMA: Is your momma a llama? “No, es mi tio” (Spanish for, “No, it’s my uncle”)

46
Q

other pneumonic for SABA,LABA, SAMA, LAMA

A

SABA is the shorter word of the two Beta AGONISTS, but SABA is longer word…
Albuterol
Salmeterol

But with Muscarinic ANTAGONISTS, since they are anti- it’s backwards…SAMA is a longer word, and LAMA is shorter…
Ipratropium Bromide
Tiotropium

47
Q

indication for SAMA/LAMA

A

COPD (sometimes effective)

Asthma if intolerant of B2 agonists or in combo with B2 agonists

48
Q

Adverse effects of SAMA/LAMA

A

dry mouth, urinary retention (caution with BPH in elderly men),
Few other systemic side effects because poorly absorbed

49
Q

Theophylline

A

Phosphodiesterase inhibitor that works to block cAMP from being changed to 5AMP and PKA. this is also how Beta2 agonists work, BUT theophylline does it INSIDE the cell. (effect is relaxed and open bronchioles)

50
Q

side effect of Theophyline

A

NARROW THERAPEUTIC WINDOW, monitor plasma levels taken PO

  • CV effects (vasodilation, tachycardia, arrhythmias
  • CNS stimulation: anxiety, tremor, convulsions
  • GI effects: N/V
51
Q

MOA for theophylline

A

COPD (improves diaphragm contraction)
Asthma
blocks activation of adenosine receptor on smooth muscle (decreased contraction) and mast cells (decreased histamine release)
increases histone deacetylation (decreasing cytokine production/release)

52
Q

how does Theophylline work with other drugs

A

in COPD, increase muscle contractility, improving ventilatory function may increase ICS effect

53
Q

Montelukast

A

PO
leukotriene receptor agonist
LT pathway inhibitor so inhibits bronchoconstriction

54
Q

indication for montelukast

A

add on for mild-moderate asthma who aren’t compliant with ICS, or not well-controlled.
not used with COPD

55
Q

negative side effects of montelukast

A

hepatic dysfunction

neuropsychiatric events

56
Q

Omalizumab

A

SQ
IgE Inhibitor
humanized anti IgE monoclonal AB that binds to Fc portion so it can’t bind to mast cells

57
Q

Indication for Omalizumab

A

reduces use of corticosteroids used for allergy rhinitis prophylaxis

58
Q

problems with omalizumab

A

expensive, possible anaphylaxis within 2 hours
WIDE variation in response
NEEDS TO BE MONITORED