mid term Flashcards

(54 cards)

1
Q

abbreviation BID

A

twice daily

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2
Q

abbreviation PRN

A

as needed

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3
Q

abreviation NPO

A

nothing by mouth

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4
Q

abbreviation Q4h

A

every 4 hours

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5
Q

drug administration

A

how drugs are delivered to the body

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6
Q

routes of administration

A

enteral
parenteral
transdermal
inhalation
topical

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7
Q

pharmacokinetics

A

what the body does to the drug

-absorption
-distribution
-metabolism
-elimination

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8
Q

primary organ for excretion

A

kidney

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9
Q

primary organ for metabolism

A

liver

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10
Q

drug half life affect dosing frequency

A

short T 1/2- more frequently
long T 1/2 life- less often

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11
Q

what percentage of inhaled aerosol reaches the lower respiratory tract with current devices?

A

10-30%

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12
Q

pharmacodynamics

A

what the drug does to the body

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13
Q

L/T ratio

A

proportion of drug availability from the lung out of the total systemically available drug

-higher ratio=more efficient aerosol drug delivery to resp trach

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14
Q

Bioavailability
oral vs inhaled

A

proportion of drug that reaches systemic circulation

*oral-not 100%–>first pass effect, very little reach systemic circulation

*inhaled- 100%–>surpasses first pass effect, higher amount reach circulation

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15
Q

pharacogenetics

A

patients response to drugs due to hereditary differences

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16
Q

agonist vs antagonist

A

agonist- drug or chemical that binds to corresponding receptor and initiates cellular effect

antagonist- drug or chemical that is able to ind to receptor but cause no response

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17
Q

what is the parasympathetic system

A

“rest and digest”
-decrease Hr
-decrease pupil dilation(miosis)
-increase mucus
-increase digestion
-bronchoconstriction

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18
Q

what is the sympathetic system

A

‘fight or flight’
-increase Hr
-increaseBP
-increase pupil dilation(mydriasis)
-bronchodilation
-decrease digestion
-

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19
Q

what is the neuotransmitter for parasympathetic system

A

acetycholine

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20
Q

what is the neurotransmitter for sympathetic system

A

norepinephrine

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21
Q

receptor site for the parasympathetic system and acetylcholine effects

A

M1- CNS
M2- heart–decrease HR
M3- smooth muscle and submucosal glands–bronchoconstriction

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22
Q

receptor sites for sympathetic system and epinephrine effects

A

alpha 1- vessels- vasoconstriction
beta 1- heart- increase hr
beta2- lungs- bronchodilation

23
Q

overstimulation of parasympathetic system leads to what?

A

SLUD
salivation, lacrimation, urination, defecation

24
Q

what inactivates acetylcholine at parasympathetic terminal receptor site

A

cholinesterase

25
agent/drug that inhibits parasympathetic system effects/ blocks acetylcholine
parasympatholytic/ anticholinergic agent
26
agent/drug that mimics parasympathetic nervous system/ mimics acetylcholine
parasympathomimetic/ cholinergic agent
27
a direct acting cholinergic agent used in bronchial challenge test
methacholine-bronchoconstriction
28
agent/drug that mimics sympathetic system effects
sympathomimetic/adrenergic agent
29
agent/drug that inhibits the effect of sympathetic system
sympatholytics/ antiadrenergic agent
30
what enzyme breaks down epinephrine
COMT and MAO
31
why do parasympatholytic drugs like atropine increase Hr
-block acetyolcholine receptors *anticholinergic agent
32
what effect does adrenergic stimulation have on bronchial smooth muscle
dilation epinephrine stimulates beta 2 receptors
33
what effect does propranolol have on bronchodilator therapy in asthma
propranolol is a beta blocker antagonistic effect
34
how are drugs that block acetylcholine receptors classified
anticholinergic agents
35
3 types of adrenergic bronchodilators
ultra short- <3 hrs short acting- 4-6 hrs long acting- 12-24hrs
36
clinical indication for adrenergic bronchodilators
relaxation of smooth airway muscle in the presence of reversible obstruction -asthma, bronchitis, emphysema, bronchiectasis
37
ultra short acting agent
racemic epinephrine - used for the alpha 1: vasconstriction relieve inflammation
38
short acting agent
"rescue" 4-6hrs -albuterol -levabuterol
39
long acting agents
12-24 hrs maintenance, control bronchospasm, and control nocturnal symptoms -salmeterol -formoterol -arformoterol -indacaterol -olodaterol
40
inhaltion route benefits
-rapid onset -smaller doses -reduce side effects -drug delivered directly to target organ -relatively safe
41
continuous nebulization of albuterol
manage asthma especially during acute exacerbations -reduce frequent treatment -constantly stimulating beta 2 receptors
42
primary indication for anticholinergic bronchodilator
COPD maintenance
43
benefit of combined beta 2 agonist and anticholinergic
beta 2- keep airways open anticholinergic- will prevent bronchoconstriction ex: combivent, duoneb
44
Ipratropium bromide
-atrovent-MDI,SVN,Nasal -short acting, treats acute bronchoconstriction -6 hrs -used more frequently
45
tiotroprium bromide
-spirva-DPI, once daily -long lasting, maintenance therapy of bronchoconstriction -24hrs
46
how do corticosteroids benefit patients with COPD
reduce inflammation prevent exacerbations reduce mucus production improve symptoms
47
explain the anti-inflammatory mechanism of inhaled corticosteroids asthma management
-inhibit inflammatory response -reduce mucus production -reduce airways swelling
48
how can systemic corticosteroids suppress the hypothalamic-pituitary- adrenal HPA axis
decrease production of cortisol
49
primary inflammation cells for asthma and copd
asthma- mast cells, eosinophil copd-neutrophils
50
asthmatic reaction
early-exposed to allergens trigger response-->peak 15 min-1hr, activation of mast cells-->release of histamine=immediate bronchoconstriction late-response 6-8 hrs, cells involved: eosinophils, neutrophils and t cells= prolonged inflammation
51
strategies to prevent oral thrush in pt using inhaled corticosteroids
minimal dose use reservoir rinse mouth after use
52
how do spacers affect drug delivery and side effects in MDI use
reduce orophrangeal deposition and increase lung deposition
53
strategies to increase lung deposition of inhaled medication
-educating on proper techniques -breath holding
54
why do COPD patients have hypoxemia and hypercapnia
air trapping and limitations to airflow