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PHARMACOLOGY > pharmacotherapy & adrenergic drugs > Flashcards

pharmacotherapy & adrenergic drugs Flashcards

1
Q

Cholinesterase inhibitors (CI) mechanism of action

A
  • prevent breakdown of ACh by acetylcholinesterase
  • increase amt of ACh in the neurologic junction
  • more ACh is present to activate receptors,
  • INDIRECT CHOLINERGIC AGONISTS
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2
Q

what are the two types of cholinesterase inhibitors

A
  • reversible

- irreversible

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3
Q

what are the reverse cholinesterase inhibitors drug

A

Neostigmine
Physotigmine
Pyridostigmine

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4
Q

muscular effects of reversible cholinesterase inhibitors

A

therapeutic dose- increase force of muscle contraction

toxic dose- decrease force muscle contraction

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5
Q

CNS effects of reversible cholinesterase inhibitors

A

therapeutic doses - mild stimulation

toxic doses- depress CNS function and respiratory drive at toxic doses

(must cross BBB)

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6
Q

indication of Neostigmine

A
  • M. gravy,
  • reversal of neuromuscular blockage
  • treats MG crisis via IV
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7
Q

counseling points for neostagmine

A

paradoxical anti-cholinesterase weakness can occur

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8
Q

indication of Physostigmine

A

reversal of anti-cholinergic toxicity (muscarinic antagonist toxicity)

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9
Q

Physostigmine counseling points

A

rapid IV administration can cause respiratory depression

  • seizures and bradycardia
  • give SLOW IV push or infusion
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10
Q

Pyridostigmine indication

A

MG

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11
Q

Pyridostigmine counseling points

A
  • do not crush ER formulation
  • time dose of IR formulation to provide maximal function
  • avoid holding or delaying doses
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12
Q

Adverse effects of Reversible Cholinesterase Inhibitors (Neostigmine
Physotigmine
Pyridostigmine)

A
  • Bradycardia
  • Hypotension
  • increased salivation, lacrimation, sweating
  • urinary urgency
  • neuromuscular blockade
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13
Q

Echothiophate (irreversible cholinesterase inhibitors) eye drops for glaucoma effect

A

increase drainage and decrease intraocular pressure

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14
Q

antidote/treatment for irreversible cholinestrerase

A

pralidoxime

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15
Q

tretaments of irreversible CIs

A
  • Atropine
  • Pralidoxime (antidote/treatment for pepticide poisoning)
  • Benzodiazepines - seizures
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16
Q

key points about pralidoxime

A
  • forces irreversible CI to dissociate from cholinesterase
  • most effective at the neuromuscular junction, cannot cross BBB,
  • MUST be given soon after exposure or will not be effective, given IV or IM via SLOW infusion
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17
Q

muscarinic agonists drugs

A

Bethanechol

Pilocarpine

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18
Q

what does muscarinic agonists bind to

A

bind to and activate muscarinic receptors

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19
Q

primary neurotransmitter of the parasympathetic NS

A

acetylcholine

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20
Q

adrenergic receptors of the sympathehtic nervous system

A
  • Dopamine, norepinephrine, epinephrine

- Beta and alpha

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21
Q

cholinergic receptors of the parasympathetic nervous system

A

Muscarinic and nicotinic

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22
Q

location of nicotinic N receptor

A

All ganglia of the autonomic nervous system (ANS)

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23
Q

location of nicotinic M receptor

A

Neuromuscular junctions (NMJ)

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24
Q

effects of nicotinic N receptors activation

A

Promotes ganglionic transmission

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25
Q

effects of nicotinic M receptors activation

A

Skeletal muscle contraction

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26
Q

clinical effects of muscarinic agonists

A

stimulate PNS (aka parasympathomimetic agents)

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27
Q

mechanism of action Bethanechol

A
  • reversible binding to muscarinic receptors

- causes ACTIVATION

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28
Q

indications of bethanechol

A

urinary retention

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29
Q

adverse effects of bethanecol

A
  • Bradycardia
  • hypotension
  • increased salivation,
  • increased gastric acid production
  • abdominal cramps and diarrhea
  • contraction of the bladder and relaxation of sphincter
  • exacerbation of asthma
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30
Q

pilocarpine mechanism of action

A

muscarinic agonist

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31
Q

indications of pilocarpine

A
  • glaucoma
  • dry mouth due to
  • Sjogren’s Syndrome
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32
Q

adverse effect of pilocarpine

A 
topical - minimal
oral - same as bethanecol
- Bradycardia
 - hypotension
- increased salivation, 
- increased gastric acid production
- abdominal cramps and diarrhea
- contraction of the bladder and relaxation of sphincter
- exacerbation of asthma
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33
Q

What are the treatments for muscarinic agonist toxicity?

A

atropine

supportive care

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34
Q

Antimuscarinic drugs

blocks the actions of

A

acetylcholine

and influence the activity of cholinergic receptors

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35
Q

other names for muscarinic antagonists

A

anti-muscarinic
muscarinic blockers
anticholinergic

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36
Q

anticholinergic drugs fro over-active bladder

A
  • Oxybutynin
  • DariFENACIN
  • SoliFENACIN
  • FesoTERODINE
  • TolTERODINE

M3 selectivity except fesoterodine and tolterodine

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37
Q

MUSCARINIC ANTAGONISTS drugs

A 
Atropine
Oxybutynin
Darifenacin
Solifenacin
Fesoterodine
Tolterodine
Scopolamine
Ipatropium
Glycopyrrolate
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38
Q

muscarnic antagonists binds to

A

bind to muscarinic receptors, competitively block ACh

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39
Q

adverse effect of atropine

A

(opposite of muscarinic activation)

  • Tachycardia
  • Decreased salivation, lacrimation, sweating
  • Decreased tone and motility
  • Decreased tone, sphincter constriction
  • Mydriasis (dry eyes)
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40
Q

lower doses of atropine are needed to affect

A

exocrine glands (lacrimal glands, salivary glands

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41
Q

higher doses of atropine are needed to affect

A

lungs and stomach

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42
Q

indications of atropine

A
  • preanesthetic medication
  • disorders of the eye
  • Bradycardia
  • GI hypertonicity
  • Muscarinic agonist poisoning
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43
Q

indication of Scopolamine

A

anti-muscarinic/muscarinic blockers/anticholinergic drug.

  • motion sickness
  • vomiting
  • decreased respiratory
  • secretions
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44
Q

indication of Ipratropium (antimuscarinic)

A
  • asthma
  • COPD
  • Rhinitis
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45
Q

counseling point of oxybutynin

A
  • Take with or without food
  • Do not crush ER tablets
  • Apply patch or gel to clean and dry skin
  • Rotate sites of topical administration
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46
Q

Darifenacin, Tolterodine counseline points

A

Do not crush ER tablets

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47
Q

Solifenacin, Fesoterodine counseling points

A

Can increase QTc at high doses - avoid with other OTc increased drugs

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48
Q

For anti-cholinergic agent to work in OAB,it must ….

A

it must inhibit M3 receptors

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49
Q

M3 receptors are specific only to bladder true or false

A

false.

M3 receptors not specific only to bladder

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50
Q

muscariinic subtype M3 response to activation

A
  • Salivation
  • Contraction (↑ pressure)
  • Increased tone & motility
  • Contraction (miosis)
  • Contraction (accommodation)
    Tearing
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51
Q

muscariinic subtype M3 impact of blockade

A
  • Dry mouth
  • Relaxation (decreased pressure)
  • Decreased tone & motility
  • Relaxation (mydriasis)
  • Relaxation (blurred vision)
  • Dry eyes
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52
Q

Adrenergic Receptors

A

alpha 1, - vasculature and smooth muscle
alpha 2 - cns
beta 1 - heart
dopamine - kidney

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53
Q

what are the two types of adrenergic agonist

A

catecholamines - do not cross BBB

noncatecholamines- able to cross BBB

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54
Q

drugs of catecholamines

A
  • Epinephrine
  • Norepinephrine = SEPTIC SHOCK
  • Isoproterenol
  • Dobutamine
  • Dopamine
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55
Q

drugs of non-catecholamines

A
  • Ephedrine
  • Phenylephrine
  • Albuterol
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56
Q

Alpha 1 receptor response of activation

A

location:
blood vessels
eyes

  • vasoconstriction
  • mydriasis (pupil dilation)
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57
Q

adverse effects of Alpha 1 activation

A
  • hypertension
  • bradycardia
  • necrosis (extravasation from IV line)
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58
Q

Beta 1 receptor response of activation

A

location: heart
- increased HR (chronotopy)
- increased force of contraction (inotropy)

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59
Q

adverse effects of beta 1 activation

A

Tachycardia
Dysrhythmias
Angina

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60
Q

Beta 2 receptor response activation

A

location:
lungs
blood vessels
uterus

  • lungs - bronchodilation
  • blood vessels -vasodilation
  • uterus - relax smooth muscle
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61
Q

adverse effect of beta 2 receptor activation

A

hyperglycemia

tremor

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62
Q

Dopamine receptor activation response

A

location:
kidney

  • renal vasodilation
63
Q

adverse effect of dopamine activation

A

minimal

64
Q

What receptors does epinephrine(catecholamine) activate?

A

alpha1,
beta1,
beta2 agonist

65
Q

What are the physiologic actions of epinephrine

A
  • vasoconstriction
  • increased HR
  • increased force of heart contraction
  • bronchodilation
66
Q

adverse effects of epinephrine

A
  • hypertensive crisis
  • tachycardia/dysrhythmias
  • angina pectoris
  • necrosis - extravasation
    hyperglycemia
67
Q

monitoring parameters of epinephrine

A

Think about drugs that counteract epinephrine

  • Beta-blockers
  • Alpha-blockers (phentolamine)
68
Q

What receptors does norepinephrine(catecholamine) activate?

A

alpha 1 and beta1 agonist

69
Q

physiologic effects of norepinephrine

A

vasoconstriction
increased HR
increased force of heart contraction

70
Q

adverse effects of norepinephrine

A

hypertension
tachycardia/dysrhythmias
angina pectoris
necrosis

71
Q

what receptors does dopamine (catecholamine) activate

A

beta1, alpha1, agonist (high doses)

72
Q

physiologic actions of dopamine

A

renal vasodilation*
increased HR
increased force of contraction
vasoconstriction

73
Q

adverse effect of dopamine (catecholamine)

A

hypertension
tachycardia/dysrhythmias
necrosis
angina pectoris

74
Q

what receptors does Isoproterenol, Dobutamine (catcholamines) activate

A

beta1 and beta2 agonist

75
Q

counseling points for Isoproterenol, Dobutamine

A
  • monitor BP, HR, ECG

- can be given peripherally

76
Q

adverse effect of Isoproterenol, Dobutamine

A

tachycardia
dysrhythmia
angina pectoris

77
Q

what receptors does Phenylephrine (non-catecholamine) activate

A

pure alpha 1 agonist

78
Q

adverse effects of Phenylephrine (non-catecholamine)

A

hypertension
bradycardia
necrosis (IV)

79
Q

what receptors does Albuterol (non-catcecholamine)

A

beta 2 receptor agonist

80
Q

adverse effects of Albuterol (non-catcecholamine)

A

minimal
tremor
tachycardia with excessive or frequent dosing

81
Q

all adrenergic agents has fast onset of action and?

A

short duration of action so continuos infusion is required

82
Q

What is the management of necrosis caused by adrenergic agents

A

Extravasation from IV line

83
Q

Which concentration of epinephrine is used for the anaphylaxis

A

More concentrated form

84
Q

less concentrated form of epinephrine are given for?

A

cardiac arrest

85
Q

What is a prototype drug?

A

Individual drug that represents a group of drugs. Often the first drug of a particular class

  • Prototype for opioid analgesic = morphine
  • Prototype for penicillin = methicillin
86
Q

What is the chemical name of a drug

A

description of the drug using nomenclature from chemistry

87
Q

What is the generic name of a drug

A

non-proprietary. Assigned by the United States Adopted names council. Only 1 generic name per drug

88
Q

What is the brand name of a drug

A

proprietary, trade. Names under which the drug is marketed. Created by drug companies. Multiple brand names for one drug9o0

89
Q

What is the role of the Controlled Substance Act?

A

Set the rules for the manufacture and distribution of drugs with abuse potential

90
Q

What kinds of drugs are categorized as Schedule I

A

heroin, LSD, Mescaline, MDMA (Ecstasy)

91
Q

What kinds of drugs are categorized as Schedule II

A

cocaine, fentanyl, dextroamphetamine

92
Q

How do Schedule II drugs compare to Schedule V drugs?

A
  • schedule 2 has high abuse potential and severe physical dependence.
  • schedule 5 has lowest abuse potential, limited physical dependence
93
Q

Describe the process for new drug development

A

Uses randomized controlled RCT design.

Compares two patients with the same disease state.
One patient gets experimental drug (treatment), one gets placebo or standard care (control).

  • Randomization = prevents allocation bias
  • Binding = participants and or researchers are unaware of what group the participants is in. Prevents personal bias
94
Q

What is the role of phase 1 testing of a drug?

A

20-100 healthy volunteers

  • Determine safety and dosage
95
Q

What is the role of phase 2 testing of a drug?

A

100-500 patient volunteers

  • Evaluate effectiveness and look for side effects
96
Q

What is the role of phase 3 testing of a drug?

A

1000-5000 patient volunteers

  • Confirm effectiveness and monitor for adverse effects from long term use
97
Q

What is the role of phase 4 testing of a drug?

A

Additional post marketing monitoring required by FDA

98
Q

What limitations of drug development does the NIH Revitalization Act of 1993 seek to address?

A
  • Minority groups
  • Women
  • Pregnant women
  • Children
  • Failure to detect all adverse events
99
Q

What are “OTC” drugs?

A

Drugs purchased without a prescription

100
Q

Where can you find information about safe handling of hazardous drugs?

A

National Institute of Occupational Safety and Health (NIOSH)

101
Q

Define: carcinogenic

A

drug having the potential to cause cancer

102
Q

Define Teratogenic

A

risk of birth defect

103
Q

genotoxic

A

drugs that can cause DNA or chromosomal damage

104
Q

What does a pregnancy risk category of X indicate?

A

Adequate well-controlled or observational studies in animals or pregnant women who have demonstrated positive evidence of fetal abnormalities. The use of the product is contraindicated in women who are or may become pregnant

105
Q

What are reputable sources for drug information?

A
  • Textbooks
  • Newsletters
  • Online (Lexicomp, Micromedex, clinical pharmacology)
106
Q

What is pharmacokinetics?

A

The study of drug movement throughout the body

107
Q

What processes make up pharmacokinetics?

A

Absorption, distribution, metabolism, elimination

108
Q

What is absorption

A

the movement of drug from site of administration to bloodstream

109
Q

What is distribution

A

the movement of drug from the blood to tissues including site of action

110
Q

What is excretion

A

the movement of drugs and metabolites out of the body

111
Q

How do drugs move across membranes in the ADME process?

A

Three primary methods

  • Channels and pores
  • Transport
  • Direct penetration of the membrane
112
Q

What is the difference between active and passive transport?

A
  • Passive transport: movement via a concentration gradient

- Active transport: require energy expenditure

113
Q

What determines if a drug can move across membranes?

A
  • All transport systems are selective
  • Drug structure determines if it will be transported
P-glycoprotein (PGP) transporters = Transmembrane protein that transports drugs 
out of the cells
- Liver = bile
- Kidneys = renal tubule (urine)
- Placenta = maternal blood 
- Intestine = intestinal lumen
  • Direct penetration of the membrane
  • Lipophilic drugs pass through membranes the easiest
  • Molecules that cannot readily cross membranes:
    ○ Polar molecules
    ○ Ions
114
Q

What pharmacokinetic process determines how quickly a drug will start working?

A 
○	Rate of dissolution
○	Surface area
○	Blood flow
○	Lipid solubility
○	Route of administration
115
Q

Pros IM and SQ

A

o Permits use of poorly soluble drugs

o Permits use of depot formulations

116
Q

What is the difference between the capillary system in the central nervous system and the rest of the body?

A
  • Most drugs must exit the blood to have an effect
  • Drugs exit the blood at capillary beds
    o Large spaces between cells for drugs to pass through
    o Movement to interstitial space is easy
  • The blood-brain-barrier (BBB) in the central nervous system (CNS) prevents this easy passage
    o Tight junctions exist between cells
    o Drugs must be lipophilic or have specific transporters
117
Q

What impact does protein binding have on drug pharmacokinetics? Are drug effects carried out by free or bound drug?

A
  • Drugs can bind to proteins in the blood

Proteins are larger than drugs and will remain
in the bloodstream
- Drug molecules bound to protein cannot
leave the blood
- Drug molecules unbound or free can leave

Protein binding:

  • Can restrict distribution
  • Source of drug-drug interactions
118
Q

What is the major enzyme system involved in drug metabolism?

A
  • Most drug metabolism occurs in the liver by the cytochrome P450 (CYP450) enzyme system
  • CYP450 can be further broken down into subcategories: CYP3A4, CYP2C9
119
Q

What happens when drugs are metabolized?

A 
○	Drug inactivation
○	Accelerated renal clearance of drugs
○	Increased therapeutic action (active metabolites)
○	Activation of prodrugs
○	Increased or decreased drug toxicity
120
Q
  • What is the first pass effect?
A
  • impacts drugs administered orally
  • After absorption from the GI tract, the drug goes to the liver via the portal circulation
  • Some drugs undergo rapid hepatic inactivation
  • The liver has potential to inactivate all drug before it reaches site of action
121
Q

How are most drugs removed from the body/which organ plays the largest role?

A
  • most common kidneys.

- non renal routes: feces, bile, lungs

122
Q

What is the minimum effective concentration?

A

smallest concentration that will cause an effect

Toxic concentration: plasma levels above this will have toxic effects

Therapeutic range: range of levelsbetween the MEC and toxic concentration

123
Q

What does it mean if a drug has a wide therapeutic range?

A

wide margin of safety and less danger of producing toxic effects

124
Q

Drug levels rise during

A

absorption/distribution

125
Q

Drug levels fall during

A

(metabolism/excretion)

126
Q

Drug will exert therapeutic effect until levels fall below…

A

Drug will exert therapeutic effect until levels fall below MEC

127
Q

What does it mean if a drug has a narrow therapeutic range?

A

small differences in dose or blood conc can lead to serious therapeutic failures/ ADE that are life threatening.

128
Q

Define half-life.

A

Time required for the drug to reduce by 50%

129
Q

How does a short vs. long half-life impact dosing frequency?

A

Short: dosing more frequent

Long: less frequent

130
Q

After how many half-lives is 100% of drug removed from the body?

A

5

131
Q

Why would a loading dose of drug be administered?

A
  • A large dose of drug given to reach close to plateau levels (administered and elimination is equal)
132
Q

What is pharmacodynamics?

A

Drug actions to target cells and their corresponding response. What drug does to the body and how it does it.

133
Q

What factors impact a patient’s response to a drug?

A
  • Physiologic variables: age, gender, weight
  • Pathologic variables: changes in organ function
  • Genetic variables: difference in enzyme that metabolizes drug
134
Q

What is an agonist? How does it have its effect?

A
  • Activates receptors or mimics the effects of endogenous molecule
  • can make processes go slower or faster according to physiologic action of the receptor it binds to
135
Q

What is a partial agonist? How does it have its effect?

A
  • Moderate activity.

- Max effect of a partial agonist is still less than a full agonist.

136
Q

What is an antagonist? How does it have its effect?

A
  • Prevents receptor activation
  • Have no effects on their own receptors
  • produce effects by preventing activation of receptors by endogenous substances
137
Q

What is a drug-drug interaction?

A
  • Action of one drug may be increased or decreased by the presence of another drug
  • Can occur anytime a pt takes more than one drug
  • Interactions can be intended and desires/ unintended and undesired
138
Q

What are the consequences? of DDI

A
  • Intensify effects of another drug: Additive interaction; Increased therapeutic and ADE
  • Create a unique response: new reaction not seen with either drug individually
  • Reduce effects of other drugs: inhibitory interaction; decreased therapeutic and ADE.
139
Q

How can we reduce the risk of drug-drug interactions?

A
  • Minimize number of drugs taken
  • Complete thorough drug history
  • Ask about illicit drugs
  • Adjust dosage of meds impacted by inhibitors and inducers
  • Monitor for signs and symptoms of toxicity
140
Q

What is an adverse drug reaction?

A
  • Any noxious, unintended, undesired effect that occurs at normal drug dpses
141
Q

How can we reduce the risk of adverse drug reactions?

A
  • Education
  • Anticipation: target evaluation of at-risk organ based on med’s ADR; monitor patient for expected ADR
  • Individualize therapy: avoid allergic meds, select meds with mild ADR, use harmful ones only when benefits>risk
142
Q

What are the 10 rights regarding drugs?

A
  • drug
  • dose
  • patient
  • route
  • time
  • reason
  • documentation
  • education
  • evaluation
  • right to refuse
143
Q

Why are nurses so critical for drug safety?

A
  • Intervene when there is an issue
  • Last line of defense
  • Administer med appropriately, ethically, legally
144
Q

What is a medication error?

A
  • Any preventable event that may cause harm while the meds is in control of healthcare professional, patient or consumer.

Wrong patient, drug, dose, route, time, dosage form, infusion rate.

145
Q

What is an indirect vs. direct medication error?

A
  • Direct: cause harm directly. Eg. Overdose

- Indirect: by not adequately treating. Eg, antibiotic dose too low or ineffective

146
Q

Which errors are most commonly fatal?

A

overdose,
wrong dose
wrong route

147
Q

How can we help reduce medication errors?

A
  • create ‘just culture’ environment
  • encourage family members and patient for active care
  • have necessary tools to dispense and administer meds
  • replace handwritten orders with computerized physician order only
  • include clinical pharmacist on rounds in ICUs
  • barcode scanning
  • Incorporate medication reconciliation on admission and discharge
148
Q

what are the Beers Criteria?

A

-Potentially inappropriate drugs for older pts: that require dose adjustments due to changes in kidney functioning; DDI

149
Q

what group of people are at risk for more intense and prolonged drug responses

A

neonates and infants

150
Q

what group of people requires higher doses of medication

A

children

151
Q

metabolism remains high in children over 1 year but starts to decrease at what age?

A

starts to decrease at age 2

152
Q

beta blocking drugs are _____ effective in older adults

A

less

153
Q

warfarins are _____ effecting in older adult

A

more

PHARMACOLOGY (7 decks)

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