pharmacotherapy & adrenergic drugs Flashcards
(153 cards)
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
2
Q
what are the two types of cholinesterase inhibitors
A
- reversible
- irreversible
3
Q
what are the reverse cholinesterase inhibitors drug
A
Neostigmine
Physotigmine
Pyridostigmine
4
Q
muscular effects of reversible cholinesterase inhibitors
A
therapeutic dose- increase force of muscle contraction
toxic dose- decrease force muscle contraction
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)
6
Q
indication of Neostigmine
A
- M. gravy,
- reversal of neuromuscular blockage
- treats MG crisis via IV
7
Q
counseling points for neostagmine
A
paradoxical anti-cholinesterase weakness can occur
8
Q
indication of Physostigmine
A
reversal of anti-cholinergic toxicity (muscarinic antagonist toxicity)
9
Q
Physostigmine counseling points
A
rapid IV administration can cause respiratory depression
- seizures and bradycardia
- give SLOW IV push or infusion
10
Q
Pyridostigmine indication
A
MG
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
12
Q
Adverse effects of Reversible Cholinesterase Inhibitors (Neostigmine
Physotigmine
Pyridostigmine)
A
- Bradycardia
- Hypotension
- increased salivation, lacrimation, sweating
- urinary urgency
- neuromuscular blockade
13
Q
Echothiophate (irreversible cholinesterase inhibitors) eye drops for glaucoma effect
A
increase drainage and decrease intraocular pressure
14
Q
antidote/treatment for irreversible cholinestrerase
A
pralidoxime
15
Q
tretaments of irreversible CIs
A
- Atropine
- Pralidoxime (antidote/treatment for pepticide poisoning)
- Benzodiazepines - seizures
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
17
Q
muscarinic agonists drugs
A
Bethanechol
Pilocarpine
18
Q
what does muscarinic agonists bind to
A
bind to and activate muscarinic receptors
19
Q
primary neurotransmitter of the parasympathetic NS
A
acetylcholine
20
Q
adrenergic receptors of the sympathehtic nervous system
A
- Dopamine, norepinephrine, epinephrine
- Beta and alpha
21
Q
cholinergic receptors of the parasympathetic nervous system
A
Muscarinic and nicotinic
22
Q
location of nicotinic N receptor
A
All ganglia of the autonomic nervous system (ANS)
23
Q
location of nicotinic M receptor
A
Neuromuscular junctions (NMJ)
24
Q
effects of nicotinic N receptors activation
A
Promotes ganglionic transmission
25
effects of nicotinic M receptors activation
Skeletal muscle contraction
26
clinical effects of muscarinic agonists
stimulate PNS (aka parasympathomimetic agents)
27
mechanism of action Bethanechol
- reversible binding to muscarinic receptors
| - causes ACTIVATION
28
indications of bethanechol
urinary retention
29
adverse effects of bethanecol
- Bradycardia
- hypotension
- increased salivation,
- increased gastric acid production
- abdominal cramps and diarrhea
- contraction of the bladder and relaxation of sphincter
- exacerbation of asthma
30
pilocarpine mechanism of action
muscarinic agonist
31
indications of pilocarpine
- glaucoma
- dry mouth due to
- Sjogren's Syndrome
32
adverse effect of pilocarpine
```
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
```
33
What are the treatments for muscarinic agonist toxicity?
atropine
| supportive care
34
Antimuscarinic drugs
| blocks the actions of
acetylcholine
and influence the activity of cholinergic receptors
35
other names for muscarinic antagonists
anti-muscarinic
muscarinic blockers
anticholinergic
36
anticholinergic drugs fro over-active bladder
- Oxybutynin
- DariFENACIN
- SoliFENACIN
- FesoTERODINE
- TolTERODINE
M3 selectivity except fesoterodine and tolterodine
37
MUSCARINIC ANTAGONISTS drugs
```
Atropine
Oxybutynin
Darifenacin
Solifenacin
Fesoterodine
Tolterodine
Scopolamine
Ipatropium
Glycopyrrolate
```
38
muscarnic antagonists binds to
bind to muscarinic receptors, competitively block ACh
39
adverse effect of atropine
(opposite of muscarinic activation)
- Tachycardia
- Decreased salivation, lacrimation, sweating
- Decreased tone and motility
- Decreased tone, sphincter constriction
- Mydriasis (dry eyes)
40
lower doses of atropine are needed to affect
exocrine glands (lacrimal glands, salivary glands
41
higher doses of atropine are needed to affect
lungs and stomach
42
indications of atropine
- preanesthetic medication
- disorders of the eye
- Bradycardia
- GI hypertonicity
- Muscarinic agonist poisoning
43
indication of Scopolamine
anti-muscarinic/muscarinic blockers/anticholinergic drug.
- motion sickness
- vomiting
- decreased respiratory
- secretions
44
indication of Ipratropium (antimuscarinic)
- asthma
- COPD
- Rhinitis
45
counseling point of oxybutynin
- Take with or without food
- Do not crush ER tablets
- Apply patch or gel to clean and dry skin
- Rotate sites of topical administration
46
Darifenacin, Tolterodine counseline points
Do not crush ER tablets
47
Solifenacin, Fesoterodine counseling points
Can increase QTc at high doses - avoid with other OTc increased drugs
48
For anti-cholinergic agent to work in OAB,it must ....
it must inhibit M3 receptors
49
M3 receptors are specific only to bladder true or false
false.
| M3 receptors not specific only to bladder
50
muscariinic subtype M3 response to activation
- Salivation
- Contraction (↑ pressure)
- Increased tone & motility
- Contraction (miosis)
- Contraction (accommodation)
Tearing
51
muscariinic subtype M3 impact of blockade
- Dry mouth
- Relaxation (decreased pressure)
- Decreased tone & motility
- Relaxation (mydriasis)
- Relaxation (blurred vision)
- Dry eyes
52
Adrenergic Receptors
alpha 1, - vasculature and smooth muscle
alpha 2 - cns
beta 1 - heart
dopamine - kidney
53
what are the two types of adrenergic agonist
catecholamines - do not cross BBB
noncatecholamines- able to cross BBB
54
drugs of catecholamines
- Epinephrine
- Norepinephrine = SEPTIC SHOCK
- Isoproterenol
- Dobutamine
- Dopamine
55
drugs of non-catecholamines
- Ephedrine
- Phenylephrine
- Albuterol
56
Alpha 1 receptor response of activation
location:
blood vessels
eyes
- vasoconstriction
- mydriasis (pupil dilation)
57
adverse effects of Alpha 1 activation
- hypertension
- bradycardia
- necrosis (extravasation from IV line)
58
Beta 1 receptor response of activation
location: heart
- increased HR (chronotopy)
- increased force of contraction (inotropy)
59
adverse effects of beta 1 activation
Tachycardia
Dysrhythmias
Angina
60
Beta 2 receptor response activation
location:
lungs
blood vessels
uterus
- lungs - bronchodilation
- blood vessels -vasodilation
- uterus - relax smooth muscle
61
adverse effect of beta 2 receptor activation
hyperglycemia
| tremor
62
Dopamine receptor activation response
location:
kidney
- renal vasodilation
63
adverse effect of dopamine activation
minimal
64
What receptors does epinephrine(catecholamine) activate?
alpha1,
beta1,
beta2 agonist
65
What are the physiologic actions of epinephrine
- vasoconstriction
- increased HR
- increased force of heart contraction
- bronchodilation
66
adverse effects of epinephrine
- hypertensive crisis
- tachycardia/dysrhythmias
- angina pectoris
- necrosis - extravasation
hyperglycemia
67
monitoring parameters of epinephrine
Think about drugs that counteract epinephrine
- Beta-blockers
- Alpha-blockers (phentolamine)
68
What receptors does norepinephrine(catecholamine) activate?
alpha 1 and beta1 agonist
69
physiologic effects of norepinephrine
vasoconstriction
increased HR
increased force of heart contraction
70
adverse effects of norepinephrine
hypertension
tachycardia/dysrhythmias
angina pectoris
necrosis
71
what receptors does dopamine (catecholamine) activate
beta1, alpha1, agonist (high doses)
72
physiologic actions of dopamine
renal vasodilation*
increased HR
increased force of contraction
vasoconstriction
73
adverse effect of dopamine (catecholamine)
hypertension
tachycardia/dysrhythmias
necrosis
angina pectoris
74
what receptors does Isoproterenol, Dobutamine (catcholamines) activate
beta1 and beta2 agonist
75
counseling points for Isoproterenol, Dobutamine
- monitor BP, HR, ECG
| - can be given peripherally
76
adverse effect of Isoproterenol, Dobutamine
tachycardia
dysrhythmia
angina pectoris
77
what receptors does Phenylephrine (non-catecholamine) activate
pure alpha 1 agonist
78
adverse effects of Phenylephrine (non-catecholamine)
hypertension
bradycardia
necrosis (IV)
79
what receptors does Albuterol (non-catcecholamine)
beta 2 receptor agonist
80
adverse effects of Albuterol (non-catcecholamine)
minimal
tremor
tachycardia with excessive or frequent dosing
81
all adrenergic agents has fast onset of action and?
short duration of action so continuos infusion is required
82
What is the management of necrosis caused by adrenergic agents
Extravasation from IV line
83
Which concentration of epinephrine is used for the anaphylaxis
More concentrated form
84
less concentrated form of epinephrine are given for?
cardiac arrest
85
What is a prototype drug?
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
What is the chemical name of a drug
description of the drug using nomenclature from chemistry
87
What is the generic name of a drug
non-proprietary. Assigned by the United States Adopted names council. Only 1 generic name per drug
88
What is the brand name of a drug
proprietary, trade. Names under which the drug is marketed. Created by drug companies. Multiple brand names for one drug9o0
89
What is the role of the Controlled Substance Act?
Set the rules for the manufacture and distribution of drugs with abuse potential
90
What kinds of drugs are categorized as Schedule I
heroin, LSD, Mescaline, MDMA (Ecstasy)
91
What kinds of drugs are categorized as Schedule II
cocaine, fentanyl, dextroamphetamine
92
How do Schedule II drugs compare to Schedule V drugs?
- schedule 2 has high abuse potential and severe physical dependence.
- schedule 5 has lowest abuse potential, limited physical dependence
93
Describe the process for new drug development
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
What is the role of phase 1 testing of a drug?
20-100 healthy volunteers
- Determine safety and dosage
95
What is the role of phase 2 testing of a drug?
100-500 patient volunteers
- Evaluate effectiveness and look for side effects
96
What is the role of phase 3 testing of a drug?
1000-5000 patient volunteers
- Confirm effectiveness and monitor for adverse effects from long term use
97
What is the role of phase 4 testing of a drug?
Additional post marketing monitoring required by FDA
98
What limitations of drug development does the NIH Revitalization Act of 1993 seek to address?
- Minority groups
- Women
- Pregnant women
- Children
- Failure to detect all adverse events
99
What are “OTC” drugs?
Drugs purchased without a prescription
100
Where can you find information about safe handling of hazardous drugs?
National Institute of Occupational Safety and Health (NIOSH)
101
Define: carcinogenic
drug having the potential to cause cancer
102
Define Teratogenic
risk of birth defect
103
genotoxic
drugs that can cause DNA or chromosomal damage
104
What does a pregnancy risk category of X indicate?
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
What are reputable sources for drug information?
- Textbooks
- Newsletters
- Online (Lexicomp, Micromedex, clinical pharmacology)
106
What is pharmacokinetics?
The study of drug movement throughout the body
107
What processes make up pharmacokinetics?
Absorption, distribution, metabolism, elimination
108
What is absorption
the movement of drug from site of administration to bloodstream
109
What is distribution
the movement of drug from the blood to tissues including site of action
110
What is excretion
the movement of drugs and metabolites out of the body
111
How do drugs move across membranes in the ADME process?
Three primary methods
- Channels and pores
- Transport
- Direct penetration of the membrane
112
What is the difference between active and passive transport?
- Passive transport: movement via a concentration gradient
| - Active transport: require energy expenditure
113
What determines if a drug can move across membranes?
- 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
What pharmacokinetic process determines how quickly a drug will start working?
```
○ Rate of dissolution
○ Surface area
○ Blood flow
○ Lipid solubility
○ Route of administration
```
115
Pros IM and SQ
o Permits use of poorly soluble drugs
| o Permits use of depot formulations
116
What is the difference between the capillary system in the central nervous system and the rest of the body?
- 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
What impact does protein binding have on drug pharmacokinetics? Are drug effects carried out by free or bound drug?
- 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
What is the major enzyme system involved in drug metabolism?
- 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
What happens when drugs are metabolized?
```
○ Drug inactivation
○ Accelerated renal clearance of drugs
○ Increased therapeutic action (active metabolites)
○ Activation of prodrugs
○ Increased or decreased drug toxicity
```
120
- What is the first pass effect?
- 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
How are most drugs removed from the body/which organ plays the largest role?
- most common kidneys.
| - non renal routes: feces, bile, lungs
122
What is the minimum effective concentration?
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
What does it mean if a drug has a wide therapeutic range?
wide margin of safety and less danger of producing toxic effects
124
Drug levels rise during
absorption/distribution
125
Drug levels fall during
(metabolism/excretion)
126
Drug will exert therapeutic effect until levels fall below...
Drug will exert therapeutic effect until levels fall below MEC
127
What does it mean if a drug has a narrow therapeutic range?
small differences in dose or blood conc can lead to serious therapeutic failures/ ADE that are life threatening.
128
Define half-life.
Time required for the drug to reduce by 50%
129
How does a short vs. long half-life impact dosing frequency?
Short: dosing more frequent
Long: less frequent
130
After how many half-lives is 100% of drug removed from the body?
5
131
Why would a loading dose of drug be administered?
- A large dose of drug given to reach close to plateau levels (administered and elimination is equal)
132
What is pharmacodynamics?
Drug actions to target cells and their corresponding response. What drug does to the body and how it does it.
133
What factors impact a patient’s response to a drug?
- Physiologic variables: age, gender, weight
- Pathologic variables: changes in organ function
- Genetic variables: difference in enzyme that metabolizes drug
134
What is an agonist? How does it have its effect?
- 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
What is a partial agonist? How does it have its effect?
- Moderate activity.
| - Max effect of a partial agonist is still less than a full agonist.
136
What is an antagonist? How does it have its effect?
- Prevents receptor activation
- Have no effects on their own receptors
- produce effects by preventing activation of receptors by endogenous substances
137
What is a drug-drug interaction?
- 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
What are the consequences? of DDI
- 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
How can we reduce the risk of drug-drug interactions?
- 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
What is an adverse drug reaction?
- Any noxious, unintended, undesired effect that occurs at normal drug dpses
141
How can we reduce the risk of adverse drug reactions?
- 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
What are the 10 rights regarding drugs?
- drug
- dose
- patient
- route
- time
- reason
- documentation
- education
- evaluation
- right to refuse
143
Why are nurses so critical for drug safety?
- Intervene when there is an issue
- Last line of defense
- Administer med appropriately, ethically, legally
144
What is a medication error?
- 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
What is an indirect vs. direct medication error?
- Direct: cause harm directly. Eg. Overdose
| - Indirect: by not adequately treating. Eg, antibiotic dose too low or ineffective
146
Which errors are most commonly fatal?
overdose,
wrong dose
wrong route
147
How can we help reduce medication errors?
- 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
what are the Beers Criteria?
-Potentially inappropriate drugs for older pts: that require dose adjustments due to changes in kidney functioning; DDI
149
what group of people are at risk for more intense and prolonged drug responses
neonates and infants
150
what group of people requires higher doses of medication
children
151
metabolism remains high in children over 1 year but starts to decrease at what age?
starts to decrease at age 2
152
beta blocking drugs are _____ effective in older adults
less
153
warfarins are _____ effecting in older adult
more
