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Pharmacology Exam 2 > IV Sedatives > Flashcards

IV Sedatives Flashcards

1
Q

Define sedative

A

a drug that induces a state of calm or sleep

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2
Q

Define hypnotic

A

a drug that induces hypnosis or sleep

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3
Q

Define anxiolytic

A

any agent that reduces anxiety

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4
Q

Define sedative-hypnotics

A

drugs that reversibly depress the activity of the CNS

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5
Q

What’s the MOA of barbiturates?

A

GABA-A agonist (GABA primary inhibitory NT in brain)

increase duration of opening of chloride channels

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6
Q

What is distinct about thiobarbiturates?

A

sulfur molecule on 2nd position, increasing lipid solubility and potency

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7
Q

What are examples of thiobarbiturates?

A

thiopental, thiamylal

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8
Q

What is distinct about oxybarbiturates?

A

oxygen molecule in 2nd position

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9
Q

What are examples of thiobarbiturates?

A

methohexital, pentobarbital

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10
Q

What lowers the seizure threshold and increases potency of barbiturates?

A

adding methyl group on the nitrogen (methohexital)

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11
Q

What increases the anticonvulsant effect of barbiturates?

A

adding phenyl group at the 5 carbon (phenobarbital)

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12
Q

What are the signs and symptoms of acute intermittent porphyria?

A

1st GI severe ab pain and n/v, CNS anxiety, confusion, seizures, psychosis, coma, PNS skeletal muscle weakness, bulbar weakness

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13
Q

What is the most common and dangerous type of intermittent porphyrias?

A

acute–caused by defect in heme synthesis

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14
Q

What makes acute intermittent porphyria worse?

A

stim of ALA synthase, emotional stress, prolonged NPO status, P450 induction

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15
Q

What drugs do you avoid in acute intermittent porphyria?

A

barbiturates, etomidate, ketamine, ketorolac, amiodarone, ca channel blockers, birth control pills

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16
Q

How do you manage acute intermittent porphyria?

A

hydration!, glucose supplementation, heme arginate, prevent hypothermia. use volatiles, N20, NMB and reversals, narcs, midaz, zofran, vasopressors, and beta blockers, regional

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17
Q

What should you NOT do with barbiturates?

A

inject intra-arterially: causes vasoconstriction/crystal formation/inflammation–tissue necrosis. treat with vasodilator injections or sympathectomy

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18
Q

What is the gold standard for ECT?

A

methohexital, dose 1-1.5mg/kg

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19
Q

What is special about phenobarbital?

A

it’s excreted unchanged in urine where all the other barbs are metabolized by P450.

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20
Q

What’s the MOA of propofol?

A

direct GABA-A agonist, increases Cl conductance which causes hyperpolarization of postsynaptic cell and inhibition of postsynaptic neuron

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21
Q

Does renal dysfunction influence elimination of propofol?

A

NO

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22
Q

When does the brain conc of propofol peak?

A

approx 1 min

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23
Q

What is awakening from propofol attributed to?

A

redistribution out of brain

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24
Q

Describe Propofol Infusion Syndrome.

A

increased long chain triglycerides load impairs oxidative phosphorylation and fatty acid metabolism which starves cells of oxygen

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25
What are the risk factors of PIS?
prop dose >4mcg/kg/hr (67 mcg/kg/min), duration >48h, sepsis, catecholamine infusions, high-dose steroids, cerebral injury
26
What is the clinical presentation of PIS?
acute refractory brady to asystole and 1 or more of these: met acidosis, rhabdo, enlarged/fatty liver, renal failure, HLD, lipemia
27
What is the treatment for PIS?
discontinue propofol, maximize gas exchange, cardiac pacing, PDE inhibitors, glucagon, ECMO, CRRT
28
How long does propofol last after opened?
syringe: 6 hours, infusion: 12 hours
29
What preservative is in diprivan?
EDTA, generics have metabisulfite or benzyl alcohol
30
How do you minimize pain on injection of propofol?
inject into larger more proximal vein, give lido or opioid b/4 admin.
31
What is the most commonly used IV anesthetic as induction drug and sedative?
propofol
32
What is etomidate's MOA?
direct GABA-A agonist, increase transmembrane Cl conductance, hyperpolarizing cell and inhibiting postsynaptic neuron
33
Does etomidate have a long or short DOA?
extremely short d/t rapid distribution half-life
34
Is etomidate lipid or water soluble?
lipid: brain conc rises rapidly and extensive redistribution to organs/tissues
35
How much is etomidate protein bound?
76%, mostly albumin
36
Does etomidate cause histamine release?
No
37
Describe etomidate's adrenocortical effects
Etomidate is a 11-beta-hydroxylase and 17-alpha hydroxylase inhibitor, cortisol and aldosterone synthesis are dependent on these enzymes.
38
How long does etomidate suppress adrenocortical function?
5-8 hours, could be up to 24 hours. AVOID in sepsis or those dependent on stress response.
39
What is the major advantage of etomidate?
minimal cardiorespiratory depression
40
True/False: etomidate increases PONV.
True, incidence 30-40%
41
Does etomidate burn veins?
yes
42
What is different about the MOA of benzos compared to other GABA-A agonists?
most increase time the channel is open but benzos increase the frequency that it opens.
43
What are side effects of benzos?
anterograde amnesia, fatigue, drowsiness, when used with CNS depressant or opioids can decrease motor coordination, impair cognitive function, and increase vent depressant effects
44
Order the potency strongest to weakest of common benzos.
Lorazepam>midazolam>diazepam.
45
True/False Benzos provide retrograde amnesia.
False
46
Why is propylene glycol added to diazepam and lorazepam?
to enhance water solubility (but causes venous irritation)
47
What are some cautions with benzos?
synergistic sedative effects with CNS depressants, suppress cortisol levels, physical dependence, withdrawal, elderly have increased sensitivity and side effects, inhibition of platelet aggregation
48
Discuss some key concepts of diazepam.
enterohepatic recirculation--long half time, anticonvulsant, preventative measure against emergence delirium after ketamine admin, antispasmodic, reduces skeletal muscle tone at spinal neurons
49
Discuss key concepts of lorazepam.
more potent sedative, onset 1-2 min, peak 20-30 min, slow--limits usefulness as anticonvulsant, amnestic action can last 6-10 hours
50
What's special about oxazepam?
active metabolite of diazepam, shorter DOA
51
What's special about alprazolam?
bigger inhibition of adrenocorticotrophic hormone and cortisol secretion
52
What's special about clonazepam?
very effective at seizure prevention
53
What's special about flurazepam?
used exclusively to treat insomnia, some daytime drowsiness
54
What's special about temazepam?
used exclusively to treat insomnia, no daytime drowsiness
55
What's special about triazolam?
treats insomnia d/t difficulty falling asleep, shortest acting benzo, no daytime drowsiness
56
What's the MOA for flumazenil?
competitive GABA-A antagonist, reversal for benzos.
57
What's the DOA and dose for flumazenil?
30-60 min, 0.2mg IV titrated in 0.1mg increments q1min
58
What are the side effects of flumazenil?
does NOT increase SNS tone, anxiety, or evidence of stress, withdrawal symptoms including seizures can occur if chronic users, more reversal of sedative effects than amnestic effects
59
What's ketamine's MOA?
NMDA receptor antagonist (2ndary targets opioid, MAO, serotonin, NE, muscarinic, Na channels)
60
When is ketamine a good drug to use?
opioid induced hyperalgesia, burn patients with frequent dressing changes and pre-existing chronic pain syndromes, treat depression
61
Does ketamine have small or large protein binding.
smallest amount compared to other induction agents (12%)
62
What's the MOA of dexmedetomidine?
alpha-2 agonist: decreased cAMP which inhibits locus coeruleus in pons causing sedation
63
What are the effects of dexmedetomidine?
anesthesia, amnesia, analgesia, anti-shivering, reduces emergence delirium in kids, doesn't impair evoked potentials, useful for wake-up test in scoliosis surgery, used in preop sedation of kids: high bioavailability in nasal and buccal routes.
64
What's the MOA of scopolamine?
anticholinergic, lipid soluble tertiary amine, crosses BBB, binds to muscarinic cholinergic receptors
65
What are the clinical uses of scopolamine?
sedation IV (decreases activity of RAS, amnestic properties); antisialagogue effect; antiemetic effect TD.
66
What are scopolamine's side effects?
mydriasis and cycloplegia (careful with glaucoma); central anticholinergic syndrome (restlessness to hallucinations to unconsciousness
67
What is the reversal for scopolamine?
physostigmine 15-60 mcg/kg

Pharmacology Exam 2 (5 decks)

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