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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
Q

What are the risk factors of PIS?

A

prop dose >4mcg/kg/hr (67 mcg/kg/min), duration >48h, sepsis, catecholamine infusions, high-dose steroids, cerebral injury

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26
Q

What is the clinical presentation of PIS?

A

acute refractory brady to asystole and 1 or more of these: met acidosis, rhabdo, enlarged/fatty liver, renal failure, HLD, lipemia

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27
Q

What is the treatment for PIS?

A

discontinue propofol, maximize gas exchange, cardiac pacing, PDE inhibitors, glucagon, ECMO, CRRT

28
Q

How long does propofol last after opened?

A

syringe: 6 hours, infusion: 12 hours

29
Q

What preservative is in diprivan?

A

EDTA, generics have metabisulfite or benzyl alcohol

30
Q

How do you minimize pain on injection of propofol?

A

inject into larger more proximal vein, give lido or opioid b/4 admin.

31
Q

What is the most commonly used IV anesthetic as induction drug and sedative?

A

propofol

32
Q

What is etomidate’s MOA?

A

direct GABA-A agonist, increase transmembrane Cl conductance, hyperpolarizing cell and inhibiting postsynaptic neuron

33
Q

Does etomidate have a long or short DOA?

A

extremely short d/t rapid distribution half-life

34
Q

Is etomidate lipid or water soluble?

A

lipid: brain conc rises rapidly and extensive redistribution to organs/tissues

35
Q

How much is etomidate protein bound?

A

76%, mostly albumin

36
Q

Does etomidate cause histamine release?

A

No

37
Q

Describe etomidate’s adrenocortical effects

A

Etomidate is a 11-beta-hydroxylase and 17-alpha hydroxylase inhibitor, cortisol and aldosterone synthesis are dependent on these enzymes.

38
Q

How long does etomidate suppress adrenocortical function?

A

5-8 hours, could be up to 24 hours. AVOID in sepsis or those dependent on stress response.

39
Q

What is the major advantage of etomidate?

A

minimal cardiorespiratory depression

40
Q

True/False: etomidate increases PONV.

A

True, incidence 30-40%

41
Q

Does etomidate burn veins?

A

yes

42
Q

What is different about the MOA of benzos compared to other GABA-A agonists?

A

most increase time the channel is open but benzos increase the frequency that it opens.

43
Q

What are side effects of benzos?

A

anterograde amnesia, fatigue, drowsiness, when used with CNS depressant or opioids can decrease motor coordination, impair cognitive function, and increase vent depressant effects

44
Q

Order the potency strongest to weakest of common benzos.

A

Lorazepam>midazolam>diazepam.

45
Q

True/False Benzos provide retrograde amnesia.

A

False

46
Q

Why is propylene glycol added to diazepam and lorazepam?

A

to enhance water solubility (but causes venous irritation)

47
Q

What are some cautions with benzos?

A

synergistic sedative effects with CNS depressants, suppress cortisol levels, physical dependence, withdrawal, elderly have increased sensitivity and side effects, inhibition of platelet aggregation

48
Q

Discuss some key concepts of diazepam.

A

enterohepatic recirculation–long half time, anticonvulsant, preventative measure against emergence delirium after ketamine admin, antispasmodic, reduces skeletal muscle tone at spinal neurons

49
Q

Discuss key concepts of lorazepam.

A

more potent sedative, onset 1-2 min, peak 20-30 min, slow–limits usefulness as anticonvulsant, amnestic action can last 6-10 hours

50
Q

What’s special about oxazepam?

A

active metabolite of diazepam, shorter DOA

51
Q

What’s special about alprazolam?

A

bigger inhibition of adrenocorticotrophic hormone and cortisol secretion

52
Q

What’s special about clonazepam?

A

very effective at seizure prevention

53
Q

What’s special about flurazepam?

A

used exclusively to treat insomnia, some daytime drowsiness

54
Q

What’s special about temazepam?

A

used exclusively to treat insomnia, no daytime drowsiness

55
Q

What’s special about triazolam?

A

treats insomnia d/t difficulty falling asleep, shortest acting benzo, no daytime drowsiness

56
Q

What’s the MOA for flumazenil?

A

competitive GABA-A antagonist, reversal for benzos.

57
Q

What’s the DOA and dose for flumazenil?

A

30-60 min, 0.2mg IV titrated in 0.1mg increments q1min

58
Q

What are the side effects of flumazenil?

A

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
Q

What’s ketamine’s MOA?

A

NMDA receptor antagonist (2ndary targets opioid, MAO, serotonin, NE, muscarinic, Na channels)

60
Q

When is ketamine a good drug to use?

A

opioid induced hyperalgesia, burn patients with frequent dressing changes and pre-existing chronic pain syndromes, treat depression

61
Q

Does ketamine have small or large protein binding.

A

smallest amount compared to other induction agents (12%)

62
Q

What’s the MOA of dexmedetomidine?

A

alpha-2 agonist: decreased cAMP which inhibits locus coeruleus in pons causing sedation

63
Q

What are the effects of dexmedetomidine?

A

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
Q

What’s the MOA of scopolamine?

A

anticholinergic, lipid soluble tertiary amine, crosses BBB, binds to muscarinic cholinergic receptors

65
Q

What are the clinical uses of scopolamine?

A

sedation IV (decreases activity of RAS, amnestic properties); antisialagogue effect; antiemetic effect TD.

66
Q

What are scopolamine’s side effects?

A

mydriasis and cycloplegia (careful with glaucoma); central anticholinergic syndrome (restlessness to hallucinations to unconsciousness

67
Q

What is the reversal for scopolamine?

A

physostigmine 15-60 mcg/kg

Pharmacology Exam 2 (5 decks)

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