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Pharmacology > Barbiturates > Flashcards

Barbiturates Flashcards

1
Q

Uses of Barbiturates

A

Induction of anesthesia, seizure treatment, short painless procedures (Cardioversion/ECT) treatment of increased ICP

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2
Q

Structure of Barbiturates

A

Derived from barbituric acid

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3
Q

Structure/Pharmacokinetics of Thiobarbiturates

A

sulfur atom @ 2nds position

more lipid soluble, greater hypnotic potency, rapid onset, shorter DOA

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4
Q

Structure/PK of Methohexital

A

methyl group on N (shorter DOA)

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5
Q

Structure/PK of Oxybarbiturates

A

O2 at 2nd position (long DOA)

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6
Q

Structure/PK of Phenobarbital

A

phenyl group @ 5th position

Anticonvulsant properites

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7
Q

MOA of Barbiturates

A

increase affinity of GABA at its binding site, increased duration of GABA a activated opening of chloride channel
Can also mimic GABA action via direct activation of GABA a receptors in high doses
Also works at glutamate, adenosine, neuronal nicotinic acetylcholine receptors

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8
Q

PK of Barbiturates

A

rapid onset and wake d/t rapid uptake and redistribution out of brain to tissues (similar to other highly liphophilic drugs)
Elimination depends on metabolism
INcrease Context sensitive half times d/t drug sequestering in fat, skeletal muscle and then re-entering circulation

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9
Q

PD of Barbiturates (PO)

A

short amount of drowsiness but residual CNS effects persist

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10
Q

PD of Barbiturates (CNS)

A

offer good treatment for grand mal seizures, but replaced with benzos in favor of more specific CNS site action

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11
Q

PD of Barbiturates (Resp)

A

DD depression of medullary and pontine ventilatory centers

Large doses- depressed laryngeal/cough reflexed (but reflexes overall more active as compared to propofol

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12
Q

PD of Barbiturates (CV)

A

decreased CO, systemic arterial pressure, PVR d/t decreased venous return/peripheral pooling, direct myocardial depression

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13
Q

Thiobarbiturates

A

Thiopental, Thiamylal

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14
Q

Metabolism of Thiobarbiturates

A

hepatocytes-> hydroxythiopental (carboxylic acid derivated) which is water soluble and exerts little CNS activity -> renal excretion

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15
Q

Small amount of X is metabolized by kidney/CNS

A

Thiobarbiturates

Thiopental, Thimylal

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16
Q

SEvere liver dysfunction w/ Thiobarbiturates

A

affects metabolism due to large reserve capactiy of liver to oxidize

17
Q

THiobarbiturates and Peds

A

elimination 1/2 shorter d/t more rapid hepatic clearance

18
Q

PK of Thiobarbiturates (CNS)

A

DD changes in median nerve somatosensory evoked responses and brainstem auditory evoked responses

19
Q

Pk of THiobarbiturates (resp)

A

decreased sensitivity of medullary ventilatory center to stimulation of CO2, apnea likely especially with other CNS drugs

20
Q

PK of THiobarbiturates

A

infusion not great opt d/t long context sensitivity 1/2 time, long recovery
not great for inductino, same time to wake up as propofol, but increased incidence of N slower to reach recovery milestones

21
Q

Oxybarbiturates

A

Methohexital, pentobarbital, secobarbital

22
Q

Metabolism of Oxybarbiturates

A

liver -> inactive hydroxy derivatives

clearance higher, more dependent on liver BF than thiobarbiturates. results in shorter elimination 1/2 t

23
Q

Causes excitatory phenomena (myoclonus, hiccoughs)

A

Oxybarbiturates

Fix: decrease with opioid

24
Q

Methohexital is X more potent then thiopental

A

2.7

25
Q

PK of Oxybarbiturates (CV)

A

less effects seen than with thiobarbiturates d/t increased tachycardia reflex response with (methohexital)

26
Q

Phenobarbital

A

increased liver microsomal protein content (enzymes) = enzyme induction
s/p 2-7 days of sustained drug administeration
affects PO anticoagulants, phenytoin, TCAs, endogenous corticosteroids/bile salts/ vitamin K

27
Q

Barbiturates for Induction

A

minimal no effects on any muscles

lean body mass weight dosing

28
Q

Thiopental Dosing

A

3-5mg/kg

pediatrics: 5-6mg/kg
infants: 6-8mg/kg

29
Q

Methohexital:

A

1-2 mg/kg

20-30mg/kg rectal in uncooperative or pediatric patients

30
Q

Neurologic Treatment of Barbiturates

A

treatment of refractory increased ICP

31
Q

How do barbiturates treat ICP?

A

decreases CBV via cerebral vascoconstriction and decreased CBF which increases perfusion to metabolism ratio
55% decrease in CMRO2= burst suppression in EEG
DOse required can cause significant hypotension and has not really been shown to improve outcomes

32
Q

Cerebral Protect in Barbiturates

A

thought to be due to reversal steal of CBF, free radical scavenging, stabilizing liposomal membrane, excitatory amino acid receptor blockade
Utilized for incomplete brain ischemia situations (CEA, CPB) however such have been shown to be more effective

33
Q

Issues of Barbiturates

A

Acclerated Heme production
Intra arterial injection
Allergy Risk

Pharmacology (14 decks)

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