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Anesthesia Pharm 2017 > COCO Study Guide > Flashcards

COCO Study Guide Flashcards

1
Q

MAC Additive properties

A

drug effects sum together

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2
Q

Racemic Mixture

A

When 2 enantiomers are present in equal proportions. Thiopental and etomidate are racemic mixtures.

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3
Q

Synergism

A

When 2 drugs interact to produce a greater effect than the some total of the 2 drug’s effects.

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4
Q

Division of cardiac output - Central Compartment

A

Central compartment gets rapid uptake of drug and includes intravascular fluid, and highly perfused tissues such as the brain, heart, lungs, kidneys, and liver.

The central compartment receives 75% of CO and makes up 10% of body mass.

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5
Q

Division of cardiac output - Peripheral Compartment

A

Peripheral compartment gets slower uptake and includes less vascular tissues like fat, bone, and inactive skeletal muscle.

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6
Q

pH for ionization

A

Basic drugs will ionize at a ph lower than their pK values, while acidic drugs will ionize at a pH greater than their pK.

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7
Q

pKa

A

The pH at which a molecule or drug is 50% ionized

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8
Q

Pharmacokinetics

A

What the body does to drugs

Absorption, distribution, metabolism, elimination. Combined with drug dosing, pharmacokinetics determines concentration of drug at its target.

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9
Q

Pharmacodynamics

A

What drugs do to the body

Study of intrinsic sensitivity or responsiveness of receptors to a drug and mechanisms by which these effects occur.

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10
Q

Agonist

A

A drug that produces its clinical effect by binding to a receptor and activating it.

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11
Q

Direct Agonist

A

Binds directly to the receptor to trigger a physiological response

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12
Q

Indirect Agonist

A

Produces its effect by increasing the endogenous substrate (NT or hormone)

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13
Q

Antagonist

A

Drugs that bind to receptors without activating them and simultaneously prevents agonists from stimulation said receptor.

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14
Q

Competitive Antagonist

A

A receptor inhibitor that competes for binding sites. Can be overcome by increasing the concentration of the agonist to out compete.

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15
Q

Non-Competitive Antagonist

A

A receptor inhibitor that cannot be overcome by increasing concentration of agonist (irreversible).

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16
Q

Hyperactive

A

unusually low doses that produce pharmacological effect

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17
Q

Hypersensitive

A

Allergy to a drug or substrate

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18
Q

Hyporeactive

A

Tolerant of said drug, requiring large doses to evoke effects

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19
Q

Tachyphylaxis

A

Tolerance that develops acutely with only a few doses

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20
Q

Prodrug

A

Molecule that is not pharmacologically active until after it has been metabolized and transformed.

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21
Q

Antagonistic Effect

A

When 2 drugs interact to produce an effect lesser than the sum of the 2 drugs.

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22
Q

Midazolam (First Pass Metabolism)

A

Midazolam given PO undergoes first pass metabolism. Midazolam given IV doesn’t undergo first pass metabolism.

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23
Q

Flumazenil Metabolism

A

Flumazenil is a specific, competitive antagonist of benzodiazepines. It has a shorter half life than benzodiazepines which can result in a resedation effect after it is metabolized. It is metabolized by hepatic enzymes which account for the quickness.

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24
Q

Midazolam Drug Interacions

A

Benzos exert a synergistic sedative effect on other CNS depressants including alcohol, barbiturates, opioids, and inhaled and injected anesthetics. It is especially potentiative of ventilatory depressant effects of opioids.

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25
Q

Clinical effects of Benzos

A

Sedation, anxiolysis, anticonvulsant, anterograde amnesia.

26
Q

Premedication of Benzos in children

A

Kids get a 0.5mg/Kg (15 mg maximum) dose of midaz 30 minutes before surgery.

27
Q

Contraindications for Acute Intermittent Porphyria

A

Do No Use barbiturates such as thiopental in patients with this disorder. It will inhibit the enzyme Porphobilinogen Deaminase used to synthesize heme which can cause problems with heme synthesis. Use Benzodiazepines instead.

28
Q

Thiopental Induction Dose

A

3 - 5 mg/Kg
Onset = 30 - 40 seconds (peaks at 1 minute)
Duration = 5 - 8 minutes
Protein Binding = Approximately 80% bound to plasma protein (Albumin)

29
Q

Thiopental Burst Supression

A

Barbiturates work well to lower the CMRO2 which lowers the cerebral blood flow to injured or operable areas of the brain. Can flat line an EEG.

30
Q

Mechanism of action - Barbiturates

A

Barbiturates interact with inhibitory NT, and GABA in the CNS. They decrease the rate of dissociation of GABA from GABA receptors, thus increasing the open time of the chloride channels. This results in hyperpolarization of the cell.

31
Q

Thiopental effects on HR and BP

A

Can lead to decreased systolic BP and a compensatory increase in HR. Histamine release can also lead to decreased BP.

32
Q

GABA

A

Gamma Aminobutyric Acid (NT)

33
Q

pH of Thiopental

A

10.5, which is very basic, making it bacteriostatic because bacteria doesn’t grow well in high pHs. When mixed with acidic drugs such as Fentanyl crystals will form.

34
Q

Barbiturate side effects

A

Cardiovascular: decreases systolic BP with compensatory HR increase
Histamine Release: Can lead to low BP
Heat Loss: due to vasodilation
Ventilation: low TV and Low RR is dose dependent. Apnea with induction dose.
Laryngeal Response: Laryngo/Broncho-spasm possible even with induction dose.
EEG: Low CMRO2 up to 55%
SSEP: not affected
Hepatic/Renal: lowers the blood flow to these organs
Placenta: will transfer to baby, but won’t affect baby
Tolerance: Happens sooner, lower therapeutic index
Intra-Arterial: BAB because high pH leads to thrombophlebitis

35
Q

Supply of Thiopental

A

24 mg/ml

36
Q

Thiopental Pharmacokinetics

A

very lipid soluble so fast uptake and easily crosses the BBB and quickly redistributes, highly protein bound, slow metabolism (wake up hungover), metabolism in liver to water soluble, inactive metabolites, renal clearance of inactive water soluble metabolites.

37
Q

Thiopental Stability

A

Supplied as an anhydrous powder. In this form it is good indefinitely. When drug is mixed in solution at room temp it is good for 1 week and good for 2 weeks when refrigerated.

38
Q

Propofol in the ICU

A

Extended use of Propofol can lead to hyperlipidemia so it should not be used longer than 3 days.

39
Q

MAC dose of Propofol

A

GA and TIVA cases = 100 to 200 mcg/Kg/min

40
Q

Propofol properties

A

Oil at room temperature, insoluble in aqueous solution, 98% protein binding

41
Q

Etomidate properties

A

Water soluble at an acidic pH and lipid soluble at physiological pH, 35% glycerol, racemic mixture, 76% protein binding

42
Q

Ketamine properties

A

Derivative of PCP, low protein binding of 27%

43
Q

Side effects of Propofol

A

Allergic reaction to eggs, may decrease convulsant activity, abuse, bacterial growth, pain on injection (glycerol)

44
Q

Propofol effect on CNS

A

Lowers the CMRO2, lowers ICP, Lowers CBF, can flatline the EEG and cause anterograde amnesia

45
Q

Propofol effect on cardiovascular system

A

Lowers SBP through vasodilation, Increases HR slightly, probably through compensatory efforts

46
Q

Propofol effect on pulmonary system

A

Lowers RR, Lowers TV = dose dependent, bronchodilation, hypoxic pulmonary vasoconstriction mechanism still intact.

47
Q

Propofol effect on Hepatic/Renal system

A

No adverse side effects, but green urine with prolonged infusion

48
Q

Propofol effects (Other)

A

Lowers IOP, Lowers responsiveness to DL

49
Q

Etomidate effect on CNS

A

Lowers CMRO2 (35-45%), Lowers CBF, can flatline the EEG but also increases excitatory spikes in EEG, which can induce a seizure soe use with caution in seizure patients.

50
Q

Etomidate effect on Cardiovascular system

A

Stability - minimal changes

51
Q

Etomidate effect on Ventilation

A

induction dose probably won’t cause apnea - SV possible

52
Q

Etomidate side effects

A

Pain on injection, myoclonus, adrenocortical suppression (inhibits 11-B-Hydroxylase), which leads to decreased cortisol, induces PONV and can rarely cause hiccups.

53
Q

Ketamine effect on CNS

A

Increased ICP due to increase in CMRO2, and increase in CBF*** - can cause excitatory spikes in EEG. OK to use when monitoring SSEPs.

54
Q

Ketamine effect on Ventilation

A

Causes no depression in ventilation (SV), increases secretions, causes bronchodilation

55
Q

Ketamine effect on Cardiovascular system

A

Increases BP (systolic > diastolic), increases HR, increases CMRO2, increases CO, is a myocardial depressant, cardiac rhythm (increase in catecholamines can lead to arrhythmias)

56
Q

Ketamine treatment for emergence delirium

A

Benzodiazepines

57
Q

Propofol additives

A

1% propofol
10% soybean oil
2.25% glycerol
1.2% purified egg phosphatide

58
Q

Drugs that interact with GABA receptors

A

Benzodiazepines
Thiopental
Propofol
Etomidate

59
Q

Drugs that do not interact with GABA receptors

A

Ketamine - instead it interacts with NMDA, opioids, MAO and muscarinic receptors

60
Q

Induction Analgesia

A

Ketamine is the only induction drug that has analgesic effects

61
Q

Etomidate dose

A

IV induction dose = 0.2 - 0.6 mg/Kg
Onset = 30 seconds (peaks at 1 minute)
Duration = 3 - 5 minutes

Anesthesia Pharm 2017 (3 decks)

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