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A Baseline Pharma > Induction Agent - Ketamine > Flashcards

Induction Agent - Ketamine Flashcards

1
Q

What class of drug is Ketamine?

A. Opioid analgesic

B. Benzodiazepine

C. Phencyclidine-derivative dissociative anesthetic

D. Barbiturate

A

C. Phencyclidine-derivative dissociative anesthetic

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2
Q

What is the typical induction dose range of Ketamine for adults?

A. 0.5-1 mg/kg

B. 1-2 mg/kg

C. 2-3 mg/kg

D. 3-4 mg/kg

A

B. 1-2 mg/kg

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3
Q

For intramuscular (IM) administration, what is the dose range of Ketamine known as the “Ketamine Dart”?

A. 1-2 mg/kg

B. 2-4 mg/kg

C. 4-6 mg/kg

D. 6-8 mg/kg

A

B. 2-4 mg/kg

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4
Q

What is the infusion dose range of Ketamine for general anesthesia (GA)?

A. 10-30 mcg/kg/min

B. 30-60 mcg/kg/min

C. 30-90 mcg/kg/min

D. 90-120 mcg/kg/min

A

C. 30-90 mcg/kg/min

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5
Q

How is Ketamine typically used for analgesia after induction?

A. 0.5 mg/kg immediately after induction, then 0.25 mg/kg every 2 hours

B. 0.5 mg/kg immediately after induction, then 0.25 mg/kg every hour

C. 1 mg/kg immediately after induction, then 0.5 mg/kg every 2 hours

D. 1 mg/kg immediately after induction, then 0.5 mg/kg every hour

A

Answer: B. 0.5 mg/kg immediately after induction, then 0.25 mg/kg every hour

“We use about 20 mg after induction, then 10 mg Q1H, but not on last hour before closing”

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6
Q

What is the concentration of Ketamine typically used?

A. 1 mg/mL

B. 5 mg/mL

C. 10 mg/mL

D. 20 mg/mL

A

C. 10 mg/mL

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7
Q

What is the primary mechanism of action (MOA) of Ketamine?

A. NMDA antagonism

B. GABA-A agonism

C. Opioid receptor agonism

D. Serotonin reuptake inhibition

A

A. NMDA antagonism

Binds noncompetitively to N-methyl-D-aspartate (NMDA) receptors.
-Glutamate (most abundant excitatory neurotransmitter in CNS)
-Glycine is an obligatory co-agonist.
-Inhibits activation of NMDA receptors by glutamate and decreases the presynaptic release of glutamate.

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8
Q

MOA:How does Ketamine affect the NMDA receptor?

A. It enhances glutamate depolarization on the postsynaptic neuron

B. It blocks glutamate depolarization on the postsynaptic neuron

C. It activates glutamate receptors

D. It inhibits acetylcholine release

A

B. It blocks glutamate depolarization on the postsynaptic neuron

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9
Q

MOA: Which system does Ketamine primarily dissociate by antagonizing NMDA receptors?

A. Thalamocortical and limbic system

B. Corticospinal and somatosensory system

C. Reticular activating system and hypothalamus

D. Limbic and hypothalamic system

A

A. Thalamocortical and limbic system

NMDA antagonism (block glutamate depolarization on post synapse) causes dissociation of thalamocortical and limbic system and decrease temporal summation,

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10
Q

What are Ketamine’s other MOA?

A. Catecholamine reuptake inhibitor (NE)

B. Mu agonist

C. weak GABAa agonist

D. monoaminergic

E. cholinergic/muscarinic (N&M) –>
hypersalivation

F. subcortical neurons in spinal tract - decrease pain

G. All of the above

A

A. Catecholamine reuptake inhibitor (NE)
B. Mu agonist
C. weak GABAa agonist
D. monoaminergic
E. cholinergic/muscarinic (N&M) –> hypersalivation
F. subcortical neurons in spinal tract - decrease pain
G. All of the above

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11
Q

What is the typical onset time of Ketamine when administered intravenously (IV)?

A. 30 seconds

B. 1 minute

C. 2 minutes

D. 5 minutes

A

B. 1 minute

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12
Q

How long does it typically take for Ketamine to take effect when given intramuscularly (IM)?

A. 1 minute

B. 2 minutes

C. 4 minutes

D. 6 minutes

A

C. 4 minutes

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13
Q

What is the usual duration of action for Ketamine when administered IV?

A. 1-3 minutes

B. 5-10 minutes

C. 15-20 minutes

D. 30-45 minutes

A

B. 5-10 minutes

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14
Q

How long does the duration of Ketamine’s effects typically last when administered IM?

A. 5-10 minutes

B. 10-15 minutes

C. 12-25 minutes

D. 30-45 minutes

A

C. 12-25 minutes
(overall up to 60 min for full recovery)

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15
Q

What explains the rapid onset and relatively quick offset of Ketamine’s effects?

A. Fast metabolism by the liver

B. Rapid uptake into the brain and redistribution to fat/muscle

C. High rate of renal excretion

D. Immediate hydrolysis in the bloodstream

A

Answer: B. Rapid uptake into the brain and redistribution to fat/muscle = dec in blood concent; not d/t metabolism!)

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16
Q

What is the typical elimination half-life of Ketamine?

A. 0.5-1 hour

B. 1-2 hours

C. 2-4 hours

D. 4-6 hours

A

C. 2-4 hours

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17
Q

What is the protein binding percentage of Ketamine?

A. 2%

B. 12%

C. 50%

D. 80%

A

B. 12%
(all other inductions >80%)

18
Q

How is Ketamine primarily metabolized in the body?

A. By esterases to inactive metabolites

B. Through phase I conjugation reactions

C. By CYP450 enzymes to the norketamine metabolite

D. Via direct renal excretion

A

C. By CYP450 enzymes to the norketamine metabolite

19
Q

What is the potency of the metabolite norketamine compared to Ketamine?

A. 1/10th potency

B. 1/3rd potency

C. 1/2 potency

D. Full potency

A

B. 1/3rd potency

causes prolonged analgesia

20
Q

Where does the primary excretion of Ketamine occur?

A. Liver

B. Lungs

C. Kidneys

D. Sweat glands

A

C. Kidneys

21
Q

Which condition is a contraindication for the use of Ketamine?

A. Systemic or pulmonary hypertension

B. Increased ICP

C. MAOIs

D. Methamphetamines

E. Cocaine (increases epi)

F. Ca2+ depletion

G. Neuro trauma (CNS stimulation)

H. SNS depression

I. All of the above

A

A. Systemic or pulmonary hypertension

B. Increased ICP

C. MAOIs

D. Methamphetamines

E. Cocaine (increases epi)

F. Ca2+ depletion

G. Neuro trauma (CNS stimulation)

H. SNS depression

I. All of the above

22
Q

What precaution should be taken when using Ketamine in combination with volatile anesthetics?

A. Monitor for hyperkalemia

B. Be cautious of hypotension due to blunted sympathetic nervous system response

C. Administer additional opioids to prevent bradycardia

D. Increase fluid intake to prevent dehydration

A

B. Be cautious of hypotension due to blunted sympathetic nervous system response

23
Q

How does Ketamine affect free calcium concentration and what is the implication?

A. Increases free calcium concentration, which decreases neuromuscular block

B. inhibits free calcium concentration, which increases neuromuscular block

C. No effect on free calcium concentration

D. Decreases free calcium concentration, which decreases neuromuscular block

A

B. Inhibits free calcium concentration, which increases neuromuscular block

24
Q

Why might the neuromuscular block be prolonged when Ketamine is used in conjunction with succinylcholine?

A. Due to increased plasma cholinesterase activity

B. Due to decreased plasma cholinesterase activity

C. Due to increased calcium concentration

D. Due to enhanced sympathetic nervous system stimulation

A

Answer: B. Due to decreased plasma cholinesterase activity

25
Q

What should be monitored due to the potential effect of Ketamine on depleted catecholamine levels?

A. Blood glucose levels

B. Blood pressure and cardiac output

C. Respiratory rate

D. Liver enzyme levels

A

Answer: B. Blood pressure and cardiac output

unexpected drops in SBP/CO with depleted catecholamines

26
Q

What unexpected cardiovascular effect can occur with Ketamine in patients with depleted catecholamines?

A. Tachycardia

B. Hypertension

C. Unexpected drops in systolic blood pressure and cardiac output

D. Increased cardiac output

A

C. Unexpected drops in systolic blood pressure and cardiac output

27
Q

How does Ketamine affect platelet aggregation?

A. Enhances platelet aggregation

B. Inhibits platelet aggregation

C. Has no effect on platelet aggregation

D. Causes abnormal platelet clumping

A

Answer: B. Inhibits platelet aggregation

28
Q

Why is Versed (midazolam) administered prior to Ketamine?

A. To enhance analgesic effects

B. To prevent emergence delirium

C. To counteract hypotension

D. To reduce hypersalivation

A

B. To prevent emergence delirium

29
Q

What is a potential allergic reaction associated with Ketamine due to its preservative?

A. Sodium chloride

B. Benzethonium chloride

C. Ethanol

D. Sodium bicarbonate

A

B. Benzethonium chloride
preservative to make water soluble

30
Q

Which of the following effects does Ketamine have on cerebral physiology?

A. Decreases cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2)

B. Decreases intracranial pressure (ICP) and intraocular pressure (IOP)

C. Increases cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), intracranial pressure (ICP), and intraocular pressure (IOP), excitatory activity in EEG

D. Increases excitatory activity in EEG and decreases intracranial pressure (ICP)

A

C. Increases cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), intracranial pressure (ICP), and intraocular pressure (IOP), excitatory activity in EEG

31
Q

What cardiovascular effects are commonly associated with Ketamine use?

A. Decreases systolic blood pressure (SBP) and heart rate (HR)

B. Increases systolic blood pressure (SBP), heart rate (HR), and cardiac output (CO) due to sympathetic nervous system stimulation

C. Causes bradycardia and hypotension

D. Decreases cardiac output and increases blood pressure

A

B. Increases systolic blood pressure (SBP), heart rate (HR), and cardiac output (CO) due to sympathetic nervous system stimulation

32
Q

What pulmonary effect does Ketamine have?

A. Causes significant respiratory depression

B. Potent bronchodilation with no depression of ventilation

C. Induces severe bronchoconstriction

D. Causes a decrease in ventilation and bronchoconstriction

A

B. Potent bronchodilation with no depression of ventilation

33
Q

Which of the following is a common ocular effect of Ketamine?

A. Eye closure

B. Nystagmus and eye opening

C. Decreased intraocular pressure

D. No effect on ocular function

A

Answer: B. Nystagmus and eye opening

34
Q

What effect does Ketamine have on salivary secretions?

A. Reduces salivary secretions

B. Causes an increase in salivary secretions

C. Has no effect on salivary secretions

D. Completely inhibits salivary secretions

A

B. Causes an increase in salivary secretions

35
Q

What precaution should be taken to manage Ketamine-induced cough and laryngospasm?

A. Administer a bronchodilator

B. Use an antisialogogue such as glycopyrrolate

C. Increase fluid intake

D. Administer a sedative

A

B. Use an antisialogogue such as glycopyrrolate

36
Q

How does Ketamine affect skeletal muscle movements?

A. Causes muscle relaxation and decreases muscle tone

B. Induces hypertonus and purposeful skeletal muscle movements

C. Causes muscle paralysis

D. Has no effect on skeletal muscle movements

A

Answer: B. Induces hypertonus and purposeful skeletal muscle movements

37
Q

In which scenario is Ketamine particularly useful?

A. For patients with chronic renal failure

B. For patients with acute hypovolemia

C. For patients with severe hepatic dysfunction

D. For patients undergoing elective cosmetic surgery

A

Answer: B. For patients with acute hypovolemia

37
Q

What effect does Ketamine have on platelet aggregation?

A. Enhances platelet aggregation

B. Inhibits platelet aggregation

C. Has no effect on platelet aggregation

D. Causes abnormal platelet clumping

A

Answer: B. Inhibits platelet aggregation

38
Q

Why might Ketamine be preferred for patients with asthma or bronchospasm?

A. It causes bronchoconstriction

B. It has potent bronchodilatory effects and does not depress ventilation

C. It enhances airway secretions

D. It significantly depresses respiratory function

A

Answer: B. It has potent bronchodilatory effects and does not depress ventilation

39
Q

Ketamine is used with which patients?

A. Acute hypovolemic pts
B. asthmatic/bronchospasm,
C. MH patients,
D. CAD ‘cocktail’ patient,
E. pediatric induction (IM),
F. burn pt with dressing changes,
G. reversal of opioid tolerance,
H. restless leg syndrome (PO)
I. All of the Above

A

I. All of the Above

A Baseline Pharma (53 decks)

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