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Flashcards in CNS Pharmacology Deck (180):
0

What is the general mechanism by which most CNS drugs act?

Changing ion flow through transmembrane channels of nerve cells.

1

What are the 2 types of ion channels of neuronal membranes?

1. Voltage-gated
2. Ligand-gated

2

The ligand-gated ion channels are activated/inactivated by the interaction between neurotransmitters and receptors. How is this coupling achieved?

1. Through a receptor that acts directly on the channel protein.
2. Through a receptor that is coupled to the ion channel through a G protein.
3. Through a receptor coupled to a G protein that modulates the formation of diffusible 2nd messengers (cAMP, DAG, IP3) which secondarily modulate ion channels.

3

How are usually EPSPS generated?

Via opening of Na and Ca channels.
In some synapses, also via CLOSING OF K CHANNELS.

4

How are IPSPs generated?

Via the opening of K or Cl channels.

5

What is the major site of pharmacologic action of most important CNS drugs?

THE SYNAPSE!

6

Mention the major CNS drug action sites?

1. The action potential in the presynaptic fiber.
2. Synthesis of transmitter.
3. Storage
4. Metabolism
5. Release
6. Reuptake
7. Degradation
8. Receptor for transmitter
9. Receptor-induced effect (ionic conductance)

7

On what is the selectivity of neurons mainly based?

On the fact that different groups of neurons USE DIFFERENT NEUROTRANSMITTERS and that they are segregated into networks that subserve different CNS functions.

8

What are the 2 types of neuronal systems in the CNS?

1. Hierarchical
2. Diffuse

9

What is the role o hierarchical CNS systems?

Control of major sensory and motor functions.

10

What are the major transmitters in the hierarchical systems?

EXCITATORY : Aspartate + Glutamate.
INHIBITORY : GABA + Glycine.

11

What effects do drugs that affect the hierarchical systems have?

Profound effects on the overall excitability of the CNS.

12

What are the transmitters in diffuse CNS systems?

Usually amines - dopamine, NE, serotonin/ or peptides on metabotropic receptors.

13

What effects do drugs that affects the diffuse CNS systems have?

Marked effects on CNS functions such as appetite, attention, and emotional states.

14

What are the 3 main criteria for a chemical to be accepted as a neurotransmitter?

1. Higher concentration in the synaptic area than in other areas.
2. Be released by electrical/chemical stimulation via a CALCIUM DEPENDENT MECHANISM.
3. Produce the SAME sort of postsynaptic response that is seen with physiologic activation of the synapse.

15

What percentage of the CNS neurons has receptors for ACh?

5%

16

What muscarinic receptors are present in the CNS?

M1.

17

What is the mechanism of action of the M1 receptors in the CNS?

SLOW excitation - DECREASE in membrane permeability to K.

18

Where are nicotinic receptors in the CNS?

On the RENSHAW cells activated by motor axon collaterals in the spinal cord.

19

What is the mechanism of action of dopamine?

Slow INHIBITORY actions via G protein ACTIVATION of K channels (postsynaptically) or INACTIVATION of Ca channels (presynaptically).

20

What is the main dopamine receptor in the CNS?

D2 - In basal ganglia and widely distributed at the supraspinal level.

21

Mention 3 important dopaminergic pathways.

1. Nigrostriatal
2. Mesolimbic
3. Tuberoinfundibular

22

Where are noradrenergic neurons mainly located in the CNS?

In the brain stem and the lateral tegmental area of the pons.

23

What adrenergic receptors produce excitatory effects?

α1+β1

24

What adrenergic receptors produce inhibitory effects?

α2+β2

25

Where are neurons that utilize serotonin located?

In the RAPHE or midline regions of the pons and upper brain stem.

26

What is the mechanism of action of serotonin?

Excitation or inhibition of CNS neurons depending on the receptor subtype activated.
BOTH excitatory and inhibitory actions can occur on the SAME neuron if appropriate receptors are present.

27

How are high concentrations of glutamic acid in synaptic vesicles being achieved?

By the vesicular glutamate transporter - VGLUT.

28

Mention an important subtype of glutamate receptors.

NMDA receptors

29

Mention 2 important NMDA blockers.

1. PCP - Phencyclidine and ketamine.

30

What is the mechanism of glutamate metabotropic receptor activation ?

G protein coupled activation of PLC or AC.

31

What is the effect of GABAa receptor activation?

Opening of chloride ion channels.

32

What happens in GABAb receptor activation?

Coupled to G proteins that either open K channels or close Ca channels.

33

What are the best-defined peptides?

1. Beta-endorphin
2. Met- and Leu- enkephalin
3. Dynorphin

34

What are the 2 main differences between peptide transmitters and nonpeptide transmitters?

1. The peptides are synthesized in the cell body and transported to the nerve ending via AXONAL TRANSPORT.
2. NO REUPTAKE or specific enzyme mechanisms have been identified for terminating their actions.

35

What are the endocannabinoids?

These are widely distributed brain lipid derivatives that bind to receptors for cannabinoids found in marijuana.

36

What is the mechanism of action of endocannabidoids?

Synthesized and released POSTSYNAPTICALLY, after membrane depolarization but travel backward acting PRESYNAPTICALLY to decrease transmitter release, via their interaction with specific cannabinoid receptor CB1.

37

What are the 3 major categories of sedative-hypnotics?

1. Benzodiazepines
2. Barbiturates
3. Miscellaneous agents

38

How are most sedative-hypnotics absorbed?

Most are lipid-soluble and are absorbed well from the GI tract, with good distribution to the brain.

39

Mention 4 sedative-hypnotics with rapid onset of CNS action.

1. Thiopental
2. Eszopiclone
3. Zaleplon
4. Zolpidem

40

What is the range of duration of CNS action of sedative-hypnotics?

From just a few hours (zaleplonto more than 30h (chlordiazepoxide, clorazepate, diazepam, phenobarbital.

41

Is there a single mechanism of action for sedative-hypnotics?

NO

42

Where have been found receptors for benzodiazepines?

BZ receptors are present :
1. Thalamus
2. Limbic structure
3. Cerebral cortex

43

Where are the BZ receptors located?

They form part of GABAa receptor-chloride ion channel macromolecular complex (5 subunits with 4 transmembrane domains).

44

What is the molecular action of benzodiazepines?

Increasing the FREQUENCY of GABA-mediated chloride ion channel opening.

45

Mention a principal BZ blocker?

Flumazenil

46

What drugs are classified as inverse BZ agonists?

Certain β-carbolines that have high affinity for BZ receptors and can elicit anxiogenic and convulsant effects.

47

What is the main action of barbiturates?

DEPRESS neuronal activity in the midbrain reticular formation, facilitating and prolonging the inhibitory effects of GABA and glycine.

48

What is the molecular mechanism of action of barbiturates?

Increase the DURATION of GABA-mediated chloride ion channel opening.

49

Mention 3 hypnotics that are NOT benzodiazepines, but utilize BZ1 or ω1 receptors.

1. Zolpidem
2. Zaleplon
3. Eszopiclone

50

In contrast to benzodiazepines, where do zolpidem/zaleplon/eszopiclone bind to ?

More SELECTIVELY, to GABAa isoforms that contain α1 subunits.

51

Can the CNS depressant effects of zolpidem/zaleplon/eszopiclone antagonized by flumanezil?

YES

52

What are the effects of sedative-hypnotics on hypnosis?

1. Promote sleep onset + increase the duration of the sleep state.
2. REM is usually decreased at HIGH doses - rebound increase when withdraw.
3. Effects on sleep patterns occur frequently with newer hypnotics such as ZALEPLON/ZOLPIDEM.

53

With what sedative-hypnotics is anterograde amnesia most likely to occur?

BENZODIAZEPINES

54

What anesthetic effects can sedative-hypnotics have at high doses?

1. Loss of consciousness
2. Amnesia
3. Suppression of reflexes

55

Can anesthesia be produced by barbiturates and benzodiazepines?

OF COURSE - By most barbiturates (thiopental) and certain benzodiazepines (midazolam).

56

Can sedative-hypnotics be used as anticonvulsant medication?

Occurs with high doses of most barbiturates and some of the benzodiazepines - but this is usually at the cost of marked sedation.
SELECTIVE ANTICONVULSANT ACTION occurs only with a few of these drugs.

57

Mention 2 sedative-hypnotics that are used as anticonvulsants.

1. Phenobarbital
2. Clonazepam

58

Mention 3 sedative-hypnotics that are used in status epilepticus?

1. Diazepam
2. Lorazepam
3. Phenobarbital
In this condition - Heavy sedation is desireable.

59

Mention 2 drugs that are used as muscle relaxants.

1. Diazepam : sedative dose levels, for specific spasticity states, including CEREBRAL PALSY.
2. Meprobamate : Some selectivity as muscle relaxant.

60

In sedative-hypnotics OD, what causes death?

Medullary depression and its consequences.

61

Besides psychological dependence, what happens in physiologic dependence of sedative-hypnotics?

Physiologic dependence is an altered state that leads to an abstinence syndrome (withdrawal state) when the drug is discontinued.

62

Mention some important withdrawal signs (of shorter acting drugs mainly).

1. Anxiety
2. Tremor
3. Hyperreflexia
4. Seizures

63

What sedative-hypnotics do we use in anxiety states?

Benzodiazepines : for acute anxiety and for rapid control of panic attacks. (Alprazolam + Clonazepam greater efficacy).

64

What sedative-hypnotics do we use in sleep disorders?

For primary insomnia :
1. Estazolam
2. Flurazepam
3. Triazolam
More recently :
1. Zolpidem
2. Zaleplon
3. Eszopiclone

65

What sedative-hypnotics do we use for anesthesia?

1. Thiopental
2. Diazepam
3. Midazolam

66

What sedative-hypnotics do we use for the management of withdrawal states in persons physiologically dependent on ethanol and other sedative-hypnotics?

Longer acting benzodiazepines :
1. Chlordiazepoxide
2. Diazepam

67

What are the adverse effects of sedative-hypnotics in the psychomotor functionality?

1. Cognitive impairment
2. Decreased psychomotor skills
3. Unwanted daytime sedation

68

With what sedative-hypnotics is the toxicity of psychomotor dysfunction more prominent?

Benzodiazepines with active metabolites that have long half-lives :
1. Diazepam
2. Flurazepam
Can ALSO occur after a single dose of a short acting, such as trialozam.

69

What is the MC drug interaction of sedative-hypnotics?

ADDITIVE CNS DEPRESSION when used with :
1. Alcohols
2. Antihistamines
3. Antipsychotics
4. Opioid analgesics
5. Tricyclic antidepressants

70

With what sedative-hypnotics is OD more likely to occur?

With alcohols + barbiturates + carbamates.

71

What CNS depressant effects can flumazenil reverse ?

Effects from :
1. Benzodiazepines
2. Eszopiclone
3. Zolpidem
4. Zaleplon

72

Mention some other adverse effects of barbiturates and carbamates (but not benzos, zolpidem, zaleplon, eszopiclone).

1. INDUCERS of liver microsomal enzymes that metabolize drugs.
2. Acute intermittent porphyria (barbiturates in susceptible patients).

73

What is the Buspirone?

A selective anxiolytic, with minimal CNS depressant effect and NO anticonvulsant or muscle relaxant properties.

74

What receptor does Buspirone utilize?

5-HT1a - acts as a partial agonist.

75

Is buspirone slow or fast acting?

Slow onset of action (>1week).

76

How is buspirone metabolized?

By CYP3A4.

77

Mention some side effects of buspirone.

1. Tachycardia
2. Pupillary constriction
3. GI distress

78

What is the Ramelteon?

This novel hypnotic drug activates MELATONIN receptors in the suprachiasmatic nuclei of the CNS and DECREASES the latency of sleep onset with MINIMAL REBOUND INSOMNIA or withdrawal symptoms.

79

What are the adverse effects of ramelteon?

1. Dizziness
2. Fatigue
3. Endocrine changes : decr. testosterone + incr. prolactin.

80

Mention 3 important alcohols of pharmacologic interest.

1. Ethanol
2. Methanol
3. Ethylene glycol

81

Mention 2 drugs that we use to treat alcohol withdrawal.

1. Thiamine
2. Diazepam (and other sedative-hypnotics)

82

Mention 3 drugs that we use to treat alcohol dependence.

1. Disulfiram
2. Naltrexone
3. Acamprosate

83

Mention 2 drugs that we use to treat acute methanol/ethylene glycol intoxication.

1. Ethanol
2. Fomepizole

84

What are the two enzyme systems that metabolize ethanol to acetaldehyde?

1. Alcohol dehydrogenase (ADH)
2. Microsomal ethanol-oxidizing system (MEOS)

85

Where are the ADH family of cytosolic, NAD+ dependent enzymes?

1. Liver
2. Gut

86

The ADH system is used for metabolizing low or high doses of ethanol?

Low to moderate doses.

87

What kinetics does th ADH system have?

Zero-order kinetics - due to limited supply of the coenzyme NAD+.
Fixed ethanol metabolism 7-10g/h.

88

GI metabolism of ethanol is lower in women or in men?

Lower in WOMEN.

89

At what level and beyond does the MEOS start to contribute to ethanol metabolism?

Ethanol levels higher than 100mg/dL.

90

What is the primary isoform of cytochrome P450 that is induced by ethanol?

2E1 - Converts acetaminophen to a hepatotoxic metabolite.

91

What is the fate of acetaldehyde that is formed by oxidation of either ADH or MEOS?

Rapidly metabolized to acetate by aldehyde dehydrogenase.
Aldehyde dehydrogenase is a mitochondrial enzyme found in the liver and in many other tissues.

92

Mention some INHIBITORS of aldehyde dehydrogenase.

1. Disulfiram
2. Metronidazole
3. Oral hypoglycemics
4. Some cephalosporins

93

What are the target organs for the major ACUTE effects of ethanol?

1. CNS
2. Heart (significant depression even at low levels)
3. Vascular smooth muscle relaxation

94

What are the major acute effects of ethanol on the CNS?

1. Sedation
2. Loss of inhibition
3. Impaired judgement
4. Slurred speech
5. Ataxia

95

What are the ethanol levels for impairment of driving ability to occur in nontolerant persons?

60-80mg/dL

96

What are the levels for gross drunkenness?

120-160mg/dL

97

What can be caused by ethanol levels higher than 300mg/dL?

1. Loss of consciousness
2. Ansthesia
3. Coma
4. Fatal respiratory/cardiovascular depression

98

What ethanol levels are usually lethal?

Higher than 500mg/dL

99

What CNS depressants can cause additive effects with ethanol?

1. Sedative-hypnotics
2. Opioid agonists
3. Many M blockers
4. Many H1 blockers

100

What appears to be the mechanism of action of ethanol?

Modulation of function of a number of signaling proteins :
1. It facilitates the action of GABA at GABAa receptors.
2. Inhibits the ability of glutamate to activate NMDA receptors.
3. Modifies the activity of AC, PLC, and ion channels.

101

What is the MC complication of chronic alcohol abuse?

Liver disease :
Reversible fatty liver progressing to irreversible hepatitis/cirrhosis/liver failure.

102

What are the complications of chronic alcohol abuse in the GI system?

1. Irritation
2. Inflammation and Bleeding
3. SCARRING of the gut wall - may cause absorption defects.
4. INCREASED RISK FOR PANCREATITIS!

103

What is the MC abnormality of chronic alcohol abuse?

Peripheral neuropathy.

104

What CNS complication can occur rarely in chronic alcohol abuse?

Thiamine deficiency, along with alcohol abuse, leads to WERNICKE-KORSAKOFF syndrome :
1. Ataxia
2. Confusion
3. Paralysis of the extraocular muscles
Parenteral thiamine ASAP to prevent permanent memory disorder known as KORSAKOFF's PSYCHOSIS.

105

What endocrine abnormalities can occur with chronic alcohol abuse?

1. Gynecomastia
2. Testicular atrophy
3. Salt retention

106

What CVS complications does chronic alcohol abuse have?

1. Hypertension
2. Anemia
3. DCM
ACUTE drinking for several days may cause arrhythmias.

107

What is the fetal alcohol syndrome?

Ethanol use in pregnancy is associated with teratogenic effects that include :
1. Mental retardation (MC)
2. Growth deficiencies
3. Microcephaly
4. Characteristically underdevelopment of the midface region

108

What is the treatment for the excessive CNS depression of acute ethanol intoxication.

1. IV dextrose (standard)
2. Thiamine administration to protect against Wernicke-Korsakoff syndrome.
3. Correction of electrolyte imbalance if necessary.

109

What are the classic effects of ethanol withdrawal syndrome?

1. Insomnia
2. Tremor
3. Anxiety
4. Life-threatening seizures (severe cases)
5. Delirium tremens (DTs) (severe cases)

110

What are the peripheral effects of ethanol withdrawal syndrome?

1. Nausea
2. Vomiting
3. Diarrhea
4. Arrhythmias

111

How do we manage ethanol withdrawal syndrome?

1. Correction of electrolyte imbalance
2. Administration of thiamine + sedative-hypnotic.

112

What sedative-hypnotic do we use in management of ethanol withdrawal syndrome?

A long acting BENZODIAZEPINE (diazepam, chlordiazepoxide) UNLESS the patient has compromised liver function.
IN THIS CASE, shooort acting benzos...! (lorazepam)

113

What drugs do we use in the treatment of alcoholism?

1. Naltrexone
2. Acamprosate
3. Disulfiram

114

What are the symptoms of methanol intoxication?

1. Visual dysfunction
2. GI distress
3. Shortness of breath
4. Loss of consciousness
5. Coma

115

What is the metabolite of methanol and what symptoms does it cause?

Formaldehyde and formic acid :
1. Severe acidosis
2. Retinal damage
3. Blindness

116

How do we reduce the formation of formaldehyde from methanol?

We give FOMEPIZOLE :
Inhibitor of alcohol dehydrogenase!... or... we give ETHANOL! (competitive inhibitor).

117

What complication does ethylene glycol metabolites cause?

Oxalic acid :
1. Severe acidosis
2. RENAL damage

118

What characterizes the state of general anesthesia?

1. Unconsciousness
2. Analgesia
3. Amnesia
4. Skeletal muscle relaxation
5. Loss of reflexes

119

What are the two broad categories of general anesthetics?

1. Inhaled
2. Intravenous

120

What are the major inhaled general anesthetics?

1. Gas - NO
2. Volatile liquids (Halothane)

121

What are the major IV general anesthetics?

1. Barbiturates (thiopental)
2. Dissociative (ketamine)
3. Miscellaneous
4. Opioids (fentanyl)
5. Benzodiazepines (midazolam)

122

What are the 4 stages of anesthesia?

1. Stage 1: Analgesia
2. Stage 2: Disinhibition
3. Stage 3: Surgical anesthesia
4. Stage 4: Medullary depression

123

What happens in stage 1 of anesthesia (Analgesia)?

The patient has decreased awareness of pain, sometimes with amnesia.
Consciousness may be impaired, BUT IT IS NOT LOST.

124

What happens in the stage 2 of anesthesia (disinhibition)?

Patient appears to be delirious and excited.
Amnesia occurs.
Reflexes are enhanced.
Irregular respiration.

125

What happens in stage 3 of anesthesia (surgical anesthesia)?

Patient is unconscious and has no pain reflexes.
Very irregular respiration.
Blood pressure is maintained.

126

What happens in the stage 4 of anesthesia (medullary depression)?

Patient develops severe respiratory and cardiovascular depression that requires mechanical and pharmacologic support.

127

What do the anesthesia protocols include for more extensive surgical procedures?

1. IV drugs to INDUCE the anesthetic state.
2. Inhaled anesthetics to MAINTAIN an anesthetic state.
3. Neuromuscular blocking agents to effect muscle relaxation.

128

What is the standard method of assessing "depth of anesthesia" during surgery?

Vital sign monitoring

129

Although the mechanisms of action of general anesthetics is varied, what is the usual one?

As CNS depressants, they USUALLY increase the threshold for firing of CNS neurons.

130

To what is the potency of INHALED anesthetics roughly proportional to?

To their lipid solubility.

131

Mention some general anesthetics that facilitate GABA-inhibition at GABAa receptors.

1. INHALED anesthetics
2. Benzos and Barbiturates
3. Etomidate
4. Propofol

132

What is the MOA of ketamine?

Possibly via antagonism of glutamic on NMDA receptor.

133

What other receptor may function as a target for cartain INHALED anesthetics?

The strychnine-sensitive glycine receptor

134

CNS neurons in different regions of the brain have different sensitivities to general anesthetics. What neurons are inhibited first?

Inhibition of neurons involved in PAIN pathways occurs before inhibition of neurons in the MIDBRAIN RETICULAR FORMATION.

135

Mention 7 important agents that are currently used in anesthesia?

1. NO
2. Desflurane
3. Sevoflurane
4. Isoflurane
5. Enflurane
6. Halothane
7. Methoxyflurane

136

What are the major factors upon which the speed of conduction of the inhaled anesthetics depends?

1. Solubility (Blood:Gas partition coefficient)
2. Inspired gas partial pressure
3. Ventilation rate
4. Pulmonary blood flow
5. Arteriovenous concentration gradient

137

What happens in the inhaled anesthetic's speed of conduction at HIGH pulmonary blood flows?

The gas partial pressure rises at a slower rate --> the speed of anesthesia is reduced.

138

What is the mechanism of termination of inhaled anesthesia?

By REDISTRIBUTION of the drug from the brain to the blood and elimination through the LUNGS.

139

Which rate of recovery from anesthesia is faster? That of NO or that of halothane?

That of NO --> Low Blood:Gas partition coefficient (low blood solubility) --> Faster recovery.

140

Mention 2 newer inhaled anesthetics that have a low blood solubility.

1. Desflurane
2. Sevoflurane

141

What are the 2 important inhaled anesthetics that are metabolized by the liver enzymes to a significant extent?

1. Halothane
2. Methoxyflurane
--> Minor influence on speed of recovery, BUT play a role in potential TOXICITY.

142

How is the potency of inhaled anesthetics measured?

By the minimum alveolar anesthetic concentration (MAC).

143

What is the definition of MAC?

The alveolar concentration required to eliminate the response to a standardized painful stimulus in 50% of patients.

144

What are the CNS effects of inhaled anesthetics?

1. Decr. brain metabolic rate.
2. Decr. vascular resistance --> Incr. cerebral blood flow --> Incr. intracranial pressure.

145

What is the unique effect of enflurane in high concentrations?

Spike-and-wave activity and muscle twitching.

146

What are the major cardiovascular effects of most inhaled anesthetics?

1. Decr. BP moderately.
2. Decr. blood flow to the liver and kidney.
3. Depress myocardial function. (NO least)

147

What inhaled anesthetics decrease CO?

1. Halothane
2. Enflurane

148

What inhaled anesthetics cause peripheral vasodilation?

1. Isoflurane
2. Desflurane
3. Sevoflurane

149

What inhaled anesthetic may sensitize the myocardium to the arrhtythmogenic effects of catecholamines?

1. Halothane
2. Isoflurane (to a lesser degree)

150

What are the respiratory effects of inhaled anesthetics?

1. Dose-dependent decrease in tidal volume and minute ventilaton --> Incr. Paco2.
2. Decr. ventilatory response to hypoxia, even at subanesthetic concentrations.
3. Most are bronchodilators.

151

What inhaled anesthetic has the smallest effect on inhalation?

NO

152

What inhaled anesthetic is pulmonary irritant and may cause bronchospasm?

Desflurane

153

How can malignant hyperthermia occur as a result of inhaled anesthetics toxicity?

Inhaled anesthetics used together with neuromuscular blockers (succinylcholine).

154

What drug is indicative for treatment of malignant hyperthermia after inhaled anesthetic?

Dantrolene

155

What are the 7 major IV anesthetics?

1. Barbiturates
2. Benzodiazepines
3. Ketamine
4. Opioids
5. Propofol
6. Etomidate
7. Dexmedetomidine

156

What barbiturates are used as IV anesthetics?

1. Thiopental
2. Methohexital

157

What is the MOA of thiopental and methohexital that are used as IV anesthetics?

High lipid solubility --> rapid anesthesia <1min.

158

What is the clinical use of the barbiturates used as inhaled anesthetics?

For short surgical procedures.

159

How are the barbiturates, that are used as IV anesthetics, terminated?

By REDISTRIBUTION from the brain to other highly perfused tissues - hepatic metabolism is required for elimination from the body.

160

What benzodiazepine is used as an IV anesthetic?

Midazolam - with inhaled anesthetics and IV opioids.

161

What are the effects of Ketamine that is used as an IV anesthetic?

Produces a state of "Dissociative anesthesia" in which the patient remains conscious, but has :
1. Marked catatonia
2. Analgesia
3. Amnesia.

162

Of what chemical substance is ketamine a chemical congener?

Of the psychotomimetic agent, PHENCYCLIDINE (PCP).

163

What emergency reactions can occur during recovery from ketamine anesthesia?

1. Disorientation
2. Excitation
3. Hallucinations

164

What drugs can reduce the emergence reactions that may occur during ketamine anesthesia?

Benzodiazepines

165

What opioids are used as IV anesthetics?

1. Morphine
2. Fentanyl

166

What is the clinical use of opioids used as IV anesthetics?

For high risk patients that may not survive a full general anesthetic.

167

What respiratory effects can be caused by IV anesthetic opioids?

Chest wall rigidity --> impair ventilation - REVERSED by NALOXONE.

168

What is the definition of Neuroleptanesthesia?

A state of analgesia and amnesia.

169

How does neuroleptanesthesia occur?

When fentanyl is used together with DROPERIDOL + NO.

170

Mention 2 newer drugs that have been used as IV anesthetic opioids.

1. Alfentanil
2. Remifentanil

171

What is the main action of propofol?

Produces anesthesia as rapidly as the IV barbiturates + recovery is MORE rapid.

172

What are the main effects of propofol?

1. Antiemetic actions
2. Marked hypotension during induction of anesthesia - Decr. peripheral resistance.

173

What is the clinical use of propofol?

It is commonly used as a component of balanced anesthesia + as anesthetic in outpatient surgery.
--> Effective in producing PROLONGED SEDATION in patients in critical care settings.

174

What are the effects of etomidate?

MINIMAL effects on CV and respiratory functions.

175

What are the pharmacokinetics of etomidate?

Short duration due to redistribution.

176

What are the toxicities and interactions of etomidate?

1. No analgesia
2. PAIN on injection (may need opioid)
3. Myoclonus
4. Nausea and vomiting.

177

What is the dexmedetomidine?

An α2 agonist, centrally acting --> analgesic + hypnotic functions when used IV.

178

What are the pharmacokinetics of dexmedetomidine?

Rapid clearance --> short elimination t1/2.

179

What is the clinical use of dexmedetomidine?

For short-term sedation in ICU setting.
When used in general anesthesia --> decr. the dose requirements for BOTH inhaled/IV anesthetics.

Decks in Pharmacology Class (54):