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Term 5 Flash Cards > Drugs of abuse, anesthetics > Flashcards

Drugs of abuse, anesthetics Flashcards

1
Q

Ethanol

A

• The initial effects of ethanol are often perceived as stimulation due to suppression of inhibitory systems.

  • Ethanol influences several cellular functions:
  • GABAA receptors
  • Kir3/GIRK channels
  • Adenosine reuptake
  • Glycine receptors
  • NMDA receptors
  • 5-HT3 receptors.
  • Withdrawal syndrome may include tremor, nausea, vomiting, sweating, agitation and anxiety.
  • This may be followed by hallucinations.
  • Generalized seizures may appear after 24-48 h.
  • After 48-72 h delirium tremens may appear.
  • Delirium tremens is associated with 5-15% mortality.
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2
Q

Treatment of alcohol withdrawal

A
  • Long half-life benzodiazepines are the preferred agents: Diazepam and chlordiazepoxide.
  • Because of their long half-life, withdrawal is smoother, and rebound withdrawal symptoms are less likely to occur.
  • Lorazepam and oxazepam are intermediate- acting drugs.
  • Not as dependent on hepatic metabolism as other benzodiazepines,
  • They may be preferable in the elderly and those with liver failure.
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3
Q

Treatment of alcohol addiction

A
  • Disulfiram: Aldehyde dehydrogenase inhibitor. Used to create aversion to drinking.
  • Naltrexone: Orally available opioid antagonist. Reduces craving for alcohol.
  • Acamprosate: NMDA receptor antagonist. Prevents relapse.

Topiramate
• Facilitates GABA function, antagonizes glutamate receptors.
• May reduce cravings.
• Not FDA-approved.

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4
Q

BZOs

A
  • Can cause physical dependence and addiction.
  • Addiction is rare.
  • S/s include:tremors,anxiety, perceptual disturbances, dysphoria, psychosis, and seizures.
  • The syndrome can be life-threatening.
  • If the patient is on a short-acting drug, they are switched to a long-acting drug.
  • Diazepam is the most used agent.
  • Then the dose is gradually reduced.
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5
Q

Methylxanthines

A

• Caffeine, theophylline & theobromine.

  • Methylxanthines block presynaptic adenosine receptors.
  • Activation of adenosine receptors inhibits norepinephrine release.
  • Therefore blockade of adenosine receptors increases norepinephrine release.

CNS
• 100–200 mg caffeine (1-2 cups of coffee) cause decrease in fatigue and increased mental alertness.
• 1.5 g caffeine (12 to 15 cups of coffee) produces anxiety and tremors.
• The spinal cord is stimulated only by very high doses (2–5 g) of caffeine.

  • Tolerance can rapidly develop to the stimulating properties of caffeine.
  • Withdrawal consists of feelings of fatigue and sedation.
  • Addiction is rare.
  • Caffeine is not listed in the category of addicting stimulants.
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6
Q

Cocaine

A

• Cocaine is classified as a Schedule II drug by the DEA.

  • Cocaine inhibits dopamine, norepinephrine and serotonin reuptake.
  • The prolongation of dopaminergic effects in the brain’s limbic system produces the intense euphoria that cocaine initially causes.

CNS
• Stimulation of cortex and brainstem.
• Increases mental awareness and produces a feeling of well-being and euphoria.
• Paranoia may occur after repeated doses.
• At high doses: tremors and convulsions, followed by respiratory and vasomotor depression.

SYMPATHETIC NERVOUS SYSTEM
• Peripherally, cocaine potentiates the action of norepinephrine: fight or flight syndrome.
• Tachycardia, hypertension, pupillary dilation and peripheral vasoconstriction.

WITHDRAWAL
• Dysphoria, depression, sleepiness, fatigue, cocaine craving and bradycardia.
• Cocaine withdrawal is generally mild.
• Treatment of withdrawal symptoms is usually not required.

TREATMENT OF COCAINE ADDICTION
• Many agents, mainly antidepressants and dopamine agonists have been tested as treatments for cocaine abuse.
• None have demonstrated clear efficacy.

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7
Q

Amphetamines

A

• Amphetamines are classified as Schedule II drugs by the DEA.

  • Amphetamines increase release of catecholamines.
  • They are also weak inhibitors of MAO.
  • They are also possible direct catecholaminergic agonists in the brain.

CNS
• Behavioral effects similar to those of cocaine.
• Due to release of dopamine.
• Increased alertness, decreased fatigue, depressed appetite and insomnia.
• At high doses, psychosis and convulsions.

SYMPATHETIC NERVOUS SYSTEM
• Activate receptors through norepinephrine release.

USES
• Attention deficit syndrome: Amphetamine and methylphenidate.
• Narcolepsy: Amphetamine and methylphenidate.

TOLERANCE AND WITHDRAWAL
• Tolerance can be marked.
• An abstinence syndrome can occur upon withdrawal.
• Symptoms include increased appetite, sleepiness, exhaustion, and mental depression.
• Antidepressants may be indicated.

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8
Q

Nicotine

A
  • Full agonist of the nicotine receptor.
  • The rewarding effect of nicotine requires involvement of the ventral tegmental area, where nicotinic receptors are expressed on dopamine neurons.
  • When nicotine excites these neurons, dopamine is released.

ACTIONS
• In low doses: ganglionic stimulation by depolarization.
• At high doses: ganglionic blockade.

CNS
• Cigarette smoking or administration of low doses of nicotine produces some degree of euphoria and relaxation.
• Improves attention, learning, problem solving, and reaction time.
• High doses of nicotine result in central respiratory paralysis and severe hypotension caused by medullary paralysis.
• Nicotine is an appetite suppressant.

WITHDRAWAL
• Nicotine withdrawal is mild.
• Involves irritability and sleeplessness.
• However, nicotine is among the most addictive drugs.
• Relapse is very common.

NICOTINE REPLACEMENT THERAPY
• Nicotine can be administered by transdermal patch, gum, nasal spray, vapor inhaler or by lozenge for buccal absorption.

SUSTAINED-RELEASE BUPROPION
• Mechanism unclear.

VARENICLINE
• Partial agonist at nicotinic receptors in the CNS.

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9
Q

Opioids

A

• The most commonly abused opioids are heroin, morphine, codeine and oxycodone, and – among health professionals- meperidine and fentanyl.

  • All opioids induce strong tolerance and dependence.
  • Addiction to heroin or other short-acting opioids produces behavioural disruptions and usually is incompatible with a productive life.
  • The withdrawal syndrome is unpleasant but not life-threatening.
  • It includes dysphoria, lacrimation, rhinorrhea and yawning.

DETOXIFICATION USING OPIOID AGONISTS
• The illicit agent is replace by a long-acting opioid.
• The dose is slowly reduced.
• Drugs used: Methadone or buprenorphine.

DETOXIFICATION USING ADRENERGIC AGONISTS
• Chronic opioid intake leads to tolerance to the effects of opioids on the ANS, mediated by adrenergic pathways.
• Withdrawal leads to a rebound firing of the neurons.
• A noradrenergic storm results and is responsible for many of the withdrawal symptoms.
• Drugs used: Clonidine and lofexidine. They are a2 agonists.

DETOXIFICATION USING OPIOID ANTAGONISTS
• Naltrexone is an antagonist with a high affinity for
the mu opioid receptor.
• Naltrexone will not satisfy craving or relieve withdrawal symptoms.
• Naltrexone can be used after detoxification for patients with high motivation to remain opioid-free.

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10
Q

Marijuana

A

• delta9-tetrahydrocannabinol (delta9-THC, THC, dronabinol) produces most of the effects.

  • Two cannabinoid receptor subtypes: CB1 & CB2.
  • Both are G protein-linked receptors.
  • Both couple to Gi.
  • CB1 receptors are found primarily in the brain and mediate the psychological effects of THC.
  • CB2 receptors are present mainly on immune cells.

ACTIONS
• THC can produce euphoria, followed by drowsiness and relaxation.
• Affects short-term memory and mental activity.
• Impairs highly skilled motor activity.
• Other effects: appetite stimulation, xerostomia, visual hallucinations, delusions, enhancement of sensory activity.
• At high doses: toxic psychosis.

• Tolerance and mild physical dependence occur with continued, frequent use of the drug.

  • Dronabinol is FDA-approved for:
  • Anorexia associated with weight loss in patients with AIDS.
  • Nausea and vomiting associated with cancer chemotherapy (second line).
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11
Q

Psychedelic agents

A
  • Psychedelic drugs affect thought, perception and mood.

* They don’t cause marked psychomotor stimulation or depression.

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12
Q

LSD

A

The LSD-like group of drugs include:
• LSD
• Mescaline
• Psilocybin

• The hallucinogenic actions of LSD appear to be mediated by agonist effects at 5-HT2 receptors in the CNS.

  • LSD does not cause addiction.
  • There is no withdrawal syndrome.
  • Users may require medical attention because of “bad trips”.
  • Severe agitation may require medication: diazepam is effective.
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13
Q

PCP

A
  • Non-competitive antagonist at the NMDA subtype of glutamate receptor.
  • At higher doses it inhibits the reuptake of dopamine.
  • Phencyclidine causes dissociative anesthesia and analgesia.
  • Tolerance often develops with continued use.
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14
Q

MDMA

A
  • MDMA fosters feelings of empathy and intimacy without impairing intellectual capacities.
  • MDMA causes release of biogenic amines.
  • It most strongly increases the concentration of serotonin in the synaptic cleft.
  • Withdrawal is characterized by depression, lasting up to several weeks.
  • MDMA produces degeneration of serotonergic neurons in rats.
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15
Q

NO2

A
  • Produces euphoria and analgesia and then loss of consciousness.
  • Usually taken as 35% N2O mixed with O2.
  • Administration of 100% N2O may cause asphyxia and death.
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16
Q

Volatile organic solvents

A
  • Include gasoline, paint thinner, lighter fluid,glue and degreasers.
  • Produce sense of exhilaration and light- headedness.
  • Toxicity depends on the properties of individual solvents.
  • Implicated in cancer, cardiotoxicity, neuropathies and hepatotoxicity.
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17
Q

Organic nitrites

A
  • Amyl nitrite and butyl nitrite are used to enhance erection.
  • They are not addictive.
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18
Q

Inhaled anesthetics

A

Gases
• N2O

Volatile halogenated hydrocarbons
• Halothane 
• Enflurane 
• Isoflurane 
• Desflurane 
• Sevoflurane 
• Methoxyflurane

• Used for the maintenance of anesthesia after administration of an IV agent.

COMMON FEATURES
• Increase perfusion of brain.
• Cause bronchodilation.
• Decrease minute ventilation.
• Potency correlates with liposolubility.
• Rate of onset inversely correlates to blood solubility.
• Recovery is due to redistribution from the brain.

  • The actions of inhaled anesthetics are the consequence of direct interactions with ligand- gated ion channels.
  • Positive modulation of GABAA and glycine receptors.
  • Inhibition of nicotinic receptors.
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19
Q

Cardiovascular effects of inhaled anesthetics

A
  • Most inhaled anesthetics depress normal cardiac contractility.
  • As a result, they tend to decrease mean arterial pressure.
  • Halothane and enflurane reduce MAP mainly by myocardial depression, with little effect on PVR.
  • Isoflurane, desflurane and sevoflurane produce vasodilation and have minimal effect on cardiac output.
  • Isoflurane, desflurane and sevoflurane may be better choices for patients with impaired myocardial function.
  • N2O lowers blood pressure less than other inhaled anesthetics.
  • Halothane sensitizes the myocardium to circulating catecholamines, which may lead to ventricular arrhythmias.
  • This effect is less marked for isoflurane, sevoflurane and desflurane.
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20
Q

Respiratory effects of inhaled anesthetics

A
  • Volatile anesthetics are bronchodilators.
  • Isoflurane and desflurane are pungent: not suitable in patients with bronchospasm.
  • Halothane, sevoflurane and nitrous oxide are nonpungent.
  • Volatile anesthetics are respiratory depressants.
  • Isoflurane and enflurane are the most depressant.
  • N2O is the least depressant.
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21
Q

CNS effects of inhaled anesthetics

A
  • Inhaled anesthetics increase intracranial pressure.
  • Undesirable in patients who already have increased intracranial pressure because of brain tumor or head injury.
  • N2O increases blood flow the least.
  • Enflurane at high concentrations may cause tonic- clonic movements.
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22
Q

Other effects of N2O

A
  • N2O exchanges with nitrogen in air-containing cavities in the body.
  • N2O enters the cavity faster than nitrogen escapes.
  • Therefore, it increases the volume and/or pressure of the cavity.
  • N2O should be avoided in the following clinical settings:
  • Pneumothorax
  • Obstructed middle ear
  • Air embolus
  • Obstructed loop of bowel
  • Intraocular air bubble
  • Pulmonary bulla
  • Intracranial air
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23
Q

Halothane SE

A
  • Some individuals exposed to halothane may develop a potentially severe and life-threatening hepatitis.
  • There is no specific treatment
  • Liver transplantation may be required.
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24
Q

Methoxyflurane SE

A
  • Methoxyflurane has nephrotoxic potential.

* Due to fluoride released during metabolism.

25
Q

Chronic N2O toxicity

A

Hematotoxicity
• Prolonged exposure to N2O decreases methionine synthase activity and causes megaloblastic anemia.
• Potential occupational hazard for staff working in poorly ventilated dental operating suites.

26
Q

IV anesthetics

A
  • Barbiturates
  • Propofol
  • Ketamine
  • Etomidate
27
Q

Ultrashort-acting barbiturates

A

Thiopental and Methohexital
• Used for induction of anesthesia and for short surgical procedures.

• Their anesthetic effects are terminated by redistribution from the brain to other tissues, but hepatic metabolism is required for their elimination from the body.

  • They decrease intracranial pressure.
  • They do not produce analgesia.
  • They may cause hyperalgesia.
  • May cause apnea, coughing, chest wall spasm, laryngospasm and bronchospasm: a concern for asthmatic patients.
28
Q

Propofol

A
  • Most popular IV anesthetic.
  • Postoperative vomiting is uncommon. Antiemetic.
  • Used for induction and maintenance of anesthesia.
  • Produces no analgesia.
  • Rapidly metabolized in the liver.
  • Potent respiratory depressant.
  • Reduces intracranial pressure.
  • Causes hypotension, through decreased PVR.
  • Fospropofol: prodrug converted to propofol in vivo.
29
Q

Etomidate

A
  • Primarily used for anesthetic induction of patients at risk for hypotension.
  • Causes minimal cardiovascular and respiratory depression.
  • No analgesic effects.
  • Reduces intracranial pressure. Associated with nausea and vomiting.
  • May inhibit steroidogenesis, with decreased plasma levels of hydrocortisone.
30
Q

Ketamine

A
  • Produces dissociative anesthesia, characterized by catatonia, amnesia and analgesia, with or without loss of consciousness.
  • Mechanism of action may involve blockade of NMDA receptors.
  • Only IV anesthetic that possesses both analgesic properties and the ability to produce CV stimulation.

• Increases intracranial pressure.
• Causes sensory and perceptual illusions, and
vivid dreams (‘emergence phenomena’).
• Diazepam, midazolam, or propofol reduce the incidence of these phenomena.

31
Q

Neuroleptic-opioid combinations

A
  • When a potent opioid analgesic, such as fentanyl, is combined with a neuroleptic such as droperidol, neurolept analgesia is established.
  • Neurolept analgesia can be converted to neurolept anesthesia by the concurrent administration of 65% N2O in O2.
32
Q

Adjuncts to anesthetics

A
  • Benzodiazepines. For their anxiolytic and anterograde amnesic properties.
  • Opioids. For analgesia.
  • Neuromuscular blockers. To achieve muscle relaxation.
  • Antiemetics, eg ondansetron. To prevent possible aspiration of stomach contents.
  • Antimuscarinics, eg scopolamine
  • For its amnesic effects
  • To prevent salivation and bronchial secretions
  • To protect the heart from bradycardia caused by inhalation agents and neuromuscular blockers.
33
Q

Local anesthetics chemistry

A

• Ester links (as in procaine) are more prone to hydrolysis than amide links, therefore esters usually have a shorter duration of action.

  • Local anesthetics are weak bases with pK values around 8.0 – 9.0.
  • Therefore the larger fraction in the body fluids at physiologic pH will be the cationic form.

Prolongation of action by vasoconstrictors
• Also, in spinal anesthesia, epinephrine acts on a2-adrenoceptors, which inhibit release of substance P.
• The vasoconstrictor may cause untoward reactions: There may be delayed wound healing, tissue edema, or necrosis.

Metabolism and excretion
• Ester-linked local anesthetics are metabolized by tissue and plasma esterases (pseudocholinesterases).
• Amide-linked local anesthetics are in general degraded by liver microsomal cytochrome P450.

  • The smaller and more lipophilic the molecule, the faster the onset.
  • Potency is also positively correlated with lipophilicity.
  • Liposoluble agents such as tetracaine, bupivacaine and ropivacaine are more potent and have longer durations of action.
34
Q

Local anesthetics clinical pharmacology

A

• The choice of local anesthetics for a specific procedure is usually based on the duration of action required.
• Procaine and chloroprocaine are short-acting
• Lidocaine, mepivacaine, and prilocaine are
intermediate-acting.
• Tetracaine, bupivacaine, etidocaine and ropivacaine are long-acting.

35
Q

Organ effects of local anesthetics

A

CNS
• CNS stimulation: restlessness and tremor that may proceed to clonic convulsions.
• CNS stimulation is followed by CNS depression. Death is usually due to respiratory failure.
• More serious toxic reactions: due to convulsions from excessive blood levels.
• When large doses must be given, premedication with a benzodiazepine provides significant prophylaxis against seizures.

Peripheral nervous system
• At excessively high concentrations, all local anesthetics can be toxic to nerve tissue.

CVS
• Local anesthetics block sodium channels and thus depress cardiac pacemaker activity, excitability and conduction.
• With the exception of cocaine they also depress strength of cardiac contraction and cause arteriolar dilation, leading to hypotension.
• Cocaine may cause vasoconstriction and hypertension; also cardiac arrhythmias.
• Bupivacaine is more cardiotoxic than other local anesthetics.

Blood
• Large doses of prilocaine during regional anesthesia may lead to accumulation of the metabolite o-toluidine, an oxidizing agent capable of converting hemoglobin to methemoglobin.

36
Q

Allergic rxns

A
  • The ester type local anesthetics are metabolized to p-aminobenzoic acid derivatives.
  • These metabolites are responsible for allergic reactions in a small percentage of the population.
  • Amides are not metabolized to p-aminobenzoic acid.
  • Allergic reactions to agents of the amide group are extremely rare.
37
Q

Management of adverse effects

A
  • Supportive treatment of the cardiovascular system includes IV fluids and, when appropriate, vasopressors (preferably those that stimulate the myocardium, such as ephedrine).
  • Convulsions may be controlled with oxygen and by IV diazepam or ultrashort-acting barbiturates, or succinylcholine.
  • If hypotension occurs, it should be controlled by vasoconstrictors given IM or IV.
  • Allergic reactions should be treated according to their severity.
  • Mild cutaneous reactions may be treated with diphenhydramine.
  • More serious reactions should be treated with epinephrine SC.
38
Q

Drug interactions

A
  • Procaine is hydrolyzed in vivo to produce paraaminobenzoic acid (PABA), which inhibits the action of sulfonamides.
  • Large doses should not be administered to patients taking sulfonamide drugs.
39
Q

Succinylcholine

A

• Depolarizing blocker consisting of two acetylcholine molecules linked end-to-end.

  • Activates the nicotinic receptor and depolarizes the junction.
  • This causes fasciculations.
  • Succinylcholine is not metabolized effectively by acetylcholinesterase.
  • The membrane remains depolarized and unresponsive to additional impulses.
  • Flaccid paralysis results.
  • The onset of neuromuscular blockade is very rapid, usually <1 minute.
  • Because of its rapid hydrolysis by plasma pseudocholinesterase, duration of block is 5-10 minutes.
  • Neuromuscular blockade by succinylcholine (and mivacurium) may be prolonged in patients with an abnormal variant of butyrylcholinesterase.
  • Treated with mechanical ventilation until muscle function returns to normal.
  • Because of the rarity of these variants, plasma cholinesterase testing is not routine clinical procedure.

SE
• Succinylcholine activates all autonomic cholinoceptors:
• Nicotinic receptors in both sympathetic and parasympathetic ganglia
• Muscarinic receptors in the heart.

BRADYCARDIA
• Due to activation of muscarinic receptors.
• Can be prevented by thiopental, atropine, ganglionic blockers and non-depolarizing muscle relaxants.

HISTAMINE RELEASE
• Succinylcholine has a slight tendency to release histamine.

MUSCLE PAIN
• Important postoperative complaint.
• Due to damage produced by the unsynchronized contractions of adjacent muscle fibers.HYPERKALEMIA
• Due to loss of tissue potassium during depolarization.
• Risk is enhanced in patients with burns or muscle trauma.
• May lead to cardiac arrest or circulatory collapse.

INCREASED INTRAOCULAR PRESSURE
• Due to extraocular muscle contractions.

INCREASED INTRAGASTRIC PRESSURE
• Fasciculations mav increase intragastric pressure.
• May cause emesis and aspiration of gastric contents.

MALIGNANT HYPERTHERMIA
• Most cases are due to combination of succinylcholine and an halogenated anesthetic.
• Treatment: dantrolene.

• No CNS effects due to their inability to penetrate the blood-brain barrier.

40
Q

Nondepolarizing blockers

A
  • Their action can be overcome by increasing the concentration of acetylcholine in the synapse.
  • This can be achieved with neostigmine or edrophonium.
  • During anesthesia, nondepolarizing blockers first cause motor weakness
  • Ultimately,skeletal muscles become totally flaccid and inexcitable to stimulation.
  • Drugs that are excreted by the kidney typically have longer half-lives, leading to longer durations of action.
  • Drugs eliminated by the liver tend to have shorter half-lives and durations of action.
41
Q

PK of neuromuscular blockers

A
  • Neuromuscular blockers contain quaternary ammonium groups.
  • They are highly polar and poorly soluble in lipid.
  • Inactiveifgivenbymouth.
  • Penetrate membranes very poorly.
  • DonotentercellsorcrosstheBBB.
  • Always given IV or IM.
42
Q

Non-depolarizing blocker durations

A

SHORT- ACTING
• Mivacurium

INTERMEDIATE-ACTING
• Atracurium
• Cisatracurium
• Rocuronium
• Vecuronium

LONG-ACTING
• Tubocurarine
• Pancuronium

43
Q

Benzylisoquinolines

A
  • Atracurium - Enzymatic & nonenzymatic ester hydrolysis. 45
  • Cisatracurium - Spontaneous. 45
  • Mivacurium - Plasma pseudocholinesterase. 15
  • Tubocurarine - Renal (40%). 80
44
Q

Ammoniosteroids

A
  • Pancuronium - Enzymatic & nonenzymatic ester hydrolysis. 90
  • Rocuronium - Hepatic (80%) and renal. 30
  • Vecuronium - Hepatic (80%) and renal. 45
45
Q

Metabolism of nondepolarizing blockers

A
  • Atracurium is inactivated by hydrolysis by nonspecific plasma esterases and by a spontaneous reaction.
  • No increase in half-life in patients with renal failure.
  • One of atracurium metabolites is laudanosine.
  • Laudanosine, may cause hypotension and seizures.
  • Cisatracurium, a stereoisomer of atracurium forms much less laudanosine.
  • Cisatracurium also causes less histamine release.
  • Cisatracurium has largely replaced atracurium in clinical practice.

• Mivacurium has short duration of action.
• Hydrolysis by plasma butyrylcholinesterase is
the primary mechanism for inactivation.
• Not dependent on liver or kidney.

  • Rocuronium has the most rapid onset among nondepolarizing blockers.
  • Can be used as alternative to succinylcholine for rapid sequence intubation.
46
Q

SE’s of nondepolarizing blockers

A
  • Some benzylisoquinolines may cause hypotension due to histamine release and ganglionic blockade.
  • Some ammoniosteroids may produce tachycardia due to blockade of muscarinic receptors, which may lead to arrhythmias.

HISTAMINE RELEASE
• Tubocurarine, and to a lesser extent, mivacurium and atracurium may release histamine.
• Antihistamines are useful particularly if given before the neuromuscular blocker.

GANGLION BLOCKADE
• Tubocurarine may block nicotinic receptors of
the autonomic ganglia and the adrenal medulla.
• This causes hypotension and tachycardia.

BLOCKADE OF CARDIAC M2 RECEPTORS
• The ammoniosteroid pancuronium causes moderate tachycardia due to blockade of cardiac M2 receptors.
• The cardiovascular effects of pancuronium are usually not a problem.

47
Q

Depolarizing blocker CIs

A
  • History of malignant hyperthermia
  • History of skeletal muscle myopathies.
  • Major burns.
  • Multiple trauma
  • Denervation of skeletal muscle
  • Upper motor neuron injury.
48
Q

Reversal of nondepolarizing neuromuscular blockade

A
  • Acetylcholinesterase inhibitors can be used in the treatment of overdose of competitive blockers.
  • Also, upon completion of a surgical procedure many anaesthesiologists use neostigmine or edrophonium to reverse competitive blockade.
  • Atropine or glycopyrrolate are used concomitantly to prevent bradycardia.
49
Q

Diazepam

A

• Acts in CNS. Facilitates action of GABA at GABAA receptors

50
Q

Baclofen

A

• Acts in CNS. GABA agonist at GABAB receptors.

51
Q

Tizanidine

A

• Acts in CNS. Agonist at a2-adrenoceptors in the CNS.

52
Q

Gabapentin

A

• Acts in CNS. Increases GABA release.

53
Q

Progabide

A

• Acts in CNS. GABAA and GABAB agonist.

54
Q

Glycine

A

• Acts in CNS. Inhibitory amino acid neurotransmitter.

55
Q

Idrocilamide, Riluzole

A
  • Act in CNS. New agents for the treatment of ALS.

* Mechanism of action may involve inhibition of glutamatergic transmission in the CNS.

56
Q

Dantrolene

A
  • Acts on skeletal muscle. Interferes with the release of Ca2+ by binding to the ryanodine receptor in the SR of skeletal muscle.
  • Also used in malignant hyperthermia.
57
Q

Botulinum toxin

A

• Acts on skeletal muscle. Botulinum toxin is now finding increased application in the treatment of more generalized spastic disorders, e.g. cerebral palsy.

58
Q

Drugs for acute spasm

A
  • Used for relief of acute muscle spasm caused by local trauma or strain.
  • Most drugs are sedatives or act on spinal cord or brain stem.
  • Cyclobenzaprine is the prototype.
  • Strong antimuscarinic actions.
  • Causes sedation in most patients and confusion and transient visual hallucinations in some.

Term 5 Flash Cards (16 decks)

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