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SRNAPharmacology II > VALLEY Review FINAL > Flashcards

VALLEY Review FINAL Flashcards

1
Q

• What is LD50/ED50?

A

The ratio is the therapeu,c index (TI). Defined by the dose that is lethal in 50% of subjects (LD50) divided by the dose that produces the desired effect (ED50). The larger the TI , the greater the margin of safety

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2
Q

What is the elimination half life (T1/2) of a drug? What two factors determine T1/2?

A

Elimination half life is time it takes for the plasma concentration to fall by one half. T1/2 is directly related to volume of distribution and inversely related to clearance. T1/2=Vd/Cl

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3
Q

Explain first order and zero order kinetics?

A

With first order a percentage of drug in eliminated per unit of time. With zero order kinetics a fixed amount of drug is eliminated per unit of time

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4
Q

What is the equation for Volume of distribution? How is is calculated?

A

Vd=Q/Cpp, where Vd is the volume of distribution, Q is the dose of drug injected and Cp is the plasma concentration of drug after distribution.

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5
Q

Diffusion of a drug across a membrane is propor,onal on the concentration gradient. Diffusion is also dependent on what 3 other factors?

A

Lipid solubility,
thickness of the membrane,
molecular weight of the substance.

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6
Q

The degree of protein binding is dependant on what primary factor?

A

The amount of protein in the blood

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7
Q

What is the most important determinant of build up of an an intravenous anesthetic in a given tissue?What other factors will effect drug concentration in tissues?

A

Blood flow to the tissue

Lipid solubility, ionization

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8
Q

Drugs absorbed from GI tract must first pass through what organ?

A

Liver first pass effect

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9
Q

What agents used in anesthesia are weak bases? •

A

Weak bases include; all opioids, benzodiazepines, etomidate, propofol, and ketamine.

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10
Q

What is an acid? Define weak acid?

A

Hydrogen ion or proton donor.• A weak acid is not ionized 100% in solution

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11
Q

What agents used in anesthesia are weak acids?

A

Barbiturates

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12
Q

What happens to the concentration of weak acid in nonionized form as pH falls?

A

Concentration increases (Rule: acid + acid=more non-ionized)

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13
Q

A weak acid with a pH of 7.8 will be more than 50% or less than 50% non-ionized at pH of 7.4 ?

A

More than 50% non-ionized

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14
Q

Do drugs that are weak acids form salts with posi,ve ions such as sodium or nega,ve ions such as Sulfate or Chloride?

A

Positive ions

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15
Q

A new drug, Z sulfate, has a pKa of 8.0. Will this drug be more than 50% ionized or les than 50% ionized at normal body pH?

A

The drug is a weak base therefore more than 50% ionized.

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16
Q

• What are six central nervous system action of benzodiazepines?

A

• Antianxiety, sedative, hypnotic,

anticonvulsant, amnestic, muscle relaxant

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17
Q

• How do benzodiazepines modify GABAergic transmission?

A

Benzodiazepines attach to the receptor adjacent to the GABA-A receptor and enhance the actions of GABA

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18
Q

At what anatomical site do benzodiazepines

work?

A

Reticular activating system (RAS)

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19
Q

Can withdrawal of benzodiazepines occur?

A 
Withdrawal	symptoms	(agitation,	insomnia,	
tremulousness)	can	occur.
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20
Q

What is the extent of protein binding of diazepine, midazolam and lorazepam in a healthy adult?

A

• Benzodiazepines are extensively protein bound. Diazepam and lorazepam are 98%, midazolam is 94%

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21
Q

• Are Diazepam and lorazepam freely water soluble?

A

• No

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22
Q

• What is the elimination half time of midazolam

A

• 1.7-2.6 hours

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23
Q

When is midazolam soluble in water? Midazolam

comes in solu#on with what pH?

A

Midazolam is water soluble when pH is < 4.0. Midazolam is available in solution with pH of 3.5.

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24
Q

• How are benzodiazepines metabolized?

A

Midazolam, diazepam are oxidized in the liver, lorazepam is conjugated in the liver

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25
Q

Clinical effects of benzodiazepines • Can small doses of benzodiazepines affect respiration?

A

Premedication normally have little effect on respiration and PaCo². Small doses can depress ventilation in geriatric patients.

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26
Q

• What pharmacological agents are used to

treat withdrawal from alcohol?

A

• Benzopiazepines (chlordiazepoxide, lorazepam).

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27
Q

• Why are benzodiazepines good premedications for a patient receiving a regional anesthetic?

A

The powerful antianxiety and amnesia actions of benzodiazepines

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28
Q

List three drugs that may be used to antagonize the central nervous sytem depression produced by benzodiazepines? • Which of these agents is specific?

A

• Flumazenil is a competitive antagonist for benzodiazepines. Physostigmine (Antilirium®) and aminophylline are nonspecific antagonist for benzodiazepines

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29
Q

• What is the half life of Flumazenil?

A

Approximately 60 minutes

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30
Q

• When is Flumazenil indicated?

A

Flumazenil is indicated for benzodiazepine overdose, or for reversal of sedative effects produced by benzodiazepines during general anesthesia, or during surgical procedures

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31
Q

• How should Flumazenil be used?

A

A series of small doses over 1-3 minutes up to 1mg usually reverses the therapeutic effects. Repetitive small doses up to 5mg over 2-10 min for benzodiazepine overdoses.

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32
Q

Which IV agents will decrease ICP?

A

Barbiturates, opioids, benzodiazepines, etomidate, and propofol. •

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33
Q

Name two non opioid induc&on agents that are associated with excitatory phenomena during induc&on? •

A

Methohexital and etomidate •

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34
Q

What agent is related chemically to Phencyclidine “angel dust”

A

Ketamine

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35
Q

• How does ketamine produce dissociative anesthesia?

A

• Ketamine produces dissociation between the

thalamocortical system and the limbic system

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36
Q

The CNS actions of ketamine appear to be primarily related to its action on what receptor?

A

• NMDA (N-methyl-D-aspartate)

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37
Q

• What other receptors does ketamine work on? •

A

Non NMDA glutamate receptors,
nicotinic receptors,
muscarinic receptors, and opioid receptors.

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38
Q

Barbiturates, benzodiazepines, propofol and etomidate produce their CNS actions by working on what receptor?

A

GABA

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39
Q

• What is responsible for the short elimination half life of ketamine?

A

Extensive hepatic metabolism

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40
Q

How is propofol eliminated?

A

Hepatic metabolism

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41
Q

The dysphoria (emergence delirium) associated with ketamine is caused by what? ••

A

due to depression of auditory and visual relay nuclei leading to misperception and/or misinterpretation of auditory and visual stimuli. Loss of skin and musculoskeletal sensations produces a sensation of bodily detachment or floating

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42
Q

What receptor does ketamine interact with to produce dysphoria?

A

Kappa, antagonism of muscarinic receptor, and possibly the sigma receptor

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43
Q

What drug would you give to a patient that becomes agitated and hallucinogenic during emergence from ketamine anesthesia?

A

A benzo such as midazolam

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44
Q

In what group of patents is ketamine contraindicated in?

A

Pts with Increased ICP

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45
Q

Does ketamine produce bronchodilation or bonchoconstriction?

A

Bronchodilation

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46
Q

Which nonopioid induction agent is associated with increase airway secretion?

A

Ketamine

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47
Q

Co-administration of what drug may be helpful to prevent excessive secretions with ketamine?

A

Glycopyrrolate

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48
Q

Which non-opioid induction agent is associated with increases in BP, HR and myocardial contractility?

A

Ketamine

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49
Q

Does ketamine depress pharyngeal and laryngeal reflexes?

A

No, these reflexes remain intact •

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50
Q

Venous thrombosis and phlebitis are most likely with what non-opioid anesthetics? Why?

A

Diazepam, lorazepam, and etomidate. Because these agents are dissolved in propyleneglycol

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51
Q

Which induction agent directly depresses the adrenal cortex

A

Etomidate

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52
Q

What are four potential complications during recovery from etomidate?

A

1) Suppression of adrenocortical response to stress
2) Nausea and vomiting
3) low plasma cortisol concentrations
4) depressed immune response.

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53
Q

What are five measurable cardiovascular effects of ketamine?

A

Increases in: mean aortic pressure, pulmonary artery pressure, CVP, HR, and cardiac index.

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54
Q

How does ketamine produce these CV effects?

A

SNS stimulation

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55
Q

What effect does etomidate have on cerebral blood flow, ICP and cerebral oxygen consumption? •

A

Etomidate, a potent vasoconstrictor decreases cerebral blood flow, ICP and cerebral oxygen consumption

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56
Q

What nonopioid induction agent best maintains cardiovascular stability?

A

Etomidate

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57
Q

How does the BP response to an induction dose of propofol differ from that of thiopental? What causes this effect?

A

The decrease in BP produced by propofol is greater than that produced by thiopental The effect is caused by a Decrease in SVR

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58
Q

How does propofol decrease BP and cardiac output?

A

Arterial vasodilation, and a decrease in myocardial contractility.

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59
Q

What is the most important advantage of propofol over other IV induction agents?

A

Faster and more complete awakening

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60
Q

What other actions of propofol enhance this drugs usefulness?

A

Antiemetic and pruritic effects

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61
Q

What is the IV induction dose of ketamine?

A

1-2mg/kg IV

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62
Q

What is the IM induction dose of ketamine?

A

5-10mg/kg IM

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63
Q

What drugs cannot be mixed with ketamine?

A

Any alkaline solutions such as barbiturates and diazepam

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64
Q

Which nonopioid induction agent depresses ventilation the least?

A

Ketamine

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65
Q

Which nonopioid induction agent produces profound analgesia?

A

Ketamine

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66
Q

• What are possible disadvantages of propofol use?

A

Allergic reactions to phenol nucleus and diisopropyl side chain.
Prolonged myoclonus has been reported caution in patients with uncontrolled epilepsy.
Potential for bacterial contamination. propofol strongly supports the growth of e-coli and pseudomonas aeruginosa
Propofol pain at injection site

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67
Q

What is the major inhibitory neurotransmitter of the CNS?

A

GABA • •

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68
Q

What ion channel is opened by this neurotransmitter?

A

Chloride

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69
Q

How do barbiturates modify GABAergic transmission?

A

By attaching to receptors nearby the GABA receptors and prolonging the attachment of GABA to its receptor.

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70
Q

Where do barbiturates work?

A

Reticular activating system (RAS)

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71
Q

What happens to onset, duration of action, and elimination of thiopental in the patient with acidosis? why

A

Thiopental is weak acid, and is therefore un-ionized in the presence of acidosis. Onset of action is faster, duration of action is shorter, and elimination will be slower (due to increase in Vd)

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72
Q

Thiopental will have a pronounced effect in a patient with liver disease and associated hypoalbuminemia? Why?

A

72-86% of thiopental is bound to albumin. In liver disease and hypoalbuminemia these is an increase in “free” frac5on of drug leading to pronounced effects

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73
Q

How are the actions of general IV anesthetics terminated?

A

Redistribution

74
Q

What is the pH of a barbiturate containing solution?

A

pH of solutions containing barbiturates is > 9.0

75
Q

Barbiturates should not be mixed with what types of solutions? Why

A

Acidic solution such as LR. Precipitation will occur

76
Q

How long does it take for thiopental to reach the brain?

A

LOC in 10-15 seconds

77
Q

What is the elimination half life of thiopental?

A

11.6 hours

78
Q

What are the cardiovascular effects of induction doses of thiopental?

A

In normovolemic patients there is a mild and transient fall in BP due to peripheral vasodilation

79
Q

What is the primary rationale for barbiturate therapy in head injury patients?

A

Barbiturates can quickly lower ICP

80
Q

What induction agents are appropriate for pa5ents with increased ICP?

A

Thiopental, etomidate, propofol, midazolam

81
Q

Does an induction dose of thiopental ordinarily obtund the laryngeal reflexes?

82
Q

Does an induction dose of thiopental produce good analgesia?

A

No. barbiturates including thiopental may cause hyperalgesia with subanesthetic doses.

83
Q

What are the disadvantages of the barbiturates as induction agents?

A

Lack specificity of effect in the CNS
Have a lower therapeutic index than benzodiazepines
Result in tolerance more easily than benzodiazepines Have a greater liability for abuse
High affinity for drug interactions
Paradoxical excitation especially in the elderly
Decrease in pain threshold with small doses
“Hangover effect”

84
Q

What is some of the unique properties of methohexital compared to thiopental?

A

• The principle disadvantage of methohexital is increased incidence of excitatory phenomena such as involuntary skeletal muscle movements (myoclonus), and hiccough.. High doses of methohexital is associated with seizures in approximately 1/3 of patients.

85
Q

List the barbiturates from highest to least potent?

A

Relaive potency of barbiturates used for IV induction, assuming thiopental is 1, thiamylal is 1.1, and methohexital is 2.5.

86
Q

What is the mechanism of apnea after thiopental administration?

A

Thiopental is a potent respiratory depressant. It reduces the sensitivity of the central respiratory center for CO2

87
Q

List three signs and symptoms of intra-arterial thiopental injection?

A

1) Arterial spasm with intense pain down the arm
2) blanching of skin with disappearance of pulses distally
3) eventual cyanosis and possible gangrene

88
Q

Which class of drugs can used to treat inadvertent intra-arterial injection of thiopental?

A

Nonselective alpha blockers phenoxybenzamine, phentolamine.

89
Q

Do induction doses of barbiturates cause hepatic enzyme induction?

90
Q

The use of barbiturates is absolutely contraindicated in which two disease states?

A

Status asthmaticus; porphyria

91
Q

What barbiturates release histamine?

A

Thiopental, thiamylal.

92
Q

How are the opioid receptors classified?

A

Mu, kappa, delta

93
Q

What receptor is responsible for the analgesic effects of the opioids?

94
Q

What opioid receptor is responsible for the adverse effects of opioids?

95
Q

Stimulation of what opioid receptor will decrease shivering?

96
Q

What opioids can be used to decrease post-operative shivering?

A

The opioid agonist meperidine, or the agonist antagonist butorphanol-Stadol®

97
Q

• What is the mechanism of action of intrathecally or epidurally (Neuraxial) administered opioids?

A

inhibit substance P release

98
Q

Explain the differences in onset and duration of action of the different opioids when given via intrathecal route? •

What drug characteritic is responsible for these differences?

• What is the clinical significance of these differences

A

• Hydrophillic opioids such as morphine cross lipid membranes slowly. After intrathecal placement, morphine diffuses out of the intrathecal space slowly, (Onset of action is slow and duration of action is prolonged). With lipophilic opioids such as fentanyl, diffusion out of CSF is rapid, resulting in rapid onset of ac

99
Q

Late respiratory depression associated with

100
Q

NO late respiratory depression

101
Q

Early respiratory depression

102
Q

What are potential side effects of neuraxial opioids?

A

Pruritis, nausea, urinary retention

103
Q

Does stimulation of mu-1 have high or low abuse potential?

104
Q

Does stimulation of mu-2 have high or low abuse potential?

105
Q

Physical dependence with this opioid receptor

106
Q

List four common side effects of intrathecal (spinal) opioid administration?

A

Pruritis, most common (60%)
Urinary retention (50%)
Nausea and vomiting (20-30%),
Respiratory depression (5-7%)

107
Q

At what anatomical locations do opioids work to produce spinal analgesia?

A

Substantia gelatinosa of the spinal cord,

108
Q

What opioid receptors promote respiratory depression?

109
Q

What opioid depresses myocardial contractility and increases heart rate?

A

Meperidine

110
Q

What is the major clinical implications of the opioid-induced decrease in gastrointestinal tone and motility?

A

Delays gastric emptying and increases risk of aspiration

111
Q

How do opioids (except meperidine) produce bradycardia?

A

With the exception of meperidine, opioids stimulate the vagal nuleus in the medulla, which increases vagal impulses to the heart.

112
Q

Does opioid-induced spasm of sphincter of Oddi cause pain?

113
Q

What agents can be used to reverse this effect?

A

Glucagon, Naloxone, NTG

114
Q

• The incidence and severity of opioid-induced skeletal muscle rigidity may be increased by what inhalation agent?

115
Q

What are the two most common side effect of fentanyl (IV)? •

A

• Severe respiratory depression, Nausea and vomiting •

116
Q

How do opioids cause nausea and vomiting?

A

By stimulating the chemoreceptor trigger zone.

117
Q

What narcotic should be avoided in patients on MAO inhibitors?

A

MEPERIDINE

118
Q

• What opioid agonist cause histamine release?

A

Morphine and Meperidine

119
Q

Why might blood pressure decrease after administration of sufentanil?

A

• Sufentanil may produce a dose dependent decrease in heart rate , probably by stimulation of the vagal nucleus in the medulla

120
Q

Metabolism of alfentanyl

A

Remifentanil is metabolized to inactive metabolites by blood and tissue nonspecific esterases. Remifentanil has T½ 10-30 min.

121
Q

What are the clinical significance of these metabolites?

A

Morphine-6-glucoronide is an active metabolite which can accumulate in patients with renal impairment leading to respiratory depression. Normeperidine is an active metabolite that can also accumulate in patents with renal impairment and lead to CNS excitation.

122
Q

List the metabolites of morphine, meperidine, and fentanyl?

A

Morphine’s principle metabolites are morphine-3- glucuronide and 5-10% of metabolites is morphine-6- glucruronide.

Meperidine’s hepatic metabolism is extensive with 90% of drug metabolized to normeperidine and meperidinic acid.

Fentanil is metabolized in the liver to norfentanil

123
Q

List the opioid agonist from fastest onset of action to slowest?
RASFM

A

1) Remifentanil,
2) Alfentanil, 3) Sufentanil,
4) Fentanyl,
5) Morphine, Meperidine

124
Q

• List the opioids agonist from shortest to longest duration of action?

A

1) Remifentanil (shortest)
2) Alfentanil 3) Morphine
4) Sufentanil
5) Meperidine 6) Fentanyl (longest)

125
Q

List the opioids agonist from highest to lowest potency?

A

1) Sufentanil (2000-4000x morphine),
2) Remifentanil 470x morphine,
3) Fentanyl 50-100 x morphine,
4) Alfentanil 10 x morphine,
5) Morphine,
6) Meperidine 0.1 x morphine

126
Q

List the opioids agonist from highest to lowest lipid solubility?

A

Sufentanyl, remi

127
Q

Most potent opioid

A

Sufentanyl

128
Q

Highest lipid soluble opiods

A

Sufentanyl

129
Q

Naloxone has affinity for what opioid receptors?

A

Mu (strongest)

130
Q

What is the duration of action of naloxone?

A

60 minutes

131
Q

• What four adverse cardiopulmonary changes may develop if large doses of naloxone are given?

A

Hypertension, cardiac dysrhythmias (V-fib), pulmonary edema, and tachycardia.

132
Q

Succinylcholine interacts with what receptor at the neuromuscular junc3on? •

133
Q

What could cause HR/BP to increase in response to succinylcholine?

A

Succinylcholine stimulates nicotinic receptors at the autonomic ganglia.

134
Q

How are the actions of succinylcholine and acetylcholine terminated?

A

Succinylcholine is hydrolyzed by plasmacholinesterases. Acetylcholine is hydrolyzed by true tissue cholinesterases at the NMJ

135
Q

What are 2 other names for plasma cholinesterases

A

Pseudocholiesterases, plasma cholinesterases, butyrocholinesterases.

136
Q

Describe the two phases of succinylcholine

metabolism?

A

• Step 1 : succinylcholine is metabolized by plasma cholinesterases to succinylmonocholine + choline.
Step 2: succinylmonocholine is metabolized by by plasma cholinesterases to succinic acid + choline.

137
Q

What are 11 possible complications associated with succinylcholine administration?

A
  1. Hyperkalemia
  2. Bradycadria
  3. Increase heart rate/BP
  4. Skeletal muscle myalgia
  5. Allergic reac3ons
  6. Triggering Malignant hyperthermia
  7. Masseter Spasms
  8. Myoglobinuria
  9. Increase intraocular pressure
  10. Increase intragastric pressure
  11. Increase ICP
138
Q

Why is succinylcholine contraindicated in pa3ents with nerve damage?

A

When motor nerves to skeletal muscles are damaged, nicotinic receptors of the skeletal muscle cell up regulate. These extrajunctional nicotinic receptors are exceptionally responsive to succinylcholine. Potassium leaves the cells in excessive quantities when succinylcholine triggers these channels to open leading to hyperkalemia

139
Q

How should you treat the bradycardia caused by succinylcholine?

A

Prior administration of atropine

140
Q

After succinylcholine administration to a normal patient, how much can serum K be elevated?

A

• 0.5-1 mEq/l

141
Q

List 5 conditions that may accentuate succinylcholine-induced hyperkalemia?

A

Unhealed 3rd degree burns 2. Denervation os skeletal muscle (praplegia, hemiplegia) 3. Severe skeletal muscle trauma 4. Upper motor neuron injury (head injury, Parkinson’s, CVA) 5. Muscular dystophy

142
Q

• What chemical group do all muscle relaxants have in common? • What is the significance of this?

A

• Quaternary ammonium group • This means that all muscle relaxants are completely ionized, highly water soluble

143
Q

• Muscle relaxants distribute primarily to what body compartment?

A

Extracellular fluid compartment

144
Q

• By what mechanism does pancuronium increase heart rate? • Pancuronium increase HR by what percentage?

A

Pancuronium competitively inhibits acetylcholine from attaching to muscarinic receptors of the SA node (atropine-like effect) • 10-15%

145
Q

What is the priming principle for nondepolarizing muscle relaxants

A

• A subtherapeutic dose of a non-depolarizing agent (10% of the ED95) is given, followed in 3-5 minutes by the remainder of the dose. It is speculated that the primary dose will occupy 50-70% of the receptors and the large subsequent dose rapidly blocks the remaining receptors causing a prompt onset of action

146
Q

Hoffman elimination is dependant on what two factors? •

A

Temperature and pH. The rate of Hoffman elimination is slowed by acidosis or decreases in body temperature

147
Q

What is the metabolite of ester hydrolysis of atracurium that although unlikely can cause CNS stimulation?

A

• Laudanosine

148
Q

List 4 muscle relaxants that least us the kidneys as a route of elimination?

A

Succinylcholine, atracurium, cisatracurium, and mivacurium

149
Q

Does fade occur with non-depolarizing NMB?

150
Q

Does fade occur with phase I block with succinylcholine?

151
Q

Does post-tetanic potentation occur with non-depolarizing NMB?

152
Q

Does post-tetanic potentation occur with phase I block from succinylcholine

153
Q

What drugs can increase the effects of nondepolarizing NMB agents? •

A 
Volatile anesthetics
Aminoglycoside 
Antibiotics
Cardiac an3dysrythmics 
Local anesthe3cs 
Diure3cs 
Magnesium 
Lithium •
Ganglionic Blockers
Cyclosporins
154
Q

What agent can lead to resistance to nondepolarizing NMB agents?

A

• Patients chronically treated with phenytoin are resistant to the effects of NMB. Higher doses may be needed.

155
Q

• What lab test assesses plasma pseudocholinesterase?

156
Q

What are the four anticholinesterase drugs that have NMB reversal effects? • • •

A

• Edrophonium, neostigmine, pyridostigmine, physostigmine

157
Q

Which of these are tertiary amines? anticholinesterase

A

Physostigmine

158
Q

Which of these are quarternary amines? •

A

• Edrophonium, neostigmine, pyridostigmine

159
Q

Explain how these agents work?

A

They competively inhibits acetylcholine from attaching to sites on the acetcholinesterase molecule. Acetylcholine concentrations are therefore substantially increased.

160
Q

How does neos#gmine and pyridos#mine bind to acetycholinesterase?

A

Covalentlly

161
Q

• How does edrophonium bind to acetylcholinesterase?

A

Electrostatic binding

162
Q

Which agents appear to work presynaptically?

A

Neogstimine

163
Q

Cholinesterase agents work at what receptor?

A

These agents indirectly stimulate muscarinic and nicotinic receptors by increasing the concentration of acetylcholine at the receptor sites.

164
Q

• What are five effects of the muscarinic
receptor stimulating properties of
anticholinesterase drugs?

A
  1. Bradycardia
  2. Increase salivary and bronchial secre#ons
  3. Bronchoconstriction
  4. Hyperperistalsis of GI tract
  5. Miosis
165
Q

• What is the treatment for cholinergic crisis?

A

• Atopine, pralidoxime (2-Pam)

166
Q

Identify 3 anticholinergic drugs used to

inhibit muscarinic receptors?

A

Atropine, glycopyrrolate, scopolamine

167
Q

Antimuscarinics suppress which division of the autonomic nervous system?

A

Parasympathetic division of the autonomic nervous system. They antagonize the effects of acetylcholine on tissues innervated by postganglionic parasympathetic nerves at the muscarinic receptor.

168
Q

How does atropine and other antimuscarinics increase heart rate?

A

• By competitively antagonizing acetylcholine
released from the vagus nerve at muscarinic
receptors of the SA node.

169
Q

What are the clinical uses of antimuscarinics agents?

Clinical Uses

A
  1. Antisialagogue
  2. Sedation and amnesia
  3. Increase heart rate
  4. Bronchodilation
  5. Reversal of cholinergic crisis
170
Q

Which antimuscarinic has the greatest and

which has the least antisialagogue effect?

A

• Greatest=scopolamine, least=atropine

171
Q

Which antimuscarinic has the greatest and

which has the least sedative effects?

A

Greatest=scopalamine, least=glycopyrrolate

172
Q

Which antimuscarinic has the greatest and

which has the least effect on heart rate?

A

Greatest=atropine, least=scopolamine

173
Q

Do antimuscarinics relax smooth muscle?

A

Yes, Ipatropium (Atrovent is given as MDI)

174
Q

Do antimuscarinics interfere with sweating?

A

Yes. Large doses of atropine may increase

body temperature

175
Q

How does atropine promote gastroesophageal

reflux

A

By decreasing the tone of lower esophageal sphincter.

176
Q

• The action of what antimuscarinic parallels the more

rapid onset of edrophonium?

A

• Atropine

177
Q

What is the concern of giving scopolamine to the

elderly (>76yrs) or young (<13yrs)?

A

Scopolamine may cause restlessness and confusion

178
Q

Which antimuscarinic can trigger the central anticholinergic syndrome?

A

Scopolamine, and to a lesser extent atropine

179
Q

What are CNS symptoms of central anticholinergic

syndrome?

A

Confusion, restlessness, agitation, delirium and

hallucinations, somnolence and coma.

180
Q

What are peripheral symptoms of anticholinergic

crisis?

A

Dry mouth, blurred vision, tachycardia, dry and
flushed skin, rash and fever (especially in
children)

181
Q

What group of patients are susceptible to

anticholinergic syndrome?

A

Small children and infants, and the elderly

182
Q

How is anticholinergic syndrome treated?

A

IV physostigmine (Antilirium®)

SRNAPharmacology II (32 decks)

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