Anxiolytics and antipsychotics Flashcards

1
Q

Widely prescribed for anxiety, insomnia and muscle spasm

A

Benzodiazepines

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2
Q

Food for short tem use and situational anxiety

A

Benzodiazepines

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3
Q

Can be used with panic disorder due to quick onset

A

benzodiazepine

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4
Q

Non benzodiazepine

A

Buspirone (Busbar)

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5
Q

Used for treatment of anxiety disorder, but NOT panic disorder due to its slow onset

A

Buspirone (Busbar)

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6
Q

Has sedative and muscle relaxant properties

A

Benzodiazepines

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7
Q

Lacks sedative, skeletal muscle and anti-seizure effect

A

Buspirone (Busbar)

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8
Q

Not good for pre op anxiety

A

Buspirone (Busbar)

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9
Q

Does not produce dependance

A

Buspirone (Busbar)

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10
Q

which has less of a tendency to form tolerance, benzos or barbituates?

A

Benzos

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11
Q

Which has more tendency for abuse benzos or narcotics?

A

Narcotics

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12
Q

Benzos mechanism of action

A

Facilitates the action of GABA by enhancing the affinity for GABA, they DO NOT effect GABA directly

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13
Q

How do GABA receptors work?

A

GABA is an inhibatory receptor that when activated passes Cl- ions that hyperpolarize the cell and meke the mebrane resistant to excitation

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14
Q

5 pharmacologic effects of Benzodiazepines

A
  1. Anxiolysis
  2. Sedation
  3. Anterograde Amnesia
  4. Anticonvulasant action
  5. Muscle relaxaton at the spinal level
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15
Q

Benzos absorbtion

A
  1. highly protein bound
  2. highly lipid sluable
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16
Q

Benzos Metabolism

A

Metabolized by CYP 450 system - caution in patients with liver disease

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17
Q

Benzos elimination

A

Eliminated via the kidneys

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18
Q

RARE CNS effect of Benzos

A

Paradoxical Excitement

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19
Q

CNS effects of Benzos

A
  1. decreased CBF and decreased CMRO2
  2. Preserves cerebrovascular response to CO2
  3. Does Not procuce isoelectric EEG
  4. Does not attenuate ICP response to laryngoscopy
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20
Q

Benzos and Respiratory Effects

A
  1. Dose dependant decrease in ventilation
  2. hypoxemia and hypoventilation enhanced in presence of opioids
  3. CO2 curve Flattens- does NOT shift
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21
Q

CO2 curves for benzos and narcotics

A

Benzos - CO2 curve flattens and does not shift

Narcotics- CO2 curve shifts to the right

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22
Q

Benzos Cardiovascular Effects

A
  1. At induction doses decreases SVR- so we see a drop in BP
  2. CO unchanged
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23
Q

Benzos and Laryngoscopy

A

Even at induction doses Benzos DO NOT attenuated the SNS response to laryngoscopy

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24
Q

Water soluable preperation

A

Midazolam/Versed

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25
Q

comercially prepared in organic solvents including propylene glycol and benzyl alcohol

A

Diazepam / Valium

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26
Q

Imidazole ring: pH 3.5 whith an open ring and when it comes to physiologic pH of 7.4 the ring closes speeding the effect of action and increasing lipid solubility

A

Midazolam/Versed

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27
Q

Viscous: pH 6.6-6.9

A

Diazepam / Valium

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28
Q

Very highh affininty for Benzo receptor on GABA

A

Midazolam / Versed

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29
Q

2-3 x the ptency of diazepam

A

Midazolam / Versed

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30
Q

Painful IV and IM injection

A

Diazepam / Vallium

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31
Q

90-98% protein bound

A

Midazolam / Versed

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32
Q

5-10x the potency of Diazepam

A

Lorazepam / Ativan

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33
Q

Most Potent Amnestic of the Benzos used in anesthetic practice

A

Lorazepam / Ativan

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34
Q

Has Propylene glycol as solvent

A

Lorazepam / Ativan

35
Q

Rapid redistribution and short duration due to its lipid solubility

A

Midazolam / Versed

36
Q

Metabolized by the CY P450 System

A

Midazolam / Versed

37
Q

Mostly used for premedication, works well in kids

A

Midazolam / Versed

38
Q

Midazolam / Versed

Premedication/ Pediatric dose:

A

0.5 mg/kg PO

39
Q

Midazolam / Versed

IV sedation / Adults dose

A

1 -2.5 mg

up to 5 mg

if patient is really anxious or large

40
Q

Midazolam / Versed

Induction dose

A

0. 1 - 0.2 mg/kg over 30-60 sec

41
Q

Midazolam / Versed

Maintinece dose

A

Incramental or Infusion

42
Q

Highly lipid soluable and extremly long duration of action

Highly protein bound

A

Diazepam / Valium

43
Q

Metabolites are Pharmacologically INACTVE

A

Lorazepam / Ativan

44
Q

Lorazipam / Ativan

Elimination 1/2 time

A

10 - 20 hours

45
Q

metabolism is less influenced by alterations in hepatic function, age and other drugs

A

Lorazepam / Ativan

46
Q

Active metabolite of Diazepam / Valium and its Elimination 1/2 Time

A

Desmethyldiazepam

41 - 96 hours

47
Q

Rapidly ablsorbed from GI tract in PO dosages

A

Diazepam / Valium

48
Q

Elimination 1/2 Time Diazepam / Valium in Healty volunters

A

21 - 37 hours

it increases with age

49
Q

Diazepam / Valium

Premedication / Oral dose

A

10 - 15 mg

50
Q

Diazepam / Valium

Premedication / IV Dose

A

0.2 mg/kg - (it reduces MAC)

51
Q

Diazepam / Valium

Induction dose

A

0.5 - 1.0 mg/kg IV

52
Q

Diazepam / Valium

Anticonvulsant Dose

A

0.1 mg/kg IV

53
Q

Why are menzos anticonvulsants?

A

They inhibit the limbic system in the hippocampus of the brain

54
Q

Non- selective CNS depression

A

Barbituates - this is why they are not anticonvulsants

55
Q

Lorazepam / Ativan

Premedication / PO dose

A

50 mcg/kg

MAX Dose 4mg

56
Q

Drug that can cause Neuroleptic Malignant syndrome

A

Phenothiazines and Thioxanthenes

57
Q

Phenothiazines and Thioxanthenes mechanism of action

A

Blockade of dopamine receptors in the basal ganglia and limbic portions of the forebrain

58
Q

because Phenothiazines and Thioxanthenes interfere with dopamine they…

A

extrapyramidal side effects

59
Q

Phenothiazines and Thioxanthenes acheive antiemetic effects by

A

Blocking the chemoreceptor trigger sone of the medulla

60
Q

Erratic patterns of absorbtion fter PO administration, but highly lipid soluable and highly protein bound

A

Phenothiazines and Thioxanthenes

61
Q

Phenothiazines and Thioxanthenes metabolism

A
  1. oxidation in liver with conjugation
  2. most have inactve metabolites
  3. T1/2 10-20 hours- longer in elderly
62
Q

the problem with Phenothiazines and Thioxanthenes side effects is that ______________ due to the blockade of ______________ in the forebrain.

Because of this blockade the brain __________ dopamine receptors and they are _________ sensitive

A

The effects get worse

dopamine receptors

upregulates

MORE

63
Q

Extrapyramidal side effecs of Phenothiazines and Thioxanthenes

A
  1. Tardive dyskinesia
  2. Acute dystonic reactions
64
Q
  1. Abnormal involutary movements of tongue, face, neck, extremeties.
  2. Gait issues.
  3. Skeletal muscle groups involved in breathing and swallowing are involved
  4. occurs in 20% of patients over 1 year of therapy (elderly and women more susceptable)
  5. Ususally Perminent (Must stop Treatment)
A

Tardive Dyskinesia caused by Phenothiazines and Thioxanthenes

65
Q
  1. Usually in the first few weeks of therapy
  2. Acute skeletal muscle rigidity and cramping of face, neck, or back
  3. Respiratory distress from laryngodyskinesia - laryngospasm that is not life threatening - have hoarsness
  4. Responds well to diphenhydramine 25- 50mg IV
A

Acute dystonic reactions caused by Phenothiazines and Thioxanthenes

66
Q

Phenothiazines and Thioxanthenes cause Cardiovascular effect, what are they, and why do they occur

A
  1. Decreases in BP - due to vasomotor reflexes/ peripheral alpha adrenergic blockade
  2. Relaxant effect on smooth muscle
  3. NO direct cardiac depression
  4. NO
  5. Can see prolonged QT on ECG
67
Q

Due to the antagonism of _________, ________ and _________ receptors, Phenothiazines and Thioxanthenes causes _________ that develops a tolerance with chronic therapy.

Likewise, the ____________ is decreased and _______________ is acheived by _________ and does not happen at the __________.

A
  1. alpha 1
  2. muscarinic
  3. histamine
  4. sedation
  5. Seizure threshold
  6. Skeletal muscle relaxation
  7. CNS deprsseion
  8. Neuromuscular Junction
68
Q
  1. Develops over 28-48 hours
  2. Hyperthemia
  3. Hypertonocity of skeletal muslesInstability of autonomic NS
  4. Fluctuation LOC
A

Neuroleptic Malignant syndrome caused by Phenothiazines and Thioxanthenes

69
Q

Distinguishing feature fo Neuroleptic Malignant syndrome from Malignat Hypertermia.

A

With Neuroleptic malignant syndrome a non-depolarizing muscle relaxant will produce flaccid paralysis whein with Malignant hyperthermia it will not.

70
Q

When interact with causes sedative effects, Ventilatory depression aand analgesic properties

A

Phenothiazines and Thioxanthenes and opioids

71
Q

The ___________ stomp and __________ shuffle refet to some of the _______________ of ____________.

A

Taialaxine, Thorazine

extrapyrimidal side effects

Phenothiazines and Thioxanthenes

72
Q

Used to be used in the OR as an anti emetic

A

Droperodol

73
Q

ICU delerium and anxiety

A

Haloperodol (Haladol)

74
Q

Haloperridol and Droperidol are

A

Butyrophenones

75
Q

Butyrophenones promarily have _________ and ___________ side effects.

A

CNS and Cardiovascular

76
Q

Does Not cause Amnesia

Noes not have any anticonvulsant activity

A

Butyrophenomes

77
Q

name the Butyrophenomes​

A

haloperidol

droperidol

78
Q

Cause extrapyrimindal effects, cerebral vasoconstrictor

A

Haloperidol

Droperidol

79
Q

Haloperidol and Droperidol are _____________ that do not decresese_________.

A

Cerebral vasoconstrictors

Crerebral metabolic oxygen consumption

80
Q

can cause dysphoria

A

Haloperidol

Droperidol

81
Q

Haloperidol and Droperidol cardiovascular effects include, a minimal decrease in _________ due to ____________, it is a prominit ___________ that protects aginst __________induced dysrhythmias it acts by stabilizing ____________. It can also cause ______________ and _____________ at doses as low as _____________.

A

blood pressure; alpha blockade; antidysrhythmic; epinepehrine; cardiac cell membranes; prolonged QT interval; torsodes de pointes; 0.625-1.25mg.

82
Q

Has a black box warning, what is it?

A

Droperidol

All patiens must get 12 lead prior to administration of droperidol - prolonged QT

Must be monitored for 2-3 hours

83
Q

Used to be combined with fentanyl to cause a neurolept anesthesia, but it cause a dysphoria

I used to be used often as an antiemetic

A

Droperidol

84
Q
A