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Spring 2020 - Pharmacology 1 > Induction Agents - Quiz 2 > Flashcards

Induction Agents - Quiz 2 Flashcards

1
Q

What helps moves neurotransmitters to the endplate to release itself to the synapse then to the receptor?

A

Calciuim

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2
Q

What is broken down to form GABA

A

Glutamate

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3
Q

What kind of an effect does the GABA Agonist have?

A

Inhibitory Neurotransmitter

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4
Q

How does Glutamate work?

A

Released by calcium –> binds with NMDA –> Influx of Positively charged ions

Excitatory Effect

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5
Q

How can the effects of Glutamate be blocked?

A

Ketamine - Noncompetitive Antagonist

(also rapid antidepressant)

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6
Q

How does the Alpha2 Receptor Negative Feedback Loop Work?

A

Excess Norepi binds to presynaptic alpha2 receptor and inhibits release of Norepi

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7
Q

How does Precedex work?

A

Binds to presynaptic alpha2 receptors, blocking release of Norepi = sedation

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8
Q

Location of Baroreceptors

A

Aortic Arch, Carotid Body - signals travel to medulla and regulate heart rate, arterial, and venous tone according MAP

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9
Q

What nerves do baroreceptor impules travel through?

A

Vagus, Glossopharyngeal, and Hering’s

Action: Inhibits/Stimulates sympathetic/parasympathetic system

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10
Q

Central Chemoreceptors

A

Respond to pH and CO2 changes

(Peripheral Chemoreceptors responds to O2)

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11
Q

Advantages of IV Anesthesia

A

Rapid onset of General Anesthesia (30 sec - 1 min)

Can be used for maintenance of General Anesthesia

Provides sedation for MAC

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12
Q

How long does it normally take for a patient to wake back up from induction meds?

A

9 Minutes

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13
Q

Disadvantages of IV Anesthesia

A

There is no ONE med that provides hypnosis, amnesia, analgesia, and immobility.

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14
Q

What is Balanced Anesthesia

A

Use of Multiple drugs

  • Inhalation agents
  • IV induction agents
  • Sedative/Hypnotic
  • Opioids
  • Neuromuscular Blockade
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15
Q

Are IV Induction Agents hydrophilic or lipophilic?

A

All are Lipophilic - for rapid onset in brain and spinal cord

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16
Q

Body Mass % of Normal Adult

A
  • Vessel Rich: 10%
  • Vessel Poor: 20%
  • Fat: 20%
  • Muscle: 50%
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17
Q

Blood Flow % of Cardiac Output

A
  • Vessel Rich: 75%
  • Vessel Poor: <1%
  • Fat: 6%
  • Muscle: 19%
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18
Q

How is the effect of a Single Dose of IV Induction agent stopped?

A

Distribution, Not Metabolism

Drug redistributed to less perfused tissues: vessel rich & poor

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19
Q

When does metabolism of IV Induction medications come into play?

A

When multiple doses are given and when there’s a buildup of the drug

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20
Q

IV Bolus Three Compartment Model

A

Med goes to general circulation –> distributes to vessel rich organs –> rapid redistribution to vessel poor (shallow) –> slow distribution to peripheral compartments (deep) –> metabolism

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21
Q

What are the vessel rich organs?

A

Brain

Liver

Kidneys

Gut

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22
Q

What are the Vessel Poor Organs

A

Shallow Compartment

Muscles

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23
Q

What is part of the Deep Compartment?

A

Fat

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24
Q

In what phase does distrbution last for 2-4 minutes?

A

Rapid distribution phase to vessel poor group

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25
List classes of IV Induction Agents
Barbiturates Benzos Propofol Ketamine Etomidate Precedex
26
Barbiturates
1930's - Oldest Class Sedative, Hypnotic, Anticonvulsant
27
Chemical Structure of Barbiturates
Barbituric Acid - lacks CNS Activity
28
How do hypnotic, sedative, and anticonvulsive effects occur regarding barbituric acid?
Subbing on N1, C2, C5 sites
29
Why do myoclonic jerks occur when bolus dose of induction agent is given?
Body's natural response to bolus of inhibition = Sympathetic outflow
30
Barbiturate MOA
Acts with GABA to enhance profound hyperpolarization
31
What are GABA-mimetic effects?
Barbiturates dont need GABA with higher doses as opposed to Benzos
32
How does plasma albumin effect barbiturate binding?
Decreased albumin causes higher unbound barbs
33
What causes higher unbound fraction of barbiturate?
Decreased plasma protein concentration * Uremia * Liver disease * 3rd Trimester
34
What drugs compete with Barbiturates?
Aspirin Naproxen Indomethacin Warfarin
35
Pharmacokinetics of Barbiturates
3 Compartment Model Redistribution has major effect on duration Metabolism Inactive metabolites excreted in urine
36
CNS Effects of Barbiturates
* Rapid Loss of Consciousness * Significant post anesthesia drowsiness * No pain management properties * Decrease in O2 Consumption (CMRO2) * Decrease Cerebral Blood FLow * Decrease ICP & IOP * Anticonsulvant Properties
37
Barbiturates CV Effects
* Decrease Medullary vasomotor center * Decrease Sympathetic system * Decrease BP d/t vasodilation (transient) * Compensatory Increase in HR * Decreased venous return
38
When are exaggerated hypotensive responses seen with Barbiturates?
Hypovolemia Cardiac Tamponade Cardiomyopathy CAD Valvular Disease Large Induction Dose Rapid Drug Injection
39
Barbiturate Respiratory Effects
* Dose related respiratory depression * Laryngo/Bronchospasm * Transient apnea * Decrease stimulation by CO2 to breath * Laryngeal reflex/cough reflex suppression
40
Barbiturate Anaphylaxis
* Cause histamine release -\> vasodilation * 1 in 30,000 * Tissue necrosis if injected not in vein * Immunosuppression
41
What happens if you inject barbiturates in the artery?
Immediate Vasospasm and Constriction Intense Pain Entire Extremity Blanching Ischemic Gangrene
42
How to treat arterial injection of Barbiturates
* Dilute with injection of NS through same site * Treat vasospam with Papaverine 40-80mcg * Stellate or Brachial Plexus block to increase flow to extremity * Systemic Heparin
43
Absolute Contraindications to Barbiturates
* History of Allergic Reaction * History of Porphyria - Less than 20,000/yr * Autonomic System Disturbance * Abd Pain * Skin Lesions * HTN * Tachycardia * Seizures
44
Benzo Drugs
Librium Diazepam Serax Ativan Versed
45
Benzo MOA
Activates GABA Receptor Big Influx of Chloride Ions - Hyperpolarizes Versed has greater potency & affinity for GABA 2-3x more than diazepam
46
Why are Benzos used more in clinical Situations
Broad scope of properties with low side effect profile * Anxiolitic - amygdala, hippocampus, limbic * Sedation - brainstem & cortical receptors * Muscle relaxation - spine * Amnesia - Forebrain & hippocampus
47
Benzo Vs. Bariburates
Less abuse potential Bigger margin of safety Less significant drug interactions Dont induce liver enzymes
48
Imidazole Ring of Versed
* Open at pH:4 * Closed \> pH 4 = lipophilic = rapid onset
49
Versed Pharmacokinetics
Highly protein bound Rapid onset, but slow effect site equilibrium CYP substrate Urinary excretion
50
Benzo CNS Effects
Decreased CMRO2 Decreased CBF **CANNOT** make isoelectric EEG No ICP change Anticonvulsant Paradoxical excitement in \< 1%
51
Benzo CV Effects
Decreased BP (Versed \> Diazepam) Cardiac Output unchanged Does **NOT** prevent sympathetic response to intubation
52
Benzo Respiratory Effects
Same as Barbiturates
53
Benzo Side Effects
* Allergic rxns rare * Pain on injection - ativan, diazepam * NonRestorative sleep * Anterograde Amnesia
54
Benzo and Barb Withdrawal
Lasts weeks to months Anxiety, insomnia, seizures, coma, agitation, psychosis, mania, suicide HTN, Tachycardia, Postural Hypotension
55
Benzo & Barb Overdose
Resp. depression, hypotension, coma, confusion Use supportive therapy first before reversing
56
What is the reversal for only Benzo Overdose
Flumazenil - competitive antagonist 200 mcg q1-2 min, max 3mg/hr May cause immediate withdrawal
57
Remimazolam
Metabolism via Esterases Rapid Clearance - may only stay in 1st or 2nd compartment Less Buildup
58
Propofol
Most frequently used for induction Needs lipid vehicle so it doesnt separate out Supports bacterial growth
59
Propofol Reformulations
Swtched from EDTA to Sodium Metabisulfite Anaphylaxis and Asthmatic Episodes
60
Propofol MOA
Acts on GABA receptors
61
Propofol Pharmacokinetics
Rapid Onset Rapid Return of Consciousness (3-10 Min) Rapid Clearance - less hangover 3 Compartments CYP Substrate & Inhibitor
62
Propofol CNS Effects
Same as Benzos and Barbz
63
Propofol CV Effects
Profound dereased BP - afterload & preload Dramatic Inhibition of Baroreceptor Reflex Profound Bradycardia
64
How does Propofol supress apoptosis and inflammation
Structurally looks like Vitamin E
65
Propofol Respiratory Effects
* Potent respiratory depressant * Apnea after induction dose * Decreased response to CO2 and O2 * Big reduction in airway reflexes * Less risk of laryngo and bronchospasms than barbs
66
Other Propofol Effects
* Anti-emetic (10mcg/kg/min) * Does not potentiate muscle relaxants * Injection Pain - stay way from hand * Elevated triglycerides * Risk for PE * Antipyretic * Antioxidant
67
Propofol Infusion Syndrome
Lactic Acidosis for use \> 48 hrs or 67mcg/kg/min **Unexpected Tachycardia** Hepatomegaly
68
How do you treat Propofol Infusion Syndrome
Stop infusion Treat acidosis Support multi-system failure
69
How does propofol infusion syndrome present in kids?
Anion Gap Acidosis Bradyarrhythmia Rhabdo Liver Dysfunction MODS Hyperkalemia AKI
70
How does Propofol work in kids' bodies
* Enters mitochondria easily, stops ATP production, and stops fatty acid metabolism = fatty acid buildup * Carb deficiency makes kids more prone to these problems
71
Fospropofol (Lusedra)
Water Soluble Produg of Propofol ## Footnote **no need for lipid vehicle**
72
Fospropofol vs. Propofol
Slower Onset Stronger & Longer Duration More Itching & Paresthesia Less Pain on Injection Doesnt enter CNS until metabolized
73
Ketamine
Dissociative Anesthesia EEG Dissociation b/t thalamocortical & limbic Pt. Non Communcative Blank stare Limited skeletal movement
74
What does ketamine do well and dont do well?
Great pain control but No complete amnesia, needs a benzo **Emergence Delerium** - reduced by benzo
75
Ketamin's chemical structure is similiar to what?
PCP Partially water soluble S-enantiomer (Ketanest) is more potent, but cost $$$$$$$
76
Ketamine MOA
NMDA Noncompetitive Receptor Antagonist Inhibits C++ Influx Weak action on GABA May effect opioid, muscuranic, and monoaminergic receptors
77
How does Ketamine produce its analgesic effects?
Inhibits Nitric Oxide Synthase
78
How does Ketamine stimulate Sympathetic system?
Inhibits Catecholamine Reuptake
79
How does Ketamine produce Beta-2 agonism and respiratory relaxation?
Induces Catecholamine Release
80
Ketamine Pharmcokinetics
Not really bound to plasma proteins Leaves blood fast to be distributed to tissues Extremely lipophilic 3 Compartment Model
81
Metabolism of Ketamine
Really metabolized by liver enzymes Demethylation of ketamine to norketamine
82
What is Norketamine
Active Metabolite of Ketamine * 1/3 - 1/5 as potent * contributes to prolonged effects of ketamine * Hydroxylated then conjugated into water soluble inactive metabolites
83
Ketamine CNS Effects
**Increases** **CBF** **Increases CMRO2** Used for seizures if other meds fail May cause myoclonic jerks
84
Ketamine CV Effects
Direct Myocardia Depressant Produces significant transient Increases in BP, HR, CO Increased Cardiac Metabolic Requirment for Oxygen
85
Ketamine Respiratory Effects
**No Respiratory Depression** Respiratory response to CO2 present Transient hypoventilation Relaxes bronchial smooth muscle Increased Salivation
86
Ketamine Side Effects
Emergence Reactions: 10-30% Vivid Dreams, Out of Body Experience, Hallucinations Can last hours Nystagmus
87
What is the half-life of Flumazenil
1 Hour
88
Where do barbs bind on the GABA receptor?
Between GABAB and GABAY
89
Where do Benzos Bind on the GABA Receptor
Between GABAa and GABAY
90
Where do GABA Neurotransmitters bind on the GABA Receptor
Between GABAa and GABAB

Spring 2020 - Pharmacology 1 (11 decks)

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