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Ane Class Practice > Pharm Exam 1- S3 > Flashcards

Pharm Exam 1- S3 Flashcards

1
Q

Neurotransmission is ?

A

Process of cellular communication

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2
Q

2 ways of cellular communication?

A

Chemical-neurotransmitters
Electrical- passive / active conduction

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3
Q

Which form of cellular communication is faster?

A

Electrical

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4
Q

Input from nerves can synapse on what?

A

Dendrites
cell body
axon
nerve terminal

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5
Q

Repolarization occurs naturally from what?

A

Na-K ATPase

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6
Q

Stored vessicles in nerve terminal are release by what?

A

Exocytosis after depolarization impulse from Axon.

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7
Q

What gives the impulse for depolarization?

A

Axon

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8
Q

Passive Conduction?

A

Brownian motion causes ions to disperse evenly and Diminish. Diffusing out and even. The longer the tube the more fluid= lower concentration at end.

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9
Q

Active Conduction?

A

Pass the signal down the axon itself, “moving”. Constantly regenerated voltage and marching down. Does not diminish. Voltage-gated Na goes in and K goes out at the same time.

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10
Q

NA goes _____?
K goes ______?

A

in
out

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11
Q

Active conduction leads to _____ to restore negative polarization?

A

Na-K pump. 3:2 pump. 3 NA out and puts 2 K back in to make more negative.

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12
Q

Chloride ions influx cause ?

A

hyperpolarization. -90mv

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13
Q

Normal resting membrane potential?

A

-70mv or -80mv

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14
Q

Sodium is higher in ?

A

Extracellular fluid

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15
Q

Potassium is higher in ?

A

Intracellular fluid

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16
Q

Chemical compounds are stored where?

A

In vessicles in the nerve terminal or Bouton.

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17
Q

The cell body (Soma) action?

A

Decides “to fire or not fire” based on signal. Biochemical reaction inside that releases binding substances.

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18
Q

Dendrites action?

A

Passively transmit information to the cell body.

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19
Q

Axon Hillock action?

A

Ligand receptor zones associated with Na ion channel. Reacts to intracellular substance.
NOT voltage-gated.

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20
Q

Axon action?

A

Voltage-gated Na channels that are stimulated by axon hillock.

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21
Q

Nerve terminals (Bouton) action?

A

Voltage-gated Ca channels that trigger the fusion of Ca and Na ions to pinch vesicles off.

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22
Q

Calcium is higher where?

A

Extracellular

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23
Q

Dendritic Conduction is a ?

A

Passive electrical process

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24
Q

Axonal Conduction is a?

A

Active electrical process, involves voltage gated Na and K channels. Na-K ATPase pump to restore chemical equilibrium.

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25
Q

Signal is initiated where in Axonal conduction?

A

Axon hillock, by internally ligand-gated Na channels.

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26
Q

Nonmyelinated axons?

A

Slower, more likely to be disrupted or blocked.

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27
Q

Myelinated axons?

A

Surrounded by myelin sheaths formed from Schwann cells. FASTER, use less energy. Not as much Na-K ATPase needed.

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28
Q

Ion penetration in myelinated axons is where?

A

At the Nodes of Ranvier or gaps.

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29
Q

Saltatory Conduction?

A

Through myelinated axons which allows jumping charge to occur. Rapid conduction.

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30
Q

Cellular changes are due to ?

A

Differential ionic concentrations

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31
Q

Normal ion concentration of Na?

A

15mM Intracellular

145mM Extracellular

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32
Q

Normal ion concentration of K?

A

145mM Intracellular

5mM Extracellular

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33
Q

Normal ion concentration of Cl?

A

10mM Intracellular

150mM Extracellular

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34
Q

Normal ion concentration of Ca?

A

0.0001mM Intracellular

2mM Extracellular

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35
Q

What is the second messenger released intracellularly to increase concentration to initiate biochemical reactions?

A

Calcium

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36
Q

Maintenance of internal voltage is done by?

A

Potassium

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37
Q

Peripheral nerves are?

A

Myelinated.

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38
Q

Motor nerves synapse where?

A

in Muscle

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39
Q

Diffusion vs Electromotive force balance?

A

Diffusion is driven by High to low

Electromotive force repulsion due to negative charges

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40
Q

Which ions are under electromotive force?

A

Potassium and Sodium

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41
Q

The primary contributor to resting charge is what?

A

Potassium channels

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42
Q

The only channel open at rest is ?

A

Potassium

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43
Q

The ability to balance diffusional flow of potassium and electromotive retention of potassium at equilibrium is what?

A

Diffusion vs electromotive force balance
allows no net movement.

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44
Q

Action potential is initiated at what?

A

Axon hillock

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45
Q

Tri-state propagation?

A

Allows the system to reset itself back to refractory -50mv.

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46
Q

Hysteresis is what?

A

Structure goes from one form to another and back. 2 state system.
NOT NEUROTRANSMISSION

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47
Q

Sodium channels open(depolarize) at what mv?

A

-40mv

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48
Q

Refractory mv?

A

-50mv

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49
Q

Resting state mv?

A

-70 to -80mv

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50
Q

Hyperpolarization mv?

A

-90mv to -100mv

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51
Q

Factors that lead to increased conduction rates?

A

Myelination
High resting membrane potential(-40)
Increasing Na channel density
Increasing axonal diameter

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52
Q

Decreased capacitance?

A

Movement of ions across membrane increases the conduction rate.

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53
Q

Saltatory conduction?

A

Jumping of currents between nodes of Ranvier which increases speed of conduction.

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54
Q

Higher resting potential is what?

A

Less negative -60 or -50mv

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55
Q

Bigger axonal diameter =

A

Less resistance, increased conduction rate.

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56
Q

Synaptic transmission occurs at the end of a nerve terminal where?

A

Ca released from storage in sarcoplasm and leads to biochemical change allowing fusion of vesicles with inner cell membrane.

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57
Q

With synaptic transmission vessicles are?

A

Filled and pinched off.

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58
Q

Primary excitatory Neurotransmitters are?

A

Acetycholine
Norepinephrine/ Epinephrine
Dopamine
Serotonin (Ionophore 5-Ht3)
Glutamic acid
Aspartic acid

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59
Q

What are the two most common excitatory neurotransmitters?

A

Aspartic acid and Glutamic acid

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60
Q

Excitatory Serotonin neurotransmitters is where?

A

Ionophore 5-Ht3

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61
Q

Primary Inhibitory transmitters are?

A

GABA
Glycine
Serotonin (G-protein type receptor)

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62
Q

Functions as a diode that transmits the energy of an action potential from presynaptic to post synaptic.

A

Synapse

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63
Q

Principle inhibitory neurotransmitter in the spinal cord?

A

Glycine

Causes hyperpolarization of cell.

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64
Q

Principle inhibitory neurotransmitter in the brain?

A

GABA

Causes hyperpolarization of the cell.

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65
Q

What is the major excitatory neurotransmitter in the CNS?

A

Glutamate

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66
Q

Ligand-gated ion channels?

A

Transmit signal across the synapse

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67
Q

Voltage-gated ion channels?

A

Propagate action potentials

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68
Q

Francis Rynd in 1845

A

First hollow needles, injection of morphine to treat neuralgia.

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69
Q

Which IV anesthetic drug first administered?

A

Thiopental in 1934

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70
Q

Agent cause mild suppression of arousal and behavior, slight decrease in alertness and response to stimuli?

A

Sedative

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71
Q

Agent cause pronounced sedative effects and induction of sleep.

A

Hypnotic

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72
Q

Which drug is used to induce sleep?
Sedative or hypnotic

A

Hypnotic

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73
Q

Sedatives become hypnotics at higher doses

A
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74
Q

Alcohols?

A

Cause CNS depression, increased side effects and death with too much.

Ethanol and Chloral hydrate

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75
Q

Which drug builds up with its own metabolism. One persons dose may kill another person?

A

Phenobarbital

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76
Q

Barbituates are ?

A

Sedative, hypnotics, and not used much anymore due to low TI.

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77
Q

Benzodiazepines are?

A

Anxiolytics, cause CNS depressant, used for short term procedures, and require less anesthetic dose.
Cause anterograde amnesia!

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78
Q

Sedative/hypnotic MOA?

A

Complex, but most act on polysynaptic pathways. Increase presynaptic inhibition to shut off release. Seperate binding sites to GABA to increase Cl conduction.

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79
Q

Benzos/Barbs most believed effect?

A

Enhance the effects of GABA by decreasing depolarization.
Hyperpolarizing

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80
Q

GABA ionophore is a ?

A

Pentameric ligand-gated structure

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81
Q

Sedative/hypnotics need 2 binding sites on GABA in order to?

A

Open chloride channel allowing Cl flow in by diffusion to hyperpolarize the cell.

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82
Q

GABA binding site is ?

A

Alpha-1
Beta-2

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83
Q

What site blocks GABA and closes Cl channel?

A

Picrotoxin

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84
Q

Picrotoxin does what?

A

Blocks GABA, closes Cl channel to cause CNS stimulation leading to seizure.

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85
Q

Too much excitatory in brain leads to?

A

Seizure, epilepsy.

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86
Q

Steroid Site effect on GABA receptor complex?

A

Can enhance GABA binding.
ie: Anesthetics

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87
Q

How does Ethanol affect GABA receptor complex?

A

Decreases ratio of Inhibitory/Excitatory
Blocks more inhibitory than excitatory.
90I : 10E. now
45I: 5E

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88
Q

Where does propofol/etomidate/ barbituates bind on GABA receptor complex?

A

Alpha-1
Beta-2

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89
Q

NMDA glutamate receptor complex is a ?

A

Voltage-dependent ionophoric system.
Allowing Ca and Na ions to enter

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90
Q

NMDA glutamate receptor complex shape?

A

4 protein structure, Quadrameric

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91
Q

Ketamine acts on what receptor?

A

PCP binding site on the NMDA glutamate receptor complex. Inhibits the conductance of Ca (Excitation) in the thalamus.

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92
Q

What is also needed to bind for the Glutamate Receptor antagonist site?

A

Glycine

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93
Q

Glycine is in ?

A

the Spinal Cord, a similar action to GABA as an inhibitory neurotransmitter

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94
Q

Benzos cause mild muscle relaxant effects where?

A

Nicotinic ACh receptor inhibition.

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95
Q

2 phases of sleep?

A

Slow wave sleep (SWS)
Rapid eye movement sleep (REM)

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96
Q

Slow wave sleep (SWS) EEG shows?

A

High voltage synchronous activity.

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97
Q

Rapid Eye movement (REM) shows?

A

Skeletal muscle relaxation, 25% of overall sleep, 1-2hrs. eye movement

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98
Q

Changes to sleep pattern from hypnotic agents?

A
  1. SWS patterns shortened
  2. REM sleep depressed
  3. Total sleep is prolonged
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99
Q

Barbituates MOA?

A

Augment GABA Cl- ionophore causing hyperpolarization. Decreasing dissociation of GABA.
Different location than benzos

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100
Q

Barbituates negative affect?

A

Heavily abused and altered sleep patterns.
Highly toxic with narrow TI

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101
Q

Which drug class inhibit oxidative phosphorylation?

A

Barbituates
Slowing of cellular function

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102
Q

Which drugs exist in keto and enol tautomers forms?

A

Barbituates

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103
Q

Replacement of C-2 oxygen with sulfur results in what?
(Barb)

A

Thiopental
Greater lipid solubility

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104
Q

Addition of a phenyl group at C-5 enhancing anticonvulsant activity?
(Barb)

A

Phenobarbital

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105
Q

Addition of a methyl group to the ring N shortens duration of action?
(Barb)

A

Methohexital

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106
Q

Long-acting barbituate?

A

Phenobarbital

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107
Q

Intermediate duration barbituate?

A

Pentobarbital
Secobarbital

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108
Q

Short-acting barbituate?

A

Methohexital
Thiopental

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109
Q

Base structure of a barbiturate?

A

Barbituric acid

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110
Q

The more lipid soluble the IV agent is the ____ its onset is?

A

Shorter onset due to rapid increase in brain concentration

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111
Q

Barbituates are_____ and packaged as ____?

A

Weak acids
Packaged as sodium salt in basic form

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112
Q

Barbituate primary metabolic pathway is?

A

Hydroxylation via PHASE 1
Potent inducers of the hepatic microsomal enzyme system.
OWN METABOLISM which can metabolism other drugs faster requiring higher doses.

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113
Q

Which drug class is used for Wada speech test prior to neurosurgery?

A

Barbituates
Slow brain function and slow metabolite buildup

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114
Q

Barbituates safe for pregnancy?

A

NO, placental transfer

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115
Q

Which has greater CNS specificity
BARBS or BENZOS?

A

Benzos

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116
Q

Ultra short-acting (10-15s)
High lipid solubility
Induction or short procedures
Metabolized by P-450 system
Half life- 6hrs
Lowers pain threshold- increase sensitive
POTENT RESP DEPRESSANT
DEPRESSES MYOCARDIUM
Neuroprotective
Unavailable in the US

A

Thiopental

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117
Q

2-3 more potent than thiopental
Metabolized faster by P-450 oxidation
Faster recovery
Used in ECT to Trigger seizures
Decreased seizure threshold

A

Methohexital

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118
Q

At high doses Benzos produce?

A

Hypnosis and unconsiousness

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119
Q

Half life of Midazolam?

A

1 hour

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120
Q

Half life of Diazepam?
Half life of effect of diazepam?

A

24-36 hrs
4 days (96hrs)

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121
Q

Midazolam is metabolized via ?

A

Microsomal hydroxylation

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122
Q

Diazepam is metabolized via ?

A

Microsomal N-demethylation

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123
Q

Oxazepam is eliminated rapidly by?

A

Glucoronide conjugation, PHASE II

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124
Q

Which benzo is converted into several active metabolites that increase clinical effect?

A

Diazepam

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125
Q

Diazepam potency value?

126
Q

Diazepam is metabolized into ____ via CYP2C19?

A

Desmethyldiazepam

127
Q

Desmethyldiazepam potency value?

128
Q

Desmethyldiazepam is metabolized into _____ via CYP3A4?

129
Q

Oxazepam potency value?

130
Q

Oxazepam becomes inactive via?

A

Glucoronidation

131
Q

Diazepam is metabolized into _____ via CYP3A4?

A

Temazepam
and
Oxazepam

132
Q

Temazepam potency value?

133
Q

Temazepam becomes inactive via ?

A

Gluronidation

134
Q

Metabolism

Diazepam→Desmethyldiazepam (via CYP2C19) then →Oxazepam (via CYP3A4) then →Glucoronidation to inactive.

Diazepam→ Temazepam(via CYP3A4) then → Glucoronidation to inactive.

A

Half life of effect= 4 days

135
Q

Midazolam potency value?
Midazolam half life?

136
Q

Midazolam is metabolized into ____ via CYP3A?

A

1-Hydroxymidazolam

137
Q

1-Hydroxymidazolam potency value?
1-Hydroxymidazolam half life?

A

0.5
6 hours

138
Q

1-Hydroxymidazolam is metabolized to inactive via ____?

A

Glucuronidation(Phase II)

139
Q

Metabolism of Midazolam

Midazolam→ 1-Hydroxymidazolam (via CYP3A) → Inactive glucuronide (via Glucuronidation) → Inactive compound

140
Q

Lorazepam half life?

141
Q

Lorazepam metabolism to inactive via ______?

A

Glucuronidation

142
Q

Benzos act on which subunits of the GABA receptor?

A

Alpha and Gamma
α. γ

143
Q

Benzos receptors are found exclusively on what region of the CNS?

A

Post-synaptic

144
Q

Benzos receptor density is greatest in _____ and associated with memory formation?

A

Cerebral cortex
(Neo cortex)

145
Q

Benzos affect on
Cardiac?
Heart rate?
Respiration?
Skeletal muscle?

A

Mild cardiovascular effect, decrease in BP
HR may decrease or increase(reflexive)
Transient apnea with rapid infusion
Relaxation of skeletal muscles

146
Q

Benzos safe for pregnancy/OB?

A

NO, crosses placenta wall, fetal depression.

147
Q

Reversal drug for benzo overdose?

A

Flumazenil
Competitive antagonist

148
Q

What is used as a counterirritant and rubifacient?

A

Ethanol

Rubifacient(increase blood flow to area by local irritation)

149
Q

Bactericidal effect by disruption of cell membranes is caused by?

150
Q

Decreases mental and physical abilities by a top-down CNS depression?

151
Q

This causes cutaneous vasodilation via central mechanism leading to warming effect?

152
Q

Ethanol metabolism?

A

Ethanol → acetaldehyde → Acetic acid

153
Q

Ethanol is converted to acetaldehyde via ?

A

Alcohol dehydrogenase

154
Q

Acetaldehyde is converted to Acetic acid via?

A

Aldehyde dehydrogenase

155
Q

Which form of Ethanol metabolism is used as an energy source?

A

Acetic acid

156
Q

Methanol metabolism?

A

Methanol → Formaldehyde → Formic acid

157
Q

What damages retinal cells and leads to blindness?

A

Formaldehyde

158
Q

Which drug binds to specific GABA receptors and has greater effects on sleep (weak alpha 2 agonist) but SE are sleep walking?

A

Escopiclone (Lunesta) = 7x
Zolpidem (ambien) = 1

159
Q

Propofol (2, 6-diisopropylphenol) MOA?

A

GABA receptor agonist, decreasing the rate of GABA dissociation from the receptor. Selective modulator of γ-aminobutyric acid type A (GABAA) receptors.

160
Q

Propofol allergic reaction are due to ?

A

Soybean allergy rather than egg allergy

161
Q

Propofol induction and affects?

A

Rapid induction (15-30 secs)
Must be given slowly to avoid vessel irritation
DO NOT MIX with LIDOCAINE
Anti emetic, antipruritic, and anticonvulsant actions

162
Q

Propofol metabolism?

A

Hepatic P-450 oxidative metabolism and phase II Glucuronide sulfate conjugation.
2-3 hour half life

163
Q

Propofol duration of effect and half life?

A

Duration- 5-10 mins
Half life- 2-3 hours

164
Q

Propofol safe for pregnancy?

A

Yes, Category B

165
Q

Propofol affect on
BP
Cardiac
Respiration?

A

Decreased BP (sympathetic vasoconstriction)
Bradycardia
Depresses ventilation and apnea

166
Q

When propofol is given continously over 24 hours what can happen?

A

Lactic acidosis.
Long term use can cause propofol infusion syndrome= severe metabolic acidosis, rhabdo.

167
Q

What is the prodrug of propofol?

A

Fospropofol

168
Q

Which form of propofol has no emulsion vehicle and is water soluble?
No pain on injection

A

Fospropofol

169
Q

Toxic metabolite of Fospropofol?

A

Formaldehyde

170
Q

Which form of propofol has no preservatives and short vial life with one time vial use?

171
Q

Propofol pumps?

A

Syringe mechanical infusion pump, bis monitor for CNS activity.
Outlawed in US

172
Q

Etomidate MOA?

A

GABA receptor enhancement. Exact receptor is not clear although more selective than barbs.
Weak base, 99% unionized

173
Q

Which drug is mixed with propylene glycol as vehicle?

A

Etomidate
very painful IV

174
Q

Etomidate Metabolism?

A

Via hydrolysis of side chain ester by plasma esterase and hepatic P-450.
Half life- 2-5 hours

175
Q

Etomidate effects on
Cardiac?
Respirations?
Neuro?

A

None, cardiac stable
Increase ICP, potent cerebral vasoconstrictor

176
Q

Side effects of Etomidate?

A

Myoclonus with rapid IV
Dystonia
Depresses steroid (cortisol) synthesis in adrenals. NO long term use

177
Q

Precedex MOA?

A

Alpha-2 Agonist works on presynaptic nerve terminals to shut off the release of norepinephrine. Mimics effects of clonidine but 7x more selective.

178
Q

Precedex half life?

A

2 hours. Why continuous IV infusion is used.

179
Q

Precedex metabolism?

Precedex side effects?

A

Mainly glucuronidation(34%) and P-450 hydroxylation.
Bradycardia/hypotension due to SNS decrease.

180
Q

Remimazolam metabolism?

A

Via Plasma esterase, which is why it is 1/4 duration of midazolam

181
Q

Ketamine MOA?

A

Binds to PCP site and Blocks glutamate excitatory NMDA receptors from release.
Blocks nACh receptors and Mu receptors

Agonist at Kappa receptors

182
Q

Ketamine side effects?

A

Tachycardia
Hypertension
Increase CO
Increased ICP
Increased cerebral oxygen requirement
Dissociative Anesthesia (Catalepsy)
Emergence delirium

183
Q

Ketamine affect on Glutamate?

A

Antagonist.

184
Q

Ketamine metabolism?

A

N- demethylated P-450 to Norketamine
25% activity then further to inactive hydroxynorketamine by hydroxylation

185
Q

Active metabolite of Ketamine?

A

Norketamine (25% activity)

186
Q

Inactive metabolite of Ketamine?

A

Hydroxynorketamine

187
Q

Best IV anesthetic for pediatric patients?

188
Q

Increase in altitude does what to pO2?

189
Q

Biggest dropoff in PO2 is seen where?

A

Below 70mmHg

190
Q

Increase in pH (Alkylosis)
Decrease DPG
Decrease Temperature
Nitrogen

Oxyhemoglobin shift where?

A

Left
Increase oxygen affinity for hemoglobin

191
Q

Decrease in pH ( Acidosis)
Increase in DPG
Increase in Temperature
Increase in CO2

Oxyhemoglobin shift where?

A

Right
Decrease oxygen affinity for hemoglobin

192
Q

What is the primary drive for ventilation?

193
Q

T or F
Increased inspired O2 conc does not greatly increase blood O2?

A

True, based on dissociation curve, can have low hemoglobin or low plasma volume

194
Q

T or F
Too much oxygen can suppress respiration?

A

True, will decrease hypoxic drive due to decreased CO2

195
Q

Too much oxygen can lead to ?

A

Peroxide formation

196
Q

_____ can constrict cerebral vessels and decrease brain size in neurosurgery?

A

Hypocarbia
Increased RR (hyperventilation)

197
Q

_____ is the main drive mechanism for vasodilation of arterioles?

A

Nitric oxide

198
Q

Osmosis molecular weight cutoff?

199
Q

Based on Fick’s Law

The diffusion rate is ____ to the partial pressure gradient, membrane area, and solubility of a gas in the membrane?

A

Proportional

200
Q

Based on Fick’s Law

The diffusion rate is ____ to the membrane thickness and sq root of the molecular weight?

A

Inversely proprotional

201
Q

Which has slower diffusion rate?

20 microns
40 microns

A

40 microns slower

202
Q

Graham’s law of diffusion states that
The rate of diffusion is ___ to the square root of the molar mass?

A

Inversely proportional.
Larger mass= Slower diffusion

203
Q

Henry’s Law states that the amount of gas that will disolve in a liquid is _____ to the partial pressure of the gas in the gas phase?

A

Proportional

204
Q

Laminar Flow?

A

Moving smooth and well. Minimal resistance

205
Q

Turbulent Flow?

A

Resistance, Disruption, slows down and cannot predict.

206
Q

What type of flow is typically in bends and narrowings?

A

Turbulent flow

207
Q

The biggest change in airway resistance is based on ?

208
Q

Increased length does what to laminar flow?

209
Q

Increased viscosity does what to laminar flow?

A

Decreased flow
Increases resistance

210
Q

Bronchodilation does what to laminar flow?

A

Increases laminar flow, decreases resistance.

211
Q

T or F
Turbulent flow can be calculated?

A

False, it is due to random movement of molecules

212
Q

Which flow is seen at high flow rates in rough tubing, or kink tubes?

A

Turbulent flow

213
Q

Reynolds number
< 1000

A

Laminar Flow
Good

214
Q

Reynolds number
> 1500

A

Turbulent Flow
Bad

215
Q

In Poiseuille’s law
Flow is directly proportional to ?

A

Radius
hydrostatic pressure gradient

216
Q

In Poiseuille’s law
Flow is inversely proportional to ?

A

Viscosity
Length

217
Q

Based on Bernoulli’s principle, Increasing the fluid viscosity (through a narrowing) will cause a pressure ____ in the narrowing?

218
Q

Based on Bernoulli’s principle, Decreasing the fluid viscosity (through a narrowing) will cause a pressure ____ in the narrowing?

219
Q

Venturi principle states that narrowing in a tube ____ pressure of fluid flowing through and ____ speed?
Ex: venti-mask

A

Decrease pressure
Increases speed

220
Q

Dalton’s Law?

A

Mixture of gases exert a pressure that is the sum of the pressures of each gas.

221
Q

Boyle’s Law?

A

If pressure increases then volume decreases.

222
Q

Charles Law?

A

If temperature increases then volume increases.

223
Q

Gay Lussac’s Law?

A

If temperature increases then pressure increases.

224
Q

Ideal gas law?

A

PV= nRT

P=Atm
V= L
n= moles
R= constant 0.0821
T= temp

225
Q

All General anesthetics have a ___ TI?

A

Narrow or low TI

226
Q

The goal of Anesthetics is to produce?

A

CNS depression sufficient for unconsciousness, lack of response to stimuli

227
Q

Earliest recorded use may have been when?

A

500 BC
Oracle Delphi

228
Q

OG discovery of Inhaled anesthetics?

A

1840s
William Morton

229
Q

First Halogenated alkane agent that reduced flammability?

A

Halothane in 1956

230
Q

Alkanes caused ?

A

Cardiac toxicity

231
Q

The mixture of different compounds for their different required effects, thus allowing less toxic doses is known as ___ ___?

A

Balanced anesthesia

232
Q

Anesthesia depends on the ______ of the agent in the inspired air?

A

Partial pressure

233
Q

_____ is the agents solubility between the gaseous phase and solubility in blood?

A

Blood:Gas partition coefficient

234
Q

A low blood:gas partition coefficient means what?

A

Fast induction and fast emergence

235
Q

A high blood: gas partition coefficient means what?

A

Slow induction and slow emergence

236
Q

Inhalational absorption is dependent on?

A

FI
FA (end-tidal)
Blood:Gas partition coefficient
Oil:water partition coefficient (lipid solubility)

237
Q

Induction rate is increased by what 3 things?

A
  1. Decreased blood solubility
  2. Increased partial pressure (conc)
  3. Increased breathing rate
238
Q

Increased lipid solubility is a better measure for ___?

A

Potency due to movement into brain

239
Q

MAC values compare what?

A

Potency of gases

240
Q

MAC definition?

A

Minimum concentration at the alveolus that produces useful anesthesia in 50% of patients.

241
Q

T or F
Mac values are related to the time to reach anesthesia?

A

False, MAC values are at equilibrium

242
Q

A low MAC would mean?

A

High potency
High solubility

243
Q

A high MAC would mean?

A

Low potency
Low solubility

244
Q

The percentage of the inhaled air that is occupied by the anesthetic gas is the ___?

245
Q

What % is controlled by the anesthesia machine?

A

The Fi or % inspired air

246
Q

What is the determinant of the brain partial pressure?

A

PA
Alveolar partial pressure

247
Q

Uptake into pulmonary capillary blood depends on what?

A

Tissue solubility,
Cardiac output
partial pressure differential

248
Q

Inhaled partial pressure?

A

Pi
Delivery amount by the anesthetic machine

249
Q

Rapid absorption of one gas will create a volume decrease with the concentration of the remaining gases is called what?

A

Second gas effect

One compound drags the other across in high concentration

250
Q

What gas is best to use for second gas effect?

A

Nitrous oxide

251
Q

The higher % of nitrous oxide used will lead to _____ equilibrium or Fa/Fi?

252
Q

Fi and FD are similar except when?

A

Low flow delivery

253
Q

A high blood:Gas solubility take ___ to reach equilibrium?

254
Q

What is the most important factor for determining how quickly Fa/Fi ratio approaches a value of 1.0 and rate of induction?

A

Blood:Gas partition coefficient

255
Q

The more soluble the agent is in blood, the ____ the rate of rise of FA?

256
Q

MAC value?

A

Minimal concentration of the agent at 1 atm in the alveolus at steady state that will inhibit pain response to a one inch surgical incision in 50% of patients.
ED50
Used as measure of potency

257
Q

Things that affect MAC value?

A

decrease with age
greater in red head women
additive with each agent in combo
decreased when opiods are administered

258
Q

More lipid soluble agents tend to have ____ MAC values?

259
Q

What is a prediction of induction time?

A

Blood:Gas partition coefficient

260
Q

Steady state MAC correlates to ?

A

500 umoles per 100mL of membrane

261
Q

All Anesthetics have a common method of action is what theory?

A

Unitary Theory of Narcosis
NOT TRUE

262
Q

Meyer-Overton Theory states ?

A

Correlation between lipid solubility and potency.

More lipid soluble agents are more potent

263
Q

According to Meyer-Overton theory the most likely site of anesthetic affect is?

A

Membrane, affecting fluidity.

264
Q

Meyer-Overton linear correlation for anesthetics is between?

A

MAC and Oil:Gas partition coefficient

265
Q

Critical Volume Hypothesis by Mullins states?

A

Binding of anesthetic agent into membrane cause expansion.

Still does not explain why hydrophobic substances are poor anesthetics

266
Q

Current theory of Inhalational Anesthetics is?

A

Mainly due to interactions with specific receptor-binding sites. Different families act on different receptors.

267
Q

Which isomer is more potent isomer for anesthetics?

A

L- isomer is more potent than D-isomer.

268
Q

IV and inhalational agents depress ____ neurons, which are important in memory formation leading to amnesia?

A

Hippocampal neurons

269
Q

Inhalational agents depression ____ neurons which are the gateway for sensory information?

A

Thalamic neurons

270
Q

GABA mediated chloride ionophores are located in the ?

271
Q

Glycine mediated chloride ionophores are located?

A

Brainstem and SPINAL CORD

272
Q

GABA Ionophore is a ?
Structure?
Sites ?

A

Pentameric ligand-gated ionophore
Alpha-1 Beta-2 binding sites

273
Q

What Anesthetics bind to the NMDA receptor complex?

A

Ketamine and Nitrous oxide

274
Q

Stage 1 of GA?

A

Initiation to loss of consciousness

275
Q

Stage 2 of GA?

A

Delirium phase
LOC to Restlessness to calm state

276
Q

Stage 3 of GA?

A

Surgery performed

277
Q

Stage 4 of GA?

A

Point of imminent death

278
Q

Rapid respiration, dilated pupils and muscle contractions occur during stage?

279
Q

Blockade of Na channels leads to expanded membrane that is caused by _____ and _____?

A

Lipid Fluidization
Protein Expansion

280
Q

Non-irritating gas, sweet odor
Nonflammable
MAC= 104%
Strong 2nd gas effect
Good sedative/ excellent analgesic
MOA- Inhibit NMDA glutamate
Antagonist at AMPA, GABA and 5-HT3
Low solubility, rapid onset/emergence
RISK OF DIFFUSIONAL HYPOXIA
long term abuse inactive B12 leads to blood disorders

A

Nitrous Oxide

281
Q

Which gas do you avoid pockets of trapped air and does not cause MH?

A

Nitrous Oxide

282
Q

Which volatile anesthetic stimulated catecholamine release and cause arrhythmias. Very explosive and made peroxides?

A

Diethyl Ether

283
Q

Volatile Anesthetics ____ post-synaptic excitatory response and _____ post-synaptic inhibitory response?

A

Inhibit excitatory
Enhance inhibitory

284
Q

Pleasant smelling, non-irritant, nonexplosive
Taken up into tubing and equipment
Rapid Induction
80% cleared by lungs with 20% Liver biotransformation
MAC= 0.76%
Short rapid breathing
Cardiac depression
CATECHOLAMINES, trigger arrhythmias
POST-OP HEPATITIS- Neoantigens

285
Q

This halogenated ether underwent 50% liver metabolism via P-450 2E1
Removed from market
NEPHROTOXICITY from Free fluoride

A

Methoxyflurane

286
Q

Which 2 gases are isomers of eachother?

A

Enflurane and Isoflurane

287
Q

This gas is isomer to Isoflurane
MAC= 1.68%
High dose stimulate CNS leading to SEIZURES (reason removed from market)
Increase epileptic waves

288
Q

Which anesthetic gas lead to seizures?

289
Q

This gas has pungent odor
MAC= 1.16%
Mild analgesic effects, skeletal muscle relaxation
Cardiac depression
Cerebral blood flow maintained
No seizure risk
High B:G partition coefficient
Slow induction/ Slow emergence

A

Isoflurane

290
Q

This gas has Pungent irritating odor
Low solubility=0.42, rapid induction
MAC= 6.6%
VP= 700
Requires special vaporizer (heated)
Vd- 600L moves into tissues/fats
CO maintained, but decrease BP
No seizure risk
Weak muscle relaxant

A

Desflurane

291
Q

This gas is best mask induction. Nonpungent
Low blood solubility- 0.65.
Rapid Induction/emergence
MAC= 1.71%
Expensive
Compound A risk/ renal damage
Decrease blood pressure

A

Sevoflurane

292
Q

This gas is Inert
Odorless, nonpungent
Does not cause MH
MAC= 63-71%
NMDA glutamate receptor inhibition
Does not depress hemodynamics
No neurotoxic risk (neuroprotective)
HIGH cost
Closest to perfect Inhalational Ane

293
Q

The only anesthetic gas which alone has not shown signs of neurodegeneration?

A

Nitrous Oxide

294
Q

Limit anesthetics given to ____ due to risk of decreased cognitive function and learning disabilities?

A

Young Children

295
Q

____ can cause the breakdown of all halogenated anesthetics?

A

Soda Lime (now banned)

296
Q

Compound A formed mainly by reaction of?

A

Sevoflurane with base catalysts
(NaOH or KOH)

297
Q

Soda lime forms ______ with gas flows below_____ due to increased heat?
Temp 40-60 C

A

Carbon monoxide
2 L/min

Higher gas flows above 2L decrease temp which decreases risk.

298
Q

Carbon monoxide degradation product of ____?
Known as ___?
Can lead to ____?

A

Desflurane by dry adsorbents
Worst on Monday morning phenomena
Lead to Carboxyhemoglobinemia (left curve)

299
Q

All modern CO2 absorbents use ___ to trap CO2 as CaCO3?

A

Ca(OH)2
Calcium hydroxide

300
Q

The higher the blood:gas partition coefficient, the _____ the anesthetic concentration in the blood?

A

Higher
doesn’t want to leave blood, enters brain slow
High= slow induction

301
Q

Solubility of the anesthetic gas in the blood ____ as body temperature decreases?

302
Q

FA/FI ratio is used to represent?

A

The equilibrium between body tissues and inspired concentration.

303
Q

True or false
An increase in cardiac output reduces the rate of rise of FA/FI in high solubility agents?

304
Q

True or false
All inhalation agents decrease cerebral metabolic rate and oxygen consumption?

305
Q

Which anesthetic agent may prolong QT?

A

Sevoflurane

306
Q

Which Anesthetic agent may result in Coronary Steal?

A

Isoflurane

307
Q

How does chloride influx affect membrane potential?

A

Hyperpolarizes the cell, becomes more negative. -90mv

308
Q

How does calcium influx affect membrane potential?

A

Depolarizes the cell, becomes less negative. -40mv

309
Q

What is responsible for transmitting the signal across the synapse?

A

Ligand-gated ion channels

310
Q

What is responsible for propagating action potentials?

A

Voltage-gated ion channels

311
Q

Local anesthetics work through which channel?

A

Voltage gated Na channels.

Ane Class Practice (27 decks)

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