Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

pharm block 3 > 7 - General and Local Anesthetics > Flashcards

7 - General and Local Anesthetics Flashcards

1
Q

What are the general principals of surgical anesthesia?

A

Minimize potentially deleterious effects of anesthetic agents and techniques.

Sustain physiologic homeostasis during procedures.

Improve post-op outcomes through dampening surgical stress response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is general anesthesia?

A

State of the pt if which no movement occurs in response to a painful stimuli; reversible.

Pt not usually conscious and unaware of sensory input.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are components of general anesthetic state?

A
  1. Amnesia - absence of memory
  2. Unconsciousness (not always necessary)
  3. Analgesia - inability to interpret, respond to, and remember pain.
  4. Immobility in response to noxious stim
  5. Attenuation of autonomic responses to noxious stimuli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is the potency of anesthetics measured?

A

The dose that prevents movement in response to pain in 50% of people.

Gaseous anesthetic potency is quantified as minimal alveolar concentration (MAC) that prevents movement in 50%of patients.

For IV - free plasma concentration that causes loss of response to surg incision in 50% pts (EC50)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the advantages of using minimal alveolar concentration (MAC) as a measure of anesthetic potency?

A

Can be measured in end-tidal expired air and correlates well with the concentration of drug at its site of action (brain)

End-point easy to measure (lack of movement to pain)

Other MAC can be defined - MACawake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are common effects shared by all general anesthetics?

A

Hyperpolarize neurons: esp those that play pacemaker role. Reduce excitability.

Inhibit excitatory synaptic transmission and/or enhance inhibitory synaptic transmission.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the first target of anesthetics?

A

GABA-! receptors: most anesthetics increase GABA-A opening via allosteric effects.

Increases chloride conductance causing hyperpolarization.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Besides GABA-A receptors, what are the other targets of anesthetics?

A

Inhibition of NMDA receptors results in Na+ and Ca+ influx causing some hyperpolarization.

Other membrane-associated proteins affects: filling hydrophobic cavities in proteins and can alter movement of proteins and alter signaling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the three stages of general anesthesia?

A
  1. Premedication
  2. Induction - want something not frightening or painful; parenteral (IV usually), only pain is getting IV; only use inhaled in emergency.
  3. Maintenance - gaseous anesthetics have short half-lives; need to give continually.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the parenterally administered general anesthetics?

A

All hydrophobic molecules; given as IV bolus at once.

Partition into brain and sp cd during one pass; causes rapid induction of anesthesia.

Redistributes back out of brain as blood levels drop.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the duration of action of parenteral anesthetics?

A

It’s shorter than the half-life.

Multiple dosing is complex as storage depots come in and out of equilibrium with blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What barbiturate activates GABA-A receptors and is used to induce anesthesia 10-30 seconds after an IV injection? How long is the duration of a single dose?

A

Sodium Thiopental

Duration is 10 min at most, half life is 12 hours (can cause hangover)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What should barbiturates be reduced in combination with?

A

Other depressants as effects are additive; reduce in combo with opiates, benzodiazepines, alpha2 receptor agonists.

Intra-art injection contraindicated (inflamm and necrosis)

Can be given rectally to peds pts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the CNS, CV, and respiratory effects of barbiturates?

A

CNS depression: decrease O2 demand and decrease intracranial pressure.

CV: venodilation (reduce preload); severe drop in BP. Demand on heart reduced, so they are not contraindicated in those with coronary art disease.

Resp depression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What common parenteral general anesthetic uses a GABA-A mechanism to both induce and maintain anesthesia? What are other properties of this drug?

A

Propofol

10-30 sec induction lasts 10 min.

Antiemetic. Half life in body is 3.5 hours (less hang-over than barbiturates), good for outpatient surgeries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are unique adverse effects of propofol?

A

Elicits pain on injection, often given with lidocaine or into a large vein. Can cause initial excitation on induction.

Can CNS effects as sodium thiopental; has demonstrated abuse liability.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do the CNS and respiratory effects of propofol compare to sodium thiopental?

A

More severe reduction in BP than thiopental AND depression of myocardial contractility; blunts baroreceptors (caution in pts with intolerance to low BP)

More resp depression than thiopenal at equianesthetic doses.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What general anesthetic is used in patients at risk for hypotension and produces little or no effect on blood pressure and only a small increase in HR?

A

Etomidate

Safer than propofol or sodium thiopental in pts with hypotension or compromised baroreceptor function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are adverse effects of etomidate?

A

High incidence of pain on injection, myoclonus (jerky contraction of muscles)

Nausea and vomitting.

Supreses adrenocortical response to stress which can cause mortality (you need cortisol to combat body stress of surgery)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the adverse effects of etomidate on the CNS, CV, and Respiratory systems?

A

CNS: same as sodium thiopental

CV: far less than sodium thiopental

Respiratory: less than sodium thiopental

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What anesthetic produces dissociative anesthesia and profound analgesia? How does this drug work? How is it given?

A

Ketamine - eyes upon but unresponsive to commands.

Bronchodilator can be used for bronchospasm and NMDA receptor antagonist (reducing excitation).

Given IV, IM, oral, rectal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are adverse effects of ketamine?

A

Increase intracranial pressure from increased cerebral blood flow.

Emergence delirium (can be hallucination) , not as bad in children. HTN from sympathomiment effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What drug is a short acting benzodiazepine that is a GABA-A activator used alone for conscious sedation, anxiolysis, and amnesia during short procedures? When can it be used?

A

Midazolam

Can also be an induction agent or adjunct during local anesthesia (tooth extraction)

Useful as a pre-operative medication to decrease anxiety.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe the induction of midazolam?

A

Slower induction time and longer duration of action than sodium thiopental.

Metabolized by hydroxylation to an active metabolite,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are adverse effects of Midazolam? What can be used to reverse the adverse effects of Midazolam?

A

Respiratory depression and arrest (esp IV).

Used with caution in pts with neuromusclar disease, parkinson’s and bipolar. CV effects like sodium thiopental.

Adverse effects can be reversed by Flumazenil.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are commonalities of inhalational general anesthetic?

A

Very low therapeutic indices: LD50/ED50 can be low as 2-4.

Gaseous or readily vaporized at room temp.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

For gaseous anesthetics, when it equilibrium reached?

A

When partial pressures (not concentrations) are the same between compartments (air, blood, brain, fat).

What matters to us are the partition coefficients of the gas at each of these compartment barriers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the partition coefficients for gaseous anesthetics and what does each tell us?

A

Blood:gas coefficient determines each of absorption at alveoli

Brain:blood coefficient determines anesthetic movement into the brain

Fat:blood coefficient determines redistribution to fat.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What happens if an anesthetic has a low blood:gas partition coefficient? What if its high?

A

Low: need high amt in inspired air, induction is quick b/c equilibrium is reached quickly.; recovery is quick.

High: Need less in inspired air, induction and recovery are slow and equilibrium is reached slowly.

30
Q

What occurs with a high fat:blood partition coefficient?

A

Half-life will be long (long hangover) sue to slow release into the blood; enough gets into the brain to make the patient feel sleepy.

31
Q

Where does anesthesia occur? When is it achieved?

A

The brain - it’s achieved when the brain partial pressure is equal to the minimal alveolar concentration.

All anesthetics are lipophilic and brain is highly perfused so it gets a large share of anesthetic circulation.

This anesthesia is achieved shortly after MAC is reached in the alveoli.

32
Q

What occurs at steady state (equilibration) for giving gaseous anesthesia? How fast is it achieved?

A

No net movement of gas.
Quick for gases with low blood:gas partition coefficient

Slow for gases with high fat:blood partition coefficient

When equilibrium is reached, the concentration of inspired air will equal the concentration of end-tidal air.

33
Q

Describe the elimination of gaseous anesthesia? What does it depend on?

A

Reverse of induction; gas moves from the blood into the inspired air (which is now free of gas).

Depends on blood:gas PC. Lowest PC will be eliminated fastest.

34
Q

What effect does solubility in blood and fat have on recovery from anesthesia?

A

Low solubility in blood and fat have rapid recovery; high solubility have slower recovery AND the duration of recovery will depend on length of time anesthetic was administered.

35
Q

What is malignant hyperthermia?

A

Effect of gaseous anesthesia exposure, rare but may be fatal.

Heritable skeletal muscle disorder triggered by anesthetics: consists of muscle rigidity, hyperthermia, rapid onset tachy and hypercapnia, hyperkalemia, and metabolic acidosis.

36
Q

What gaseous anesthetic has a moderate blood:gas partition coefficient and is the most commonly used inhalational anesthetic in the US? What are some other properties of this drug?

A

Isoflurane

Moderate rates of induction and recovery; excreted unchanged in air.

Mostly used for maintenance (often with NO to reduce amt needed).

37
Q

What are adverse effects of Isoflurane?

A

Air irritant that causes coughing and decreases tidal volume and increases respiratory rate. (Overall effect is depression of respiration and increased PaCO2.)

CV: Myocardial depression causes decrease in BP, arrythmias, and cerebral vasodilation (causes increased intracranial pressure).

38
Q

What gaseous anesthetic is a volatile liquid at room temp and is used in outpatient surgeries and maintenance? Describe the solubility of this drug?

A

Desflurane

Very low solubility in blood therefore induction and recovery are rapid. Excreted unchanged in air.

39
Q

What effects do Desflurane have? How do these compare to isoflurane?

A

Skeletal muscle relaxation - good thing

CV effects: similar to isoflurane
Respiratory: worse irritant than isoflurane and can cause bronchospasm.

40
Q

What gaseous anesthetic is used in both inpatient and outpatient settings and can be used to both induce and maintain anesthesia and is NOT a respiratory irritant? What are the properties of this drug such as metabolism?

A

Sevoflurane : very low blood:gas partition coefficient and 5% is metabolized to fluoride in the liver which may cause damage.

It’s also degraded to compound A by absorbants in the admin apparatus which may cause nephrotoxicity.

41
Q

How does sevoflurane compare to isoflurane and desflurane in its effects?

A

Sevoflurane is different from the other two in that it’s NOT a respiratory irritant and it doesn’t cause as much respiratory depression.

42
Q

What are the pharmacological properties of nitrous oxide? What problems can occur when using this?

A

Very insoluble in blood, rapidly equilibrates. Uptake from air results in increased concentration of other anesthetics. 99% excreted unchanged in lungs.

During emergence can dilute oxygen so pts need to break 100% O2 to prevent hypoxia.

43
Q

What are the clinical uses of nitrous oxide?

A

Weak anesthetic, cannot get enough into the air to produce minimal alveolar concentration.

Good for sedation and analgesia at 50% concentration in inspired air.

Used together with other inhaled anesthetics to reduce dose needed.

44
Q

What are adverse effects of nitrous oxide?

A

Contraindicated in pneumothorax bc it will distribute to any pockets of air.

Negative ionotrophic effect (slow heart contractions), but also sympathomimetic so CO is preserved.

Minimal resp effects, abuse liability, prolonged exposure may cause megaloblastic anemia.

45
Q

What is the mechanism of action of local anesthetics?

A

Bind reversibly to site within pore of voltage-gated Na+ channels and block sodium entry when channel is open.

Therefore they reversibly block nerve conduction and cause sensory loss and motor paralysis of the innervated area.

46
Q

What are topical anesthetics used for?

A

Applied to skin, mucous membranes, or ulcerated surfaces.

Ophthalmic to produce anesthesia of the cornea and conjunctiva.

47
Q

What is local infiltration anesthesia and what is it used for?

A

Local injection of an agent without consideration of the course of cutaneous nerves.

Provides regional anesthesia around the sites of injection (for sewing up lacs)

48
Q

Describe nerve block anesthesia?

A

Injection of local anesthetic around individual nerves of nerve plexi that include sensory nerves from the operative site.

49
Q

Describe spinal and epidural anesthesia?

A

Epidural: into the epidural space

Spinal: solution injected into spinal fluid

50
Q

What effect do local anesthetics have on nerves? What type of nerves do they act on?

A

Act directly on nerve cells to block their ability to conduct impulses.

Act on every type of nerve fiber and blocks AP initiation and propagation on nociceptive neurons to elim pain.

Completely reversible, no nerve damage.

51
Q

How do local anesthetics bind to voltage-dependent sodium channel proteins?

A

To get from tissues into the neuron, it needs to get across the membrane and enter the pore of the channel from the inside of the neuron. The only way to do this is to have a lot of the drug in the uncharged (free base “B”) form.

Protonated form is active form at the binding site within the channel.

52
Q

What results from the inhibition of voltage gated sodium channels?

A

Slowed rate of depolarization, reduced height of AP.

Slow axonal conduction, prevents AP propagation and increases threshold potential.

No change in resting membrane potential because Na channels are not involved in it.

53
Q

Local anesthetics are frequency and voltage dependent, what does this mean?

A

Drugs gain access to channel binding site when the channel is open (BH+ binds).

They have higher affinity for the inactive channel than the unopened channel therefore resting nerves are less sensitive to local anesthetic block and nerves with + membrane potentials are more sensitive to block.

54
Q

What is the efficacy of local anesthetics affected by?

A

Local pH

Efficacy is decreased when tissue pH is decreased such as during infection of inflammation.

Too little drug can get to the site of action (too little is in the B form, the form that crosses membranes)

55
Q

What are local anesthetics co-administered with and why?

A

Vasoconstrictors such as epinephrine and phenylephrine to decrease the rate of absorption into the circulation and increase the depth and duration of anesthesia.

Loss potential for systemic toxicity.

56
Q

What is the sensitivity of neuron types to blockade?

A

Most likely to be anesthetized are the C fibers, bringing sensory info about pain into the brain. They are most sensitive because they aren’t myelinated and their diameter is small.

57
Q

What is the order of block of nerve conduction (ie in what order are effects felt)? In what order are these functions recovered?

A
  1. Pain
  2. Cold
  3. Warmth
  4. Touch
  5. Deep pressure
  6. Motor

Recovery of function occurs in the reverse order.

58
Q

What is the toxicity and adverse effects of local anesthetics?

A

Interefere with function of all organs in which conduction of impulses occurs (CNS ganglia, NMJ, muscle).

Intraneuronal injection can cause irreversible damage.

S-enantiomer less toxic than R in those with chiral centers.

59
Q

Describe the systemic toxicity of local anesthetics in the order by which they occur?

A
  1. CNS effects: convulsions, numbness, lightheadedness, muscle twitching, unconsciousness.
  2. Coma
  3. Resp arrest
  4. CV depression
60
Q

Describe the CNS toxicity associated with local anesthetics?

A

CNS stim seen first due to depression of cortical inhibitory neurons: restlessness, tremors, convulsions.

CNS depression at higher doses: drowsy, depression, resp depression, resp arrest.

Death usually caused by resp arrest.

61
Q

What is the CV toxicity associated with local anesthetics?

A

Depression of the CV system seen after CNS effects.

Decreased myocardial contractility/decreased BP. Decreased rate of induction, AV blocks, arrhythmias. Vasodilation.

62
Q

Where are amides and esters metabolize?

A

Amides: in the liver (use with caution in pts with liver disease).

Esters: metabolized by plasma cholinesterases (much quicker).

63
Q

What hypersensitivity is associated with local anesthetics?

A

Rare. Must be distinguished from effects of co-admin vasoconstrictors.

More freq with ester types.

64
Q

What local anesthetic also blocks the reuptake of norepi into presynaptic adrenergic nerves and is a potent vasoconstrictor? What type of local anesthetic is it? What is it used for?

A

Cocaine - ester

Used for topical anesthesia of the upper respiratory tract.

65
Q

What local anesthetic is short acting and the first synthetic local anesthetic that’s used for infiltration anesthesia? What type is it and what is the potency?

A

Procaine - ester

Low potency, slow onset, short duration of action.

66
Q

What long acting ester local anesthetic is widely used in spinal anesthesia and ophthalmic preps? How does its effects compare to procaine?

A

Tetracaine

More potent and longer duration of action than procain. Not used for peripheral nerve block.

67
Q

What local anesthetic has low water solubility and therefore is too slowly absorbed when applied topically to be toxic? What is the use?

A

Benzocaine - ester

Applied to wounds and ulcerated surfaces where it provides relief for long periods of time

68
Q

What local amide anesthetic has an intermediate duration of action and produces faster, more intense, longer lasting, and more extensive anesthesia compared to procaine?

A

Lidocaine - amide

Often used with vasoconstrictors to decrease toxicity - wide range of clinical uses

69
Q

What local amide anesthetic is capable of producing prolonged anesthesia and provides more sensory than motor block? How does this compare to lidocaine?

A

Bupivicaine

More cardiotoxic than lidocaine. S-enantiomer is less toxic.

70
Q

What local amide anesthetic is long acting and consists of the S-enantiomer and is suitable for epidural and regional anesthesia? How does its actions compare to bupivicaine?

A

Ropivacaine - amide

Anesthetic actions similar to bupivicaine with less cardiotoxicity. Even more motor sparing than bupivicaine.

pharm block 3 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions