Muscle Relaxants And Local Anesthetics

Front 1

Name three clinical uses of succinylcholine.

Back 1

-electroconvulsive therapy (ECT)
-muscle relaxant during short surgeries

Front 2

List three things that can moderately increase succinylcholine's duration of action.

Back 2

1. pregnancy
2. liver disease
3. renal failure

Front 3

Succinylcholine has several side effects. Many of them result from it's structural similarity to ______.

Given said structural similarity, name the receptor that is activated by Sux resulting in bradycardia.

Back 3

ACh

muscarinic

Front 4

Name all the major side effects of Sux (6)

Back 4

1. Increased pressures (ICP, Gastric, IOP)
2. Bradycardia
3. Hyperkalemia
4. Masseter Spasm
5. Malignant Hyperthermia
6. Muscle pain

Front 5

Name conditions that are cause for concern- but not exclusionary- for Sux treatment.

Hint: think about the side effects.

Back 5

1. Pre-exisiting hyperkalemia
2. Pre-exisiting high pressures (ICP, IOP)
3. Children
4. known to have atypical butarylcholinesterase

Front 6

Family history of malignant hyperthermia is an absolute exclusionary criterion for Sux treatment, as is a recent denervation injury. Explain how the latter rules out Sux treatment.

Back 6

Upregulation of nicotinic ACh receptors is a physiological response to a denervation injury. The increased number of receptors would, with Sux treatment, allow non-specific flow of potassium out of cells, and hyperkalemia would result.

Front 7

How does the concept of spare receptors apply to non-depolarizing NMJ blocking agents?

Back 7

Competitive inhibitors need to prevent activation of ~70% of the ACh receptors before muscle relaxation occurs.

Front 8

Aminoglycosides and tetracyclins ______ metabolism of non-depolarizing NMJ blockers; conversely, dilantin and phenytoin _______ their metabolism.

Back 8

Aminoglycosides and tetracyclins _increase_ metabolism of non-depolarizing NMJ blockers; conversely, dilantin and phenytoin _decrease_ their metabolism.

Front 9

Assays for NMJ block effectiveness:

Back 9

Electro monitoring
Head lift / Leg lift
Negative Inspiratory Pressure
-NIF > 50 mm H20

Front 10

Name and briefly describe (administration route, if applicable) the classes of competitive AChE blockers (3)

Back 10

1. Edrophonium: lacks a moiety that can be hydrolyzed by AChE.
2. Carbamate Inhibitors: neostigmine; enzyme attacks ester group; orally available
3. Organophosphate(insecticides): irreversibly inhibit AChE; dermally absorbed (clinically significant due to toxicity)

Front 11

Symptoms of AChEinhibitor overdose

Back 11

-Classic PS overdrive (bradycardia, secretions, etc.)
-Sweating
-NMJ: muscle fibrillation, and possibly block (paralysis)
-CNS: seizures

Front 12

Treating AChEinhibitor toxicity

Back 12

Support symptoms
Atropine
If toxicity resulted from organophosphate, there is an antidote chemical

Front 13

Uses of AChEinhibitors:

Back 13

-bladder atony (weak, can't contract)
-Mysanthenia Gravis
-Reverse non-depolarizing NMJ blocker toxicity (insecticides, nerve gas)
-Reduce IOP (Glaucoma)
-CNS: nicotinic receptors

Front 14

A rare mutation in the enzyme ___________ drastically prolongs Sux's duration of action.

Back 14

butarylcholinesterase

Front 15

Explain how inflammation can decrease a local anesthetic's ability to enter the cell.

Back 15

Inflammation can lower extracellular pH; LA (a weak base) remains protonated longer and cannot easily enter cell.

Front 16

List the three categories of neuron size and their respective sensitivities to LA.

Back 16

small: Adelta (pain) and C (temp/sympathetic sensory) fibers; most vulnerable

medium: B (sympathetic preganglionic), less vulnerable

large: A (proprioception, motor, touch/pressure), least vulnerable

Front 17

All things equal, how do the following affect a fiber's sensitivity to LA:
-position in nerve
-frequency of activity
-Myelination
-Size

Back 17

-position in nerve: increases with greater eccentricity
-frequency of activity: increases with frequency
-Myelination: increases with more myelination
-Size: increases with decreasing size

Front 18

List the determining factors for a LA's potency, onset of action, and duration of action.

Back 18

Potency: hydrophobicity
Onset: hydrophobicity, pKa
Duration: hydrophobicity, vascular access (washout), protein binding (extends life)

Front 19

List the three categories of neuron size and their respective sensitivities to LA.

Back 19

small: Adelta (pain) and C (temp/sympathetic sensory) fibers; most vulnerable

medium: B (sympathetic preganglionic), less vulnerable

large: A (proprioception, motor, touch/pressure), least vulnerable

Front 20

All things equal, how do the following affect a fiber's sensitivity to LA:
-position in nerve
-frequency of activity
-Myelination
-Size

Back 20

-position in nerve: increases with greater eccentricity
-frequency of activity: increases with frequency
-Myelination: increases with more myelination
-Size: increases with decreasing size

Front 21

List the determining factors for a LA's potency, onset of action, and duration of action.

Back 21

Potency: hydrophobicity
Onset: hydrophobicity, pKa
Duration: hydrophobicity, vascular access (washout), protein binding (extends life)

Front 22

Toxic effects on excitable cells stemming from LA overdose, in order of likelyhood of occuring:

Back 22

most likely: nervous system (oral numbness, tinnitus, drowsiness)
2nd most likely: cardiac depression (conductance, contractility, pulse all decrease, plus arrythmias)

Front 23

Metabolism difference b/w aminoesters and aminoamides

Back 23

aminoesters: plasma esterases; PABA metabolite (common allergy)
aminoamide: hepatic metabolism

Front 24

treatment for LA toxicity:

Back 24

maintain airway

drugs: barbituates/sedatives to prevent seizures; atropine to reduce PS drive; epinephrine for arrythmia

also new treatment: lipid emulsion to draw LA away from site of action

Front 25

allergic considerations with LAs

Back 25

aminoesters have problems with allergies (metabolite PABA + drug preservative)

Front 26

List the following toxicities associated with these specific agents:

Back 26

Prilocaine: methemoglobinemia (methylated hemoglobin, can't unload O2)
Bupivicaine/etidocaine: cardiac arrythmias
Benzocaine/Procaine: PABA metabolite (allergy)

Front 27

non IV LA:
topical

main concern:

Back 27

don't want to create a drug reservoir (contains prilocaine, watch out for methemoglobinemia)

Front 28

non IV LA:
subcutaneous/subdermal
which drugs?
concern?

Back 28

usually lidocaine, Bupivicaine or Ropivicaine for longer duration
concern = pain upon administering (give w/ baking soda to decrease sting)

Front 29

LA Block technique: Bier
why?
how?

Back 29

Bier block
why = anesthetize an arm
how = exsanguinate limb w/ constrictions, inject LA, wait 30 minutes for protein binding to occur, remove constrictions

Front 30

LA Block technique: plexus
why?
how?

Back 30

plexus block
why = desensitize an entire sensory area
how = hit any plexus (digit, intercostal, femoral, popliteal)

Front 31

LA Block technique: neuraxial
what are the 2 routes?
what are the differences?

Back 31

LA Block technique: neuraxial
what are the 2 routes?
what are the differences?

Front 32

epinephrine and LA: what's the connection?

Back 32

epinephrine can vasoconstrict (preventing washout); epinephrine also serves as an indicator for accidental arterial injection (tachycardia will occur)