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Pharm 2 > Test 2: Basic Overview > Flashcards

Test 2: Basic Overview Flashcards

1
Q

What are the 3 reasons for paralyzing a patient?

A

1) Intubation – to protect against vocal cord injury
2) Facilitate surgical exposure (need for immobility, sometimes makes it easier for muscles to be relaxed)
3) Increase efficacy of mechanical ventilation

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2
Q

Do Neuromuscular blocking agents produce anesthesia?

A

NO: they just produce paralysis.

Muscle relaxation DOES NOT ensure unconsciousness, amnesia or analgesia.

Always have another agent providing amnesia (volatile agent, IV agent), analgesia (opioid, etc).

MUST continually provide anesthesia while the patient is paralyzed/relaxed
Peripheral Nerve Stimulator is subjective measurement.

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3
Q

Describe the pathway of the Somatic Action Potential.

A

Motor Nerve (voluntary) → signal down Ventral side of column → skeletal muscle receptor is Nicotinic Motor End Plate with Ach NT

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4
Q

What subunits are required to be stimulated on a Nicotinic receptor for contraction to occur?

A

Both alpha subunits

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5
Q

What ions flow when a nicotinic channel is activated?

A

-Na & Ca in
-K+ out

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6
Q

What type of molecule is Acetylcholine?

A

-Quaternary ammonium ester
-Permanent positive charge independent of pH
-Ester = acid + alcohol

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7
Q

How is acetylcholine synthesized?

A

Synthesized inside the neuron from CHOLINE + ACETYL COENZYME A in a reaction controlled by the enzyme CHOLINE ACETYLTRANSFERASE

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8
Q

Where is Acetylcholine stored?

A

Stored in Synaptic Vesicles in motor nerve endings and released in the Synaptic Cleft in quanta.

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9
Q

What are quanta?

A

Packets with energy stored in them (physics definition).
-the minimal amount needed to produce the reaction.

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10
Q

Vesicles contain how many molecules of acetylcholine?

A

Vesicles each contain 5,000-10,000 molecules.

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11
Q

Acetylcholine release is dependent on ____.

A

Calcium

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12
Q

How long does it take for Acetylcholine to be hydrolyzed by Acetylcholinesterase?

A

<15 milliseconds

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13
Q

Where is Acetylcholinesterase (Ach-E) located?

A

AKA true cholinesterase AKA specific cholinesterase.
-Anchored to the external/extracellular surface of the cell membrane.

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14
Q

Where does Choline go after Ach is hydrolyzed?

A

Choline will re-enter the motor nerve terminal to be re-synthesized to Ach.

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15
Q

Each molecule of AchE degrades about _______ molecules of Ach per second.

A

Each molecule of AchE degrades about 25,000 molecules of Ach per second.

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16
Q

T/F: Acetylcholine is recycled.

A

FALSE: Ach is not recycled or re-used so it must be synthesized constantly

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17
Q

Which nerves release Acetylcholine as their neurotransmitter? (5)

A

1) Somatic motor nerves
2) Preganglionic Sympathetic nerves
3) Preganglionic Parasympathetic nerves
4) Postganglionic Parasympathetic nerves
5) Postganglionic Sympathetic sweat glands

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18
Q

What are Efferent Somatic Nerves?

A

Motor nerves that originate in the anterior (ventral) horn of the spinal cord and terminate in the skeletal muscle.

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19
Q

What are Afferent Somatic Nerves?

A

Sensory nerves that originate in the skeletal muscle and carry signals to the spinal cord’s posterior (dorsal) horn.

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20
Q

What is the resting transmembrane potential at the Neuromuscular Junction?

A

-90 mV

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21
Q

Describe the steps of neuromuscular transmission at the Neuromuscular Junction.

A

1) AP depolarizes motor nerve terminal
2) Ca influx from the interstitial space via Voltage gated Ca channels
3) Ca causes exocytosis of Ach
4) Ach diffuses down its concentration gradient, through the synaptic cleft, to the Nicotinic Acetylcholine receptor (nAchR) on the Motor End Plate of the Post synaptic Membrane.
5) When both alpha subunits of the nAchR are occupied, the Motor End Plate of the muscle cell depolarizes.
6) Cations flow through the nAchR, causing further depolarization of the membrane
-Sodium/Calcium into the cell
-Potassium out of the cell
7) Resulting Action Potential is generated along the muscle membrane to the T-tubule system opening Voltage Gated Sodium Channels and releasing Calcium from the Sarcoplasmic Reticulum (SR)
-Intracellular Calcium propagates Actin and Myosin to interdigitate generating a muscle contraction
8) Ach is promptly hydrolyzed by AchE decreasing the amount of Ach in the Synaptic Cleft
-Ion channels close causing the membrane to repolarize
-Calcium is resequestered in the SR
-Muscle Cell relaxes – awaits another AP

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22
Q

What is the effect of the influx of Calcium from the interstitial space via Voltage-Gated Calcium Channels into the pre-synaptic motor nerve terminal?

A

Calcium influx causes the release of hundreds of quanta of Ach from their Synaptic Vesicles (exocytosis)
-“Calcium in…Neurotransmitter out”

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23
Q

How is acetylcholine release effected by HYPOCalcemia?

A

Hypocalcemia = decrease in the amount of Ach released

24
Q

How is acetylcholine release effected by HYPERCalcemia?

A

Hypercalcemia = increase in the amount of Ach released

25
Q

Describe the structure of a Fetal Post-Junctional Receptor.

A

-immature, unstable

5 subunit proteins:
2 – alpha
1 – beta
1 –gamma
1 –delta

*Can exist outside the NMJ (so, not a part of paralysis. But, can absorb some of the drug you gave).

26
Q

Describe the structure of an Adult Post-Junctional Receptor.

A

-mature, stable, 5 subunit proteins (nAchR)
-Similar to the fetal but 1 –epsilon replaces the 1 – gamma subunit
-Increased cation conductance
-Shortened open time

27
Q

How many Nicotinic Receptors have to be stimulated to cause an effect?

A

500,000

There are 5 million at the NMJ.

28
Q

Where does binding occur on the Nicotinic Receptors?

A

Binding occurs at the alpha - beta and gamma-alpha interfaces.
-Remember: Both alpha subunits have to be blocked for the receptor to be activated and ions to flow.

29
Q

How is acetylcholine removed from the Motor End Plate region?

A

Acetylcholine is removed from the end plate region by both diffusion and enzymatic destruction by acetylcholinesterase enzyme.

30
Q

What conditions cause Extrajunctional Receptors to proliferate sufficiently enough to affect subsequent neuromuscular transmission?

A

-Prolonged immobilization
-Thermal Burns

31
Q

Describe Extrajunctional Receptors.

A

-Proliferate in response to physiologic or pathophysiologic stimulation
-Have gamma protein like fetal receptors
-Appear over the entire post-junctional membrane and not just the neuromuscular junction
-Highly responsive to Ach
-May produce unexpected/unwanted responses to neuromuscular blockers.

32
Q

What conditions cause Up-Regulation of Nicotinic Acetylcholine Receptors (nAchR)?

A

-Spinal cord injury
-ECT therapy
-CVA
-Thermal Injury
-Prolonged immobility
-Prolonged exposure to NMBs
-Multiple Sclerosis
-Guillian-Barre Syndrome

33
Q

What conditions cause Down-Regulation of Nicotinic Acetylcholine Receptors (nAchR)?

A

-Myasthenia Gravis
-Organophosphate poisoning
-Anticholinesterase overdose

34
Q

What is Multiple Sclerosis?

A

-Demyelinating injury in the brain and spinal cord that disrupts nervous system transmission.
-Autonomic, motor, and sensory symptoms.
-Upregulation of receptors.

35
Q

What is important to know regarding dosing of NMB with Multiple Sclerosis?

A

-AVOID SUCCINYLCHOLINE.
-Decrease the dose of NDMR.

36
Q

Can you do regional anesthesia in a patient with Multiple Sclerosis?

A

Could do an Epidural, but would avoid a spinal. Most people avoid regional in these patients.

37
Q

What is Guillain- Barre Syndrome?

A

Rapid onset muscle weakness due to immune system damage to peripheral nervous system.
-Starts at feet and progresses up (Ascending paralysis)
-Upregulation of receptors.
-Ok to use regional

38
Q

What is important to know regarding dosing of NMB with Guillain-Barre Syndrome?

A

-AVOID SUCCINYLCHOLINE.
-Decrease the dose of NDMR.

39
Q

What is Myasthenia Gravis?

A

Autoimmune, long-term, NMJ disease.
-Skeletal muscle weakness, typically seen in eyes, face, difficulty swallowing, can progress to difficulty walking.
-Treat with anti-cholinesterase (builds up the levels of Ach).
-OK to use regional

40
Q

What is important to know regarding dosing of NMB with Myasthenia Gravis?

A

-Effects of Succ will be augmented/prolonged.
-Increased sensitivity to Non-Depolarizers.

41
Q

Most of the time (aside from MS and GB) what do you need to do with your NDMR in patients with Up-regulation of receptors?

A

-Would need to increase dose of NDMR in these patients.
-Regularly check K+ levels

42
Q

What do the Prejunctional Receptors on the Motor Nerve Terminal do?

A

-Increases the synthesis and release of Ach in the presence of Ach = POSITIVE FEEDBACK
-Prevents depletion of Ach at the NMJ
-Moves more Ach vesicles towards the synaptic membrane

43
Q

Where are M1 receptors located and what are the clinical effects?

A

-CNS/Stomach
-Inc H+ ion secretion

44
Q

Where are M2 receptors located and what are the clinical effects?

A

-Heart, CNS, Airway
-Bradycardia

45
Q

Where are M3 receptors located and what are the clinical effects?

A

-CNS, Salivary Glands, Airway Smooth Muscle, Vasc Endothelial Cells
-Salivation, Bronchoconstriction, Vasodilation

46
Q

What is important to know regarding elimination of NMB agents?

A

-100% ionized at physiologic pH
-Very highly protein bound
-DO NOT cross BB barrier or placenta
-Trapped in the renal tubule after filtration b/c of the high degree of ionization. All MRs can be excreted by the kidney if other routes are not available.

47
Q

Which NMB agents are primarily eliminated via metabolism?

A

-Succinylcholine
-Atracurium
-Cisatracurium

48
Q

Which NMB agents are primarily eliminated via Biliary Excretion?

A

-Vecuronium
-Rocuronium

49
Q

Which NMB is primarily eliminated by renal excretion?

A

Pancuronium

50
Q

Which NMB agents release histamine?

A

-Succinylcholine
-Atracurium

51
Q

Which NMB causes bradycardia?

A

Succinylcholine

52
Q

Which NMB agent causes modest tachycardia due to vagolytic/anti-muscarinic effect?

A

Pancuronium
-Also has mild increase in Arterial BP

53
Q

NDMR + NDMR =

A

Augment
-additive, synergistic, augmented block

54
Q

Succ + NDMR =

A

Antagonize
-Ex: defasciculating dose needs an increased Succ dose
-Antagonism.
-Antagonizes a depolarizing block.
-Alpha subunits are containing a depolarizing molecule

55
Q

NDMR + Anticholinesterase =

A

Antagonize
(this is the whole point of reversal)

56
Q

Succ + Anticholinesterase =

A

Augment
(inhibits pseudo cholinesterases)

Pharm 2 (40 decks)

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