Chapter 27 Basic And Clinical Pharmacology

Front 1

Therapeutic group of drugs used drugs used during surgical procedures and in the intensive care unit to produce muscle paralysis.

Back 1

Neuromuscular Blockers

Front 2

Therapeutic group of drugs used to reduce spasticity in a variety of painful conditions.

Back 2

Spasmolytics.

Front 3

These drugs interfere with transmission at the neuromuscular end plate and lack central nervous system activity.

Back 3

Neuromuscular blocker

Front 4

True or False
Neuromuscular blockers are used primarily as adjuncts during general anesthesia to facilitate tracheal intubation and optimize surgical conditions while ensuring adequate ventilation.

Back 4

True

Front 5

Drugs in this group are "centrally acting" muscle relaxants that are primarily used to treat chronic back pain and painful fibromyalgic conditions

Back 5

Spasmolytics

Front 6

A spasmolytic agent that has no significant central effect and is used to treat malignant hyperthermia.

Back 6

Dantrolene

Front 7

Describe neuromuscular function.

Back 7

AP causes Ca2+ influx and the release of ACh. ACh diffuses across the synaptic cleft and activates the nicotinic receptors. ACh opens sodium and potassium channels and an end plate potential occurs. AP propagation along the entire muscle fiber occurs if the end plate potential is large.

Front 8

The binding of two ACh molecules to receptors on the _____ and ____ subunits cause opening of the channel.

Back 8

Alpha-beta
Delta-alpha

Front 9

ACh is quickly removed from the end plate region by what 2 methods?

Back 9

Diffusion
Acetylcholinesterase

Front 10

What is the function of the ACh receptor located on the presynaptic motor axon terminal?

Back 10

Activation leads to mobilization of additional transmitter for subsequent release by moving more ACh vesicles toward the synaptic membrane.

Front 11

These neuromuscular blocking agents block ACh and the prototype is d-tubocurarine.

Back 11

Nondepolarizing

Front 12

These neuromuscular blocking agents produce a blockade via excess ACh and the prototype is succinylcholine.

Back 12

Depolarizing

Front 13

Which NM blockers have a linear structure similar to ACh?

Back 13

Depolarizing

Front 14

Which NM blockers conceal the double ACh structures in a ring system?

Back 14

Non-depolarizing

Front 15

What feature is common to all currently used NM blockers?

Back 15

The presence of one or two quaternary nitrogens.

Front 16

True or False
NM blockers have limited entry into the CNS.

Back 16

True

Front 17

True or False
All NM blockers are inactive orally and MUST be administered parentally.

Back 17

True

Front 18

The rate of disappearance of a nondepolarizing NM blocker is characterized by ________ initial distribution followed by a ________ elimination phase.

Back 18

Rapid
Slower

Front 19

True or False
The volume of distribution of NM blockers is much greater than the blood volume.

Back 19

False
Slightly larger

Front 20

Drugs that are excreted by the _________ typically have longer half-lives, leading to longer durations of action.

Back 20

Kidney

Front 21

All _________ muscle relaxants are metabolized to 3, 17, and 3,17-hydroxy products.

Back 21

Steroidal

Front 22

The __-hydroxy metabolites are usually 40-80% as potent as the parent drug.

Back 22

3-hydroxy

Front 23

What happens if to the 3-hydroxy metabolite, if the parent is administered in the ICU setting for several days?

Back 23

3-hydroxy metabolite accumulation leading to prolonged paralysis.

Front 24

An intermediate-acting isoquinolone (ND)-NM blocker; its metabolite is laudanosine, which is metabolized by the liver and may cause seizures at high concentrations.

Back 24

Atracurium

Front 25

An isomer of Atracurium; it has less dependence on liver inactivation and produces less laudanosine. It is less likely to release histamine.

Back 25

Cisatracurium

Front 26

The shortest-acting isoquinolone (ND)-NM blocker; its onset of action is slower than succinylcholine. Rapidly cleared by plasma cholinesterase.

Back 26

Mivacurium

Front 27

The use of a larger dose of mivacurium to speed the onset can be associated with profound _______ release.

Back 27

Histamine

Front 28

Mivacurium duration of action may be ________ in patients with impaired renal function. Why?

Back 28

prolonged
They have lower levels of cholinesterase.

Front 29

An ultra short acting isoquinoline (ND)- NM blocker in phase III clinical trials?

Back 29

Gantacurium

Front 30

This extremely short acting (5-10 minutes) depolarizing NM blocker is rapidly hydrolyzed by butyrylcholinesterase (liver) and pseudocholinesterase (kidney).

Back 30

Succinylcholine

Front 31

What is the primary metabolite of succinylcholine?

Back 31

Succinylmonocholine

Front 32

This is a measure of the ability of the patient to metabolize succinylcholine.

Back 32

Dibucaine number.

Front 33

Normally, diibucaine inhibits normal enzyme activity by ____% and abnormal enzyme by ____%.

Back 33

80%
20%

Front 34

Which class of NM blockers act competitively with ACh at the nicotinic receptor site?

Back 34

Non-depolarizing

Front 35

True or False
In larger doses, non-depolarizing drugs can enter the pore of the ion channel to produce a more intense motor blockade.

Back 35

True

Front 36

How can muscle relaxants interfere with the mobilization of ACh at the nerve ending?

Back 36

By blocking prejunctional sodium channels

Front 37

Which class of NM blockers are agonists on the nicotinic receptor, stimulating it at [low] and blocking the pore at [high]?

Back 37

Depolarizing

Front 38

Answer Phase I or Phase II
Depolarization, prolonged flickering, unresponsive to stimuli.

Back 38

Phase I

Front 39

Answer Phase I or Phase II
Flaccid paralysis

Back 39

Phase I

Front 40

Answer Phase I or Phase II
Augmented by cholinesterase inhibitors.

Back 40

Phase I

Front 41

Answer Phase I or Phase II
Membrane repolarization; similar to nondepolarizing block.

Back 41

Phase II

Front 42

Answer Phase I or Phase II
Reversible by cholinesterase inhibitors.

Back 42

Phase II

Front 43

What is the primary use of NM blockers?

Back 43

Adjunct to anesthetics

Front 44

What (4) NM blockers produce hypotension as a result of systemic histamine release and muscarinic blockade?

Back 44

Tubocurarine, metocurine, mivacurium, and atracurium.

Front 45

Which NM- blocker produces moderate tachycardia, small increases in CO, and has no effect on vascular resistance?

Back 45

Pancuronium

Front 46

__________ may cause cardiac arrhythmia during halothane anesthesia.

Back 46

Succinylcholine

Front 47

True or False
Succinylcholine stimulates autonomic cholinoceptors, including nicotinic receptors at both sympathetic and parasympathetic ganglia and muscarinic receptors in the heart.

Back 47

True

Front 48

How can the negative inotropic and positive chronotropic responses to succinylcholine be attenuated?

Back 48

Administration of an anticholinergic (glycopyrrolate or atropine).

Front 49

True or False
Large doses of succinylcholine DO NOT produce positive inotropic and chronotropic effects.

Back 49

False

Front 50

Bradycardia can be observed following which dose of succinylcholine?

Back 50

2nd when given less than 5 minutes after initial dose.

Front 51

How can transient bradycardia be prevented? (4 ways)

Back 51

Thiopental
Atropine
Ganglionic blockers
Pretreatment with a small dose of pancuronium.

Front 52

C.J. presents to the hospital with severe burns. She also has NM disease. What can be a complication of giving her succinylcholine?

Back 52

Release of potassium which on rare occasions results in cardiac arrest.

Front 53

C.R. has open globe glaucoma. Should she be given succinylcholine for her upcoming opthalmic operation?

Back 53

No. Succinylcholine is contraindicated for these patients.

Front 54

What is the MOA of increased intraoccular pressure associated with succinylcholine?

Back 54

Tonic contraction of myofibrils, transient ocular choroidal vasodilation.

Front 55

S.H. is 5'7", 490 lbs. She is diabetic and presents to the E.R. following a serious car accident. What is a possible complication of giving this patient succinylcholine as an adjunct to anesthesia?

Back 55

Intragastric pressure; increased risks of regurgitation and aspiration of gastric contents.

Front 56

True or False
Fasciculations associated with succinylcholine may cause increased intragastric pressure in heavy muscled patients.

Back 56

True

Front 57

K.R. is an former NFL linebacker (6'3', 265 lbs.). He has just undergone surgery and has been complaining of muscle pain. What drug may have caused this?

Back 57

Succinylcholine. Pain is thought to be secondary to the unsynchronized contractions of adjacent muscle fiber just before the onset of paralysis.

Front 58

________ __________ potentiate the action of ND- NM blocking agents, but may result in malignant hyperthermia.

Back 58

Inhaled anesthetic

Front 59

Which antibiotics enhance the NM blockade?

Back 59

Aminoglycosides

Front 60

True or False
With smaller doses, local anesthetics can block ACh induced depolarization.

Back 60

Larger

Front 61

What may occur if an antiarrhythmic and NM blocking agent are given concommitantly?

Back 61

Blockage of Sodium channels.

Front 62

Myasthenia gravis ______ NM blockade.

Back 62

Enhances

Front 63

Elderly patients have prolonged duration of ND NM blockers and ________ clearance.

Back 63

Reduced.

Front 64

True or False
Severe burns patients are resistant to ND relaxants.

Back 64

True

Front 65

This drug rapidly inactivates steroidal neuromuscular blocking drugs by forming an inactive complex, which is excreted in urine.

Back 65

Sugamedex

Front 66

These cholinesterase inhibitors effectively antagonize the neuromuscular blockage by increasing the availability of ACh at the motor end plate.

Back 66

Neostigmine
Pyridostigmine

Front 67

True or False
Edrophonium reversal is more effective than neostigmine residual block.

Back 67

False
less effective

Front 68

Name (4) procedures where NM blockers are used.

Back 68

Surgical relaxation
Tracheal intubation
Control of ventilation
Treatment of convulsions.

Front 69

Characterized by an increase in tonic stretch reflexes and flexor muscle spasms together with muscle weakness.

Back 69

Spasticity

Front 70

True or False
Damage to the descending pathways in the spinal cord result in decreased excitability of the alpha motoneurons in the cord.

Back 70

False
Hyperexcitabilty

Front 71

How can you reduce the hyperactive stretch reflex?

Back 71

Reduce the activity of the Ia fibers that excite the primary motoneuron or enhance the activity of the inhibitory internuncial neurons.

Front 72

This drug acts at GABAa synapses; it is effective in patients with cord transection. Can be used in patients with muscle spasms of almost any origin.

Back 72

Diazepam.

Front 73

This drug is an agonist at GABAb; it reduces the release of excitatory transmitter in the spinal cord and brain. May reduce pain via inhibition of substance P.

Back 73

Baclofen

Front 74

How is Baclofen dosed?

Back 74

15mg BID, increasing as tolerated to 100mg QD.

Front 75

What are 2 side effects of baclofen?

Back 75

Drowsiness
Increased seizures in epileptics.

Front 76

This drug blocks excitation-contraction coupling by interfering with RyR1 and blocking opening of the Ca2+ channel.
Treats malignant hyperthermia.

Back 76

Dantrolene

Front 77

This is a local facial injection and can be used to treat generalized spastic disorders.

Back 77

Botulinum

Front 78

A GABAa and GABAb agonist that has been found to reduce spasticity.

Back 78

Progabide

Front 79

An inhibitory amino acid NT that has been found to reduce spasticity.

Back 79

Glycine

Front 80

An alpha-2-adrenoceptor agonist that inhibits nociceptive transmissions in the spinal dorsal horn. It also reinforces both presynaptic and postsynaptic inhibition in the cord.

Back 80

Tizanidine

Front 81

What are adverse effects of tizanidine?

Back 81

Drowsiness, hypotension, dry mouth, asthenia.