Pharm 27 - Skeletal Muscle Relaxants

Independent Study 101 with Team/awesome at Lake Erie College

About this deck

By: Erin Copeland
Textbook:

Basic and Clinical Pharmacology, 11th Edition (LANGE Basic Science)

Guyton and Hall Textbook of Medical Physiology: with STUDENT CONSULT Online Access (Guyton Physiology)

Marks' Basic Medical Biochemistry: A Clinical Approach, North American Edition (Point (Lippincott Williams & Wilkins))

Medical Genetics: With STUDENT CONSULT Online Access (MEDICAL GENETICS ( JORDE))

Medical Microbiology: with STUDENT CONSULT Online Access (Murray, Medical Microbiology)

Medical Physiology: Principles for Clinical Medicine (MEDICAL PHYSIOLOGY (RHOADES))

Neuroanatomy Through Clinical Cases, Second Edition

Robbins & Cotran Pathologic Basis of Disease: With STUDENT CONSULT Online Access (Robbins Pathology)

The Immune System
Created: 2012-02-13
Size: 51 flashcards
Views: 14

About StudyBlue

STUDYBLUE makes things that make you better at school. Things like online flashcards with photos and audio. Things like personalized quizzes and friendly reminders about when (and what) to study next. Think of it as a digital backpack™: access to all of your study materials online and on your phone. STUDYBLUE exists to make studying efficient and effective for every student, for free. Join us.

“Simply amazing. The flash cards are smooth, there are many different types of studying tools, and there is a great search engine. I praise you on the awesomeness.”
Dennis

Sign up (free) to study this.

Describe the 4 steps of skeletal muscle contraction

1) AP causes influx of Ca and release of Ach

2) Ach diffuses across synaptic cleft to activate nicotinic receptors on end plate

3) Binding of 2 Ach molecules to Nm receptors causes opening of the Na/K channel

4) Movement of Na and K creates end plate potential

In what 2 ways are end plate fxns blocked?

1) Antagonistic: prevent access of transmitter to its receptor and thereby prevent depolarization

2) Excess depolarizing agonist (Ach): cholinesterase inhibitor

Name the 4 long lasting neuromuscular blockers

Tubocurarine

Pancurorium

Pipercuronium

Cisatracurium

Name the 2 neuromuscular blockers with intermediate duration of action

Vecuronium

Atracurium

Name the 2 neuromuscular blockers with short duration of action

Mivacurium

Rocuronium

Succinylcholine

Duration of action (in min) of tubocurarine:

>50

Duration of action (in min) of pancurorium:

>35

Duration of action (in min) of pipercuronium:

>35

Duration of action (in min) of cisatracurium:

25-44

Duration of action (in min) of vecuronium

20-35

Duration of action (in min) of atracurium:

20-35

Duration of action (in min) of mivacurium:

10-20

Duration of action (in min) of rocuronium:

20-35

Duration of action (in min) of succinylcholine

less than 8

Why is the duration of action of succinylcholine so much less than nondepolarizing blocking agents?

Rapid hydrolysis by butyrylcholinesterase and pseudocholinesterase (in liver and plasma respectively) AND most is diffused away from end plate (only small percentage reach NMJ)

Nondepolarizing drugs have rapid distribution phase and slow elimination phase

What is the prototypic drug for depolarizing blocking agents?

Succinylcholine

What is the prototypic drug for nondepolarizing blocking agents?

d-Tubocurarine

In which order are muscles paralyzed when given nondepolarizing blockers? In which order do they recover?

Paralysis: Facial, foot and hand mm --> abdomen, trunk, paraspinous --> diaphragm

Recovery: Diaphragm --> abdomen, trunk, paraspinous --> facial, foot, hand

Which nonpolarizing NM blocker produces hypotension as a result of systemic histamine release and ganglionic blockade?

Tubocurarine

What can be given before administering tubocurarine in order to attenuate hypotension?

Antihistamine

Which nondepolarizing NM blocker causes moderate increase in heart rate and smaller increase in cardiac output with little or no change in systemic vascular resistance?

Pancuronium

Increase in HR and CO associated with pancuronium is due to what?

Primarily caused by vagolytic action

Secondarily due to release of NE from adrenergic nn., as well as a blockade of neuronal uptake of NE

Which NM blocker causes caridac arrhythmias when administered with halothane anesthesia?

Succinylcholine

How does succinylcholine cause cardiac arrhythmias?

Stimualtes nicotinic receptors at sympathetic and PS ganglia and muscarinic receptors in the heart (SA node)

Cardiac arrhythmias associated with succinylcholine can be attenuated by administration of which type of drug?

Anticholinergic

Pts with burns, nerve damage or NM disease, closed head injury or other trauma can respond to succinylcholine by releasing ________ into the blood, which may result in ____________.

Potassium (hyperkalemic)

Cardiac arrest

Myalgias are a common complain of heavily muscle pts who receive large doses of _________. The pain is thought to be secondary to the unsynchronized contractions of adjacent muscle fibers just before the onset of paralysis.

Succinylcholine

What are the 4 drug interactions you need to consider when prescribing muscle relaxants?

Anesthetics

Antibiotics

Local anesthetics and antiarrhythmic drugs

Other nondepolarizing NM blocking drugs

List the 3 side effects of administering anesthetics + muscle relaxants

1) Nervous system depression

2) Larger fraction of injected muscle relaxant reaches NMJ (inc. blood flow)

3) Decreased sensitivity of postjunctional membrane to depolarization

What causes a depression of evoked release of Ach when taken with muscle relaxants?

Antibiotics

High doses of these drugs block Ach-induced muscle contractions when given with muscle relaxants. How?

Local anesthetics and antiarrhythmic drugs; blockade of nicotinic receptor ion channels

What is the effect of taking 2 separate muscle relaxants at the same time?

End plate-deoplarizing effect of succinylcholine is antagonized by small doses of nondepolarizing blockers

Which agents are used to reverse nondepolarizing NM blockade?

(Inc. availability of Ach at motor end plate)

Neostigmine

Pyridostigmine

Edrophonium

List the clinical conditions associated with spasticity

Spinal injury

Cerebral palsy

Stroke

Describe the mechanisms underlying spasticity

Involves stretch reflex arc + higher centers in the CNS, with damage to descending pathways int he spinal cord resulting in hyperexcitability of alpha motorneurons in the cord

This drug is a GABA receptor agonist and is used for pre- and postsynaptic inhibition of motor output (antispasticity agent)

Baclofen

This drug is used for chronic spasm due to cerebral palsy, stroke, and spinal cord injury, as well as acute spasms due to muscle injury

Diazepam

What is the MoA of baclofen?

Decrease neuronal cAMP levels and Ca influx; increase K efflux; reduces motor neuron excitability and inhibits spinal reflexes

What is the MoA of diazepam?

Facilitates GABAergic transmission in CNS; binds to GABA Cl-ion channels, increasing affinity for GABA and frequency of channel opening (causes dose dependent CNS depression)

This drug is a muscle relaxant used for the Tx of malignant hyperthermia (IV) or spasms due to cerebral palsy, spinal cord injury, or MS (oral)

Dantrolene

What is the MoA of dantroline?

Blocks RyR1 Ca-release channels in the SR of skeletal mm.

This drug is used to treat spasm due to MS, stroke, and amyotrophic lateral sclerosis

Tizanidine

What is the MoA of tizanidine?

Alpha2-adrenoceptor agonist in the spinal cord; presynaptic and postsynaptic inhibition of reflex motor output

This drug is used for short-term Tx of wrinkles associated with aging around the eyes and mouth and generalized spastic disorders (eg Cerebral palsy)

Botulinum toxin (Botox)

This is a rare hertaible disorder that is triggered by general anesthetics and NM blocking drugs.

Malignant hyperthermia

Pts at risk for malignant hyperthermia have a hereditary alteration in:

Ca-induced Ca release via the RyR1 channel or and impairment of the SR to sequester Ca via Ca transporters

3 main Sx of malignant hyperthermia:

Massive muscle contraction

Lactic acid production

Increased body temp

This drug reduces Ca release during malignant hyperthermia by binding to the RyR1 receptor and blocking the opening of the channel

Dantrolene

This drug is used for relief of acute muscle spasm caused by local tissue trauma or muscle strins

Cyclobenzaprine

What is the MoA of cyclobenzaprine?

Acts on brainstem and possibly spinal cord to reduce tonic somatic muscle activity via gamma and alpha motor neurons

note the conditions for which cyclobenzarpine is ineffective

Tx muscle spasm due to cerebral palsy or spinal cord injury

About this deck

By: Erin Copeland
Textbook:

Basic and Clinical Pharmacology, 11th Edition (LANGE Basic Science)

Guyton and Hall Textbook of Medical Physiology: with STUDENT CONSULT Online Access (Guyton Physiology)

Marks' Basic Medical Biochemistry: A Clinical Approach, North American Edition (Point (Lippincott Williams & Wilkins))

Medical Genetics: With STUDENT CONSULT Online Access (MEDICAL GENETICS ( JORDE))

Medical Microbiology: with STUDENT CONSULT Online Access (Murray, Medical Microbiology)

Medical Physiology: Principles for Clinical Medicine (MEDICAL PHYSIOLOGY (RHOADES))

Neuroanatomy Through Clinical Cases, Second Edition

Robbins & Cotran Pathologic Basis of Disease: With STUDENT CONSULT Online Access (Robbins Pathology)

The Immune System
Created: 2012-02-13
Size: 51 flashcards
Views: 14

About StudyBlue

“Simply amazing. The flash cards are smooth, there are many different types of studying tools, and there is a great search engine. I praise you on the awesomeness.”
Dennis