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PHARM.M2.Neuromuscular Relaxants > Neuromuscular Blockade > Flashcards

Neuromuscular Blockade Flashcards

1
Q

NMJ Neurotransmission-ACh Release?

A

Ach is released from pre-synaptic vesicle into the synapse

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2
Q

How do the cation channels get opened?

A

binding (2 ACh) of Nicky R opens cation channels and INCREASES Na+ and K+ conductance.

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3
Q

What is a muscle twitch?

A

AP-dependent increase in intracellular calcium followed by an Cai fall due to sequestration by SR

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4
Q

Why does the axon get so close to the target?

A

ensure that NT release creates a response

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5
Q

What is Clonus?

A

reduced ability to lower Ca between stimulations due to inreased frew of stimulation leads to incomplete relaxation

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6
Q

Define tetanic contraction

A

no appreciable reduction in Cai between stimuli leads to physiological mu contraction.

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7
Q

Why is the availability of fast Na channels important?

A

propagation of AP is dependent on it. channel must be in a RESTING STATE (to maintain AP)…linked to way of inducing paralysis

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8
Q

(proper skeletal mu contraction requires 5 things)

A
  1. Ach release
  2. available Nicky R
  3. summation of EPPs to produce AP
  4. activation of fast Na+ channels
  5. increased intracellular calcium
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9
Q

What are the two types of neuro.mu relaxants acting on nicky R?

A

non-depolarizing agents (curare drugs)-competitive antagonist of Nm receptor
AND depolarizing agents-bind to nicky R, stay there; prolonged activation of Nm and membrane DEpolarization (Succinylcholine)

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10
Q

What are three examples of non-depolarizing blocking drugs?

A

D-TUBOCURARINE
PANCURONIUM
VECURONIUM

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11
Q

What is the mech of action of ND Drugs?

A
  1. mech of action: competitive ANTagnist at nicky ACH R
  2. overcome by excess ACh thru: tetanic stimulation and AChE inhibitors
  3. At higher concentrations blockade (plugging) of channel pore develops less sensitive to excess ACh inhibitors-wont to avoid this because drug will act in a NON-COMPETITIVE manner)…therefore use stimulus to know how many receptors are being used so that you dont go overboard
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12
Q

Clinical Characteristics

A

competitive binding of curare-likeD to the nicky R prevents opening of nicky R ion channel thus preventing membrane depolarization and end-plate potentials

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13
Q

What does choice of drugs depend on?

A

desired PK parameters

  • short vs. long t1/2 (depends on route of elimination…)
  • renal > hepatic clearance > plasma cholinesterase
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14
Q

Curare Info

A 
rapid distribution (dont cross BBB)
t1/2 depends on how drug is eliminated
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15
Q

Fun drugs

A

(**know how long they act RELATIVE TO EACHOTHER)
PANCURONIUM: 75-107…renal 30-80%
TUBOCURARINE: 107-237
VECURONIUM: 61.1…>25 renal (good for pt with liver failure)
MIVACURIUM: ~3-5..cholinesterase (use for renal/liver probs)
ROCURONIUM: ~60…80-90 liver

(tub>pancuro>vecuro=rocuro>miva
(two ~1hr but one eliminated by liver vs kidney)

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16
Q

Why is Receptor Reserve relevant?

A

significant R occupancy by antagonist is required before an effect (to prevent muscle twitch)=large RR (for agonist)

17
Q

RR

A

biological t1/2 of the curare compounds tend to be longer than their therapeutic effect (**duration of action)

18
Q

What about ANTAGONIST?

A

percentage of R that must be occupied by an ANTAGONIST to inhibit contraction is directly related to the RR.

19
Q

Clinical Uses of ND NM relaxants

A
  1. surgical procedures (many diff drugs); adjuvant to anesthesia during surgery-choice depends on length of surgery and liver/renal function
  2. relaxation of larynx for endotracheal intubation (rocu and micu)
  3. relaxation of chest during mechanical ventilation (choice depends on liver and renal fxn)
20
Q

Side Effects

A

non-analgesic-with these blockers wont respond to pain
apnea-paralyze respiratory muscles-MUST ventilate pt
histamine release (mivacurium)
-hypOtension, bronchospasm
musky blockade (pancuronium, rocuronium)
-increased HR and CO, troublesome for pt with CHD

21
Q

Muscle weakness followed by paralysis

A
  • affects small muscles first then large muscles of limb and trunk
  • *-order: extraocular, hands and feet, head and neck, abdomen and extremities, diaphragm-respiratory muscle (recovery is in reverse order)
22
Q

Drug Interactions

A 
Inhalation anesthetics (enhaned effect)
AB (enhance efects, particularly aminoglycosides)
23
Q

Chemical Antidotes

A

Cholinesterase inhibitors-neostigmine (can also work at musky)
Muscarinic blocker-to minimize effet of ChE inhibitor–glycopyrate

24
Q

Depolarizing Blocking D-AGONISTS major example?

A

Succinylcholine

25
Q

Succinylcholine mech of action P1?

A

Phase I: Depolarization Block

  • depolarization of mu with sustained contractions (opens cation channel to cause EPP)
  • flickering of channel due to channel blockade
  • flaccid paralysis
  • **ChE inhibitors augment blockade
26
Q

Succinylcholine mech of action P2?

A
  • *prolonged exposure to succinycholine (>~30 min, membrane becomes REPOLARIZED) leads to PII
  • mechanism unknown, may deal with R desensitization
  • R gets INSENSITIVE to ACh (and other agonists)
27
Q

***What causes DEPOLARIZATION of the membrane?

A

Plasma ChE is not available at the synapse, therefore DEPOLARIZATION of the membrane is prolonged. This results in inactivation of voltage-gated Na+ channels. The Na+ channels cant regain their resting state until the membrane is REPOLARIZED…consequently: nor further AP can be propagated=FLACCID PARALYSIS!

28
Q

PK of DEpolarizing Drugs

A
  • more rapid onset of action than non-depolarizing agents
  • rapidly metabolized inplasma by cholinesterase (not at synapse)
  • action terminated by diffusion of drug away from motor end plate
  • ***genetic variant in ChE can prolong drug action (t1/2-longer for it to be broken down)
29
Q

Clinical Uses of Succinylcholine

A

-endotracheal intubation
-control convulsion during ECST (electro-convulsive shock therapy)
(only two because of all the side effects)

30
Q

Side Effects of Succinylcholine

A
  • non analgesic
  • apnea
  • muscle pain (from fasciculations)
  • exacerbate problems if they have glaucoma or intestinal block-could be damaged because of excessive intestinal motility
  • stimulation of nicky R of autonomic ganglia and cardiac musky R in sinus node (arrhythmia, hypErtension. bradycardia)
  • hypErkalemia due to K+ release from motor end plate (associated with burns or nerve damage)
  • can initiate malignant hyperthermia (in children with undiagnosed muscle myopathies)
31
Q

Antidotes Phase I Succinylcholine

A

(no chemical ones) time for diffusion (5-10 mins) away from synapse and hydrolysis by plasma ChE

32
Q

Antidote Phase II Succinylcholine

A

Can just use ChE inhibitor to reverse paralysis

33
Q

Ci of Succinycholine

A

-fam history of malignant hyperthermia
-burns (immediate aftermath)
-major soft tissue injury (over past 7-10 days)
skeletal mu myopathies (associated with genetic variants that may initiate malignant hyperthermic response)

34
Q

(What are the indications of Spasmolytic Drugs?)

A

heightened skel.mu tone due to:

  1. release from inhibitory supraspinal control
  2. increased activity of facilitory pathways
  3. heightened excitability of alpha and gamma motor systems
35
Q

Types of Spasmolytic Drugs: BACLOFEN

A

Mech of action: GABAb agonist, reduces Ca influx, therefore reduces the release of excitatory transmitters (at that skeletal.mu)
Clinical Usages: spinal spasticity due to MS
Toxicity: drowsiness (crosses BBB)
(**intrathecal catheter-passed by spinal cord, can reduce side effects, less of drug in the brain)

36
Q

Tx of spasticity

A
  1. reduce activity of Ia fibers that excite the primary motor neuron
  2. enhance activity of inhibitory internuncial neurons (innervated by cutaneous afferents-heat, pain)
37
Q

Types of Spasmolytic Drugs: Benzodiazepines (DIAZEPAM

A

Benzo=positive allosteric modulators of GABAa R INCREASE GABA-mediated Cl- influx

MOA: facilitate GABA-mediated pre-synaptic inhibition
Clinical usages: spinal spasticity, MS
Side Effects: sedation and drowsiness

38
Q

Types of Spasmolytic: TIZANIDINE

A

Mech of action: alpha TWO adrenergic agonists
Clinical Use:
Side Effects: drowsiness and hypotension

39
Q

Types of Spasmolytic: DANTROLENE

A

Mech of Action: blocks ryadonine receptor
Clinical Usages: spasticity and malignant hyperthermia
toxicity: muscle weakness, sedation, hepatitis (inflames the liver–therefore not used that often)

PHARM.M2.Neuromuscular Relaxants (3 decks)

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