Lecture 06_Fall Flashcards by Nancy Corder

When a nerve depolarizes, ___ ions enter the neuron and ___ is released from vesicles and binds to ___ receptors on the motor-end plate of the muscle fiber

Ca ions enter, Ach is released, binds to nicotinic cholinergic receptors

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Ach is hydrolyzed by ____ into ____ and ____.

Acetylcholinesterase, acetate and choline

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Select the correct option.Depolarizing NMBAs act as Ach receptor _____ (agonist or competitive antagonist).

agonist

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Select the correct option.Non-depolarizing NMBAs act as Ach receptor _____ (agonist or competitive antagonist).

competitive antagonist

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T or F. Phase I and Phase II blocks are seen with non-depolarizing NMBAs.

False. They refer to the blocks seen with depolarizing NMBAs.

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NMBAs are quaternary ______ compounds with afinity for _____ Ach receptors.

ammonium, nicotinic

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A Phase II block resembles a ___ block.

non-depolarizing

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What % of receptors must be blocked before you observe fade with a twitch monitor?

> 70%

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What % of receptors must be blocked for complete twitch suppression?

> 90%

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What is responsible for the metabolism of sux?

plasma pseudocholinesterase

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What happens if you try to reverse a Phase I block with an AchE inhibitor?

can lead to prolonged depolarization

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What is Dibucaine

it is a local anesthetic that inhibits pseudocholinesterase

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What is A Dibucaine Number?

It is the % of pseudocholinesterase that is inhibited by dibucaine

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What is a normal Dibucaine number?

80 = normal

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What would a dibucaine number of 0-20 indicate?

a homozygous abnormal pseudocholinesterase gene that will result in prolonged NMB with Sux, lasting 4-8hrs

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What would a dibucaine number of 40-60 indicate?

a homoheterozygous abnormal pseudocholinesterase gene that will result in prolonged NMB with Sux, lasting 20-30min

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Pesticide toxicity resembles the effects of what drugs?

resembles the SLUDGE effects of AchE Inhibitors like Neostigmine

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T or F. Pancuronium can prolong the depolarizing block of Sux.

True - Pancuronium inhibits pseudocholinesterase

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T or F. Low doses of Sux causes tachycardia.

False. It binds to muscarinic cardiac Ach receptors - causes bradycardia and decreased myocardial contractility. Opposite at high doses

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Why is hyperkalemia a side effect of Sux?

Due to the sustained opening of ion channels and membrane depolarization

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Sux increases serum K+ levels by ___ mEq/L

0.5 mEq/L

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Which of the following side effects associated with Sux can be attenuated with a defasciculating does of non-depolarizering MRs? (select all that apply)

A. Myalgias
B. Increased ICP
C. Increased IOP
D. Hyperkalemia
E. Increased Gastric Pressure

A. Myalgias - Yes
B. Increased ICP - Yes
C. Increased IOP - NO!!
D. Hyperkalemia - NO!!
E. Increased Gastric Pressure - Yes

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How does neural injury lead to significant K+ release with Sux?

Rapid proliferation of extrajunctional ACh receptors with neural injury (trauma, denervation) - Widespread depolarization leads significant K+ release

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Which of the following increases risk of succinylcholine induced hyperkalemia (Potential risk within 96 hours, peaks ~7-10 days after injury, lasts 6 months or longer)?

A. 3rd degree burn injury
B. Massive skeletal trauma
C. Upper motor neuron injury
D. Denervation  muscle atrophy
E. Myopathies (myotonia, muscular dystrophy)

All of them

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A Phase II block will be seen after ___mg/kg IV Sux.

7-10 mg/kg or 30-60 min- or after a single dose in pts with atypical plasma cholinesterase

Inhalational anesthetics ____ the onset of a Phase II block.

accelerate

What are the 6 ABSOLUTE contraindications for succinylcholine?

ABSOLUTE contraindications include: 1. MH 2. dangerously elevated serum K+ 3. known myotonia or muscular dystrophy 4. >2-4 days after CNS injury (stroke, cord injury) 5. massive musculoskeletal injury 6. major burn

Succinylcholine-induced MMR can lead to _____.

rhabdomyolysis

What are 2 signs of rhabdomyolysis?

myoglobinuria and myoglobinemia

What are the 2 classes of Non-Depolarizing Neuromuscular Blocking Agents?

Benzoisoquinolines (“-acurium”) or steroidals (“-curonium”)

What is the Priming dose of Non-Depolarizing Neuromuscular Blocking Agents?

Priming dose: give 10% of intubating dose 5 min before induction

___, ____, ___, and ___ potentiate the action of Non-Depolarizing NMBAs.

1. inhalational anesthetics (DES>SEVO>ISO>HAL) 2. antibiotics (aminoglycosides – prolong steroidal NMBs) 3. phenytoin 4. Mg

___, ____, ___, and ___ prolong the action of Non-Depolarizing NMBAs.

1. hypothermia 2. acidosis 3. hypokalemia 4. hypocalcemia

What is the Defasciculating dose of Non-Depolarizing Neuromuscular Blocking Agents?

Defasciculating dose: give 10% of intubating dose 5 minutes before succinylcholine

Muscles of glottis, face, airway, diaphragm are ___ sensitive to NMB than the thumb (adductor pollicis) so the dose to block diaphragm is ___ the dose needed to block adductor pollicis.

less, twice

Cisatracurium is metabolized by _____.

Hoffman Elimination

Atracurium (isomer of cisatracurium) is degraded by ___ AND _____ bynon-specific plasma esterases

Hoffman elimination AND ester hydrolysis

What is the must common paralytic used in renal failure patietns and for ICU infusions?

Cistatracurium

Which paralyzing agent is metabolized by pseudocholinesterase but no longer available?

Mivacurium

Which paralyzing agent should be used with caution in renal failure patients and why?

Pancuronium - 40% renally cleared – caution in renal failure

What CV effect does Pancuronium have?

Increases in HR, BP, CO (block cardiacmuscarinic ACh receptors)

What is the onset time and duration of Vecuronium?

Onset = 3-4 min Duration = 35-45min

What is the onset time and duration of Rocuronium?

Onset = 2 min Duration = 30-40min

What is the onset time and duration of Nimbex

Onset = 2-4 minutes Duration = 35-40 minutes

What is the best non-depolarizer for rapid sequence intubation?

Rocuronium

What percent of Vecuronium is renally cleared?

25%

T or F. Organophosphates (pesticides) are also anticholinesterases.

TRUE

How do reversal agents work?

Cholinesterase (AChE) Inhibitors (“Anticholinesterases”) - Indirectly increase amount of ACh in the NMJ which can compete with the non-depolarizing NMB agent

AChE inhibitors are used in the diagnosis of ____.

myasthenia gravis

In excessive doses, AChE inhibitors can cause_____ leading to ____.

ACh-mediated blockade, weakness

T or F. Bronchospasm is a side effect of AChE inhibitors.

TRUE

___ is the only AChE inhibitor that crosses the Blood-Brain Barrier.

physostigmine

Which anticholinergic agent crosses the BBB?

Atropine

A pt with TOF with fade should get a ___ reversal dose.

Full

A pt with TOF without fade should get a ___ reversal dose

partial

When would you consider giving no reversal?

If the pt has sustained 5 sec tetanus or clinical evidence of adequate strength

A pt with post-tetanic twitch or no tetanic response should get a ___ reversal dose.

They should not get any reversal - they are unreversible at this point

List the clinical signs of adequate strength in order from best to least acceptable.

Sustained head lift / leg lift > negative inspiratory force > vital capacity > tidal volume

Post-tetanic count correlates with ____.

time until spontaneous recovery

Reversal agents have ____% Hepatic and ____% renal clearance.

Hepatic (25-50%) and Renal (50-75%)

What is the max dose of Neostigmine for adults?

5mg

Which reversal agent should be given with atropine and why?

Edrophonium: rapid onset of action (1-2 minutes) and short duration of effect - Give with atropine – better match with onset, duration

When would you consider using atropine with neostgmine instead of glycopyrrolate?

When you are concerned about it crossing the placenta

_____ is a tertiary amine that crosses blood-brain barrier and is used as treatment for central cholinergic toxicity

Physostigmine

T or F. You do not have to give atropine / glycopyrrolate with Physostigmine.

TRUE

Physostigmine is metabolized by ____.

plasma esterases

_____ can be used to reverse deep NMB from non-depolarizing agents, although it is not currently approved for use in the US.

Sugammadex

Sugammadex only works on non-depolarizing NMBAs with a ____ nucleus, such as ___, ____, and ___.

Steroid, Rocuronium, Vecuronium, and Pancuronium

______ could be used with rocuronium for RSI – replace succinylcholine- which would be a huge benefit due to all the contraindications associated wit Sux.

Sugammadex(If you couldn't tell by my 3 flashcards, this is sort of important to know!)

What should you remember about NMBAs in patients with Myasthenia Gravis?

They are Resistant to Sux and Sensitive to non-depolarizers (like Roc) so you can remember this with: "R to S and S to R"

___is an autoimmune neuromuscular disease where circulating antibodies block Ach receptors at the postsynaptic NMJ and cause muscle weakness.

Myasthenia Gravis

What should you remember about NMBAs in patients with Myotonia (many types)?

They will have:SUSTAINED contracture leading to hyperkalemia with SUX and A Normal response to Non-depolarizers so you can remember this with: "S with S and N with N"

What should you remember about NMBAs in patients with Muscular Dystrophy, a disease that causes loss of muscle mass?

First, it is often latent and undiagnosed in patients <10y old (esp. males) They have a normal response to non-depolarizers BUT Sux can cause hyperkalemic cardiac arrest This is why we avoid using sux in children

What should you remember about NMBAs in patients with Upper Motor Neuron Lesions: hemiplegia, quadriplegia?

starting ~2-4 days after injury for up to 6-12 months use of Sux will cause hyperK and they have a resistance to non-depolarizers below the level of the lesion

What should you remember about NMBAs in burn patients?

They are Sensitive to Sux b/c they have a proliferation of extra-junctional Ach receptors and they are Resistance to non-depolarizing agents (Roc) you can remember this with: "S to S and R to R" (sux will cause hyperK starting ~2-4 days after the burn for at least 12 months)

What is Myotonia?

abnormal delay in muscle relaxation after contraction