• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/20

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

20 Cards in this Set

  • Front
  • Back

What nerves to you twitch and what muscles do they innervate?

Ulnar Nerve-Adductor Muscle of the thumb




Facial Nerve-Orbicularis Oculi Muscle of the eye

What is the order in which the Muscles blockade with NMBA?




"Vocal Cords Die Out After Adding Muscle Paralysis Externally"

Graph demonstrating the difference between Phase one and Phase two depicted by fade.

How is a TOF Ratio calculated and what is a safe ratio for extubation?

TOF Ratio= Magnitude of 3rd twitch/Magnitude of 1st twitch




TOF Ratio of at least 0.9 is safe to extubate




TOF Ratio=.7/.75=.933

How is acetylcholine synthesized and degradated?

Synthesized by Choline Acetyltransferase from Choline and AcetylCoA in the Pre-Synaptic Nerve Terminal.




Degradated in the synaptic cleft by Acetylcholinesterase (true Cholinesterase) into Acetic Acid and Choline (gets reabsorbed)

Nicotinic Receptors, what type of receptor is it, what binds to it, what blocks it, and what electrolyte is involved?

Ligand Gated Ion Channel




Acetylcholine, Nicotine, Succinlcholine




Blocked by NDMRs




Na+ enters into the cell K+ leaves the cell

How many of the five sites on a Nicotinic receptor needs to be occupied to activate?

Two

How is the action of Succinylcholine ended?




How is Succinylcholine broken down?

Ended by diffusion off the receptor by gradient.




After 3-5 minutes due to hydrolysis by plasma cholinesterase (not true cholinesterase) enzymes.

What percentage of Succinylcholine reaches the neuromuscular junction (after metabolism)

Only 10%

What are the other two names for plasma cholinesterase?

Pseudocholinesterase and Butyrocholinesterase

What causes a prolonged effect from Succinylcholine lasting 1-3 hours instead of 3-5 minutes?

Atypical plasma cholinesterase.




Can be caused by low quantity or poor quality

What are causes of Low plasma cholinesterase (synthesized in the liver)?

Liver disease Advanced age


Malnutrition Pregnancy


Burns Oral Contraceptives


MOA Inhibitors Cytotoxic Drugs


Anticholinesterase Drugs

What is the blood test for atypical plasma cholinesterase?

Dibucaine Number (inhibits normal pseudocholinesterase activity by 80% and atypical activity by 20%)




40-60% Prolongs Succ by 100% (20-30 min)




20 and Below prolongs Succs by 4-8 hours





What are the adverse side effects of Succinylcholine?

Bradycardia


Hyperkalemia (increases by5-10meq/dL in burn, trauma, or Head injury patients)


Myalgia (muscle pain)

What are factors that increase the action of Succinylcholine?

Antibiotics


Local Anesthetics


Anticholinesterase Agents


Increased extra cellular Mg++


Inherited pseudocholinesterase defecit


Lithium

How do non-depolarizing neuromuscular blocking agents work?

Combine with the acetylcholine receptors on the nicotinic receptor at the motor end-plate.

What are the two chemical classes of NDMRs?

Steroidal (oniums)-Pancuronium, Vecuronium, Rocuronium




Benzylisoquinolinium (urium) Atricurium, cisatricurium, Mivacurium

Factors that increase Potency of NDMRs?

Aminoglycoside Antibiotics


Local Anesthetics (large doses)


Haloginated inhalation agents


Hypothermia


Magnesium Sulfate


Hypokalemia


Lithium


Loop diuretics


Antiarrhythic agents (Propranolol, Procainamide)

Factors that decrease Potency of NDMRs?

Chronic Anticonvulsant therapy




Hyperparathyroidism and Hypercalcemia




Hyperkalemia and Hypermagnesemia

How do Myasthenia Gravis and Muscle Denervation Injuries(MDI) affect the response to muscle relaxants?

Myasthenia Gravis has fewer Ach receptor (down regulates) results in increased sensitivity to NDMR and decreased sensitivity to succs




MDI chronic decrease in Ach release with upregulated receptors resulting in resistance to NDMR and increased response to Succs