• 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

1/8

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;

8 Cards in this Set

  • Front
  • Back
Non-depolarizing blockers
ending with -curium or -curonium

tubocurarine is very long lasting, hard to reverse, not used clinically
Mech of action, non-dep. blockers
compete with ACh, causes weakness followed by flaccid paralysis, direct stimulation WOULD elicit contraction
Depolarizing blockers
succinyl choline
succinyl choline mechanism
Phase I blockade: depolarization, brief fasiculations followed by flaccid paralysis

-muslce contraction can't be elicited by direct stimulation of muscle and is enhanced by increasing ACh.//

Phase II: Flaccid paralysis, endplate depolarization decreases... later becomes similar to nondepolarizing, and can be overcome with excessive ACh.
Issues with succinylcholine
contraindicated for pts less than 8 yo... causes hyperkalemia, prolonged apnea, malignant hyperthermia
What's malignant hyperthermia
life-threatening muscle rigidity, leads to severe hyperthermia, musc. metabolism, acidosis and tachycardia...

Auto. Dominant defect in ryanodine receptor or L-type Ca2+ channel...

common with succinylcholine + halothane or other inhalational anesthetics.

treat with DANTROLENE (musc. relaxant)
potentiates NMJ blockers
inhaled, and local anesthetics, Ca channel blockers, antibiotics (aminoglycosides, tetracyclines)
Myasthenia gravis etiology
most autoimmune ab against nAChRm at NMJ leading to decreased receptors. There are some congenital forms

sx: muscle weakness

Tx: pyridostigmine, immunosuppresants, thymectomy