Conductive Tissue/Muscle/NMJ Physiology Flashcards Preview

MSI Module II > Conductive Tissue/Muscle/NMJ Physiology > Flashcards

Flashcards in Conductive Tissue/Muscle/NMJ Physiology Deck (14):
1

Mechanism of action of local anesthetics

Block fast Na channels in axons (block action potentials) by binding inside the channels

***Exception: Benzocaine (a topical LA), binds outside of the Na channel rather than inside.

Drug needs to be lipid soluble to penetrate membrane

Drugs with higher lipid solubility tend to be more potent

2

Ester versus amide local anesthetic metabolism

Ester local anesthetics are quickly degraded by serum esterases → short half-life, shorter-acting

Amide local anesthetics can only be metabolized in the liver, which takes a long time → longer-acting

3

Ester local anesthetics

Procaine, Tetracaine (Pontocaine)

4

Amide local anesthetics

Lidocaine (Xylocaine)

Bupivacaine (Marcaine)

Mepivacaine (Carbocaine)

  • Good for old people and cardiac pts bc can be administered w/o epinephrine

***All of these have two "i's" in thier name

 

5

Differential sensitivity of nerve fibers

Using differential sensitivity allows these drugs to be applied to block pain but not affect sensory and/or motor fibers

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6

CNS and cardiovascular side effects of local anesthesia

Adverse reactions occur primarily in the central nervous and cardiovascular systems because these tissues are also composed of excitable membranes.

Cardiovascular effects

  • Conduction failure
  • Ventricular arrhythmias or fibrillation
  • Both effects are worse in the presence of epinephrine
  • Hypotension as a result of a combination of vasodilation effects from local anesthetics and negative inotropic forces (Which weaken the force of muscular contraction)
  • Spillage of excessive amounts of local anesthetic into general circulation can be caused by excessive local injections or tourniquet failure.

CNS effects

  • Low doses affect only excitatory neurons, causing sedation and drowsiness
  • High doses affect both excitatory and inhibitory interneurons, causing convulsions

7

Cross-bridge cycle

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8

Clinical uses and mechanism of action of botulinum toxin

Mechanism of action: blocks acetylcholine release from presynaptic terminals (results in total blockade of neuromuscular transmission)

Clinical uses: used to treat Upper Motor Neuron Disease and for chewing problems, swallowing problems, muscle spasms, hair loss, twitching of the eyelids, and excessive sweating

9

Clinical uses and mechanism of action of curare

Mechanism of action: competes with acetylcholine for nicotinic receptors on motor end plate (decreases size of end plate potential)

Clinical uses:

  • D-tubocurarine is used to relax skeletal muscles during anesthesia
  • α-bungarotoxin is used experimentally to measure the density of acetylcholine receptors on the motor end plate

10

Clinical uses and mechanism of action of acetylcholinesterase inhibitors

Mechanism of action: prolong and enhance action of acetylcholine at motor end plate by preventing its degradation

Clinical uses: used to treat myasthenia gravis

11

Subunits of troponin and their actions

Troponin blocks myosin binding sites during rest but when calcium binds to troponin (C) it exposes myosin binding site and allows for contraction.

  • Troponin C: binds to calcium leading to conformational change
  • Troponin T: binds to tropomyosin to form troponin-tropomyosin complex
  • Troponin I: binds to actin in thin myofilaments to hold the troponin-tropomyosin complex in place

12

Locations and functions of dihydropyridine receptor and ryanodine receptor in skeletal muscle fiber

Dihydropyridine Receptor: Voltage Sensitive Protein activated by AP from sarcolemma

  • Location: T-Tubules
  • Function: Activates ryanodine receptors

Ryanodine Receptor: Ca2+ Release Channel

  • Location: sarcoplasmic reticulum
  • Function: Enables muscle contraction by increasing intracellular Ca2+

13

Exitation contraction coupling in smooth muscle

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14

Excitatory versus inhibitor neurotransmitters

Excitatory:

  • Glutamate: the major excitatory neurotransmitter in the CNS

Inhibitory:

  • Glycine
  • GABA (gamma-aminobutyric acid)
  • Nitric Oxide