Module 2 Flashcards
Blocks release of Ach from presynaptic terminals
Botulinum toxin (botox)
a drug that blocks the gating action of Ach on the Ach channels by competing for ACh receptor sites on motor end plate
Curare
Inhibits acetylcholinesterase
Neostigmine
Blocks reuptake of choline into presynaptic terminal
Hemicholinium
Antibody directed against the ACh receptor
Myasthenia gravis
What is the effect of AChE inhibitor?
Blocks the degradation of ACh, causing an increase in the endplate potential, and prolongs the action of ACh at the motor endplate
- A neuromuscular disease with classic symptoms of weakness and fatigue of skeletal muscles
- Seen more commonly in females, with peak incidence at 20 to 30 years of age
- Men have a peak of incidence at around 50 to 60 years of age
Myasthenia gravis
Classic symptoms of this disease is muscle weakness that increases with repetitive muscle use (eg, chewing) and partially recovers with rest
Myasthenia gravis
- Most common muscular dystrophy
- 1 in 3500 boys (3-5 yo)
- Severe muscle wasting
- Most patients are wheelchair bound by the age of 12
- Respiratory failure in adulthood (30 to 40 years of age)
Duchenne’s muscular dystrophy
What is gower’s sign for Duchenne’s muscular dystrophy?
Using hands to push on legs to stand
- X-linked recessive
- Defect in the dystrophin gene –> deficiency of the dystrophin protein in skeletal muscle, brain, retina, and smooth muscle
Duchenne’s muscular dystrophy
- A large (427 kDa) protein present in low abundance (0.025%) in skeletal muscle
- Localized on the intracellular surface of the sarcolemma in association with several integral membrane glycoproteins (forming a dystrophin-glycoprotein complex)
Dystrophin
- Tethers Myosin to Z lines (scaffolding)
- Binds Z lines to M line
- largest protein
Titin
- Attaches to plasmalemma
- Stabilizes plasmalemma and prevents contraction-induced rupture
Dystrophin
Binds Actin to Z lines
Actinin and Capz Protein
Binds Z lines to plasma membrane
Desmin
- Occurs when contracting muscles are stretched and lengthened too vigorously
- More pain and stiffness than in not-so-vigorous muscle stretching and lengthening (cycling)
Resultant dull, aching pain develops slowly and reaches peak in 24 to 48 hours
Delayed-onset Muscle Soreness
- Pain associated with reduced range of motion, stiffness, and weakness of the affected muscles
- Pain due to inflammation near myotendinous junctions
- Slow recovery, depends on regeneration of the injured sarcomeres
Delayed-onset Muscle Soreness
- A state of contracture several hours after death
- All the muscles of the body go contraction and become rigid even without action potentials
Rigor Mortis
Rigor Mortis results from loss of all the ATP. Why?
It is required to cause separation of the cross-bridges from the actin filaments during the relaxation process
- Muscles remain in rigor until the proteins deteriorate (15 to 25 h later)
- All these events occur more rapidly at higher temperatures
Rigor Mortis
exert opposite effects but operate reciprocally (complementary) or synergistically to produce coordinated responses
Dual Innervation
Single Innervation that has sympathetic only
- sweat glands
- adrenal glands
- most blood vessels
- pilomotor muscle
Single Innervation that has parasympathetic only
- lacrimal muscle (tear glands)
- ciliary muscle (accommodation for near vision)