Introduction to Medical Sciences: Nerve and Muscle

Types of Muscles in the Human Body:
- Skeletal Muscle Cells: Long, striated fibers under voluntary control.
- Smooth Muscle Cells: Non-striated, involuntary muscle found in hollow organs.
- Cardiac Muscle Cells: Striated, involuntary muscle that makes up the heart.

Structure:
- Composed of bundles of fibers called fascicles.
- Each fiber encased by three connective tissue layers:
- Epimysium (entire muscle)
- Perimysium (fascicles)
- Endomysium (individual fibers)
- Sarcomere Structure:
- Composed of thick (myosin) and thin (actin) filaments arranged in a repeating pattern.
- Z Discs mark the boundaries of each sarcomere.
- Ultrastructure:
- Multi-nucleated with nucleus located peripherally.
- Contains abundant mitochondria for ATP production.
- Distinctive T-tubules for action potential propagation.
Function:
- Responsible for voluntary movements; contraction initiated by neuromuscular junction via action potentials.
Action Potential Phases:
- Depolarization: Rapid influx of Na+ ions.
- Repolarization: Efflux of K+ ions restores resting potential.
- Contraction Mechanism: Driven by cross-bridge cycling between actin and myosin.

Structure:
- Spindle-shaped cells, smaller than skeletal muscle, with a single central nucleus.
- Lacks striations; thick and thin filaments more randomly organized.
- Contains dense bodies that anchor actin filaments.
Types of Smooth Muscle:
- Phasic: Contracts rhythmically, found in gastrointestinal tract.
- Tonic: Maintains prolonged contraction, found in sphincters.
Contraction:
- Involves latch-bridge mechanism for sustained contraction.
- Calcium activation via calcium-calmodulin complex leading to myosin light chain phosphorylation.

Structure:
- Branching muscle fibers interconnected at intercalated discs that contain gap junctions for electrical coupling.
- Rich in mitochondria (30% of cell volume) to meet energy demands.
Function:
- Involuntary and rhythmic contraction, regulated by pacemaker potentials and electrical coupling.
Action Potential:
- Comparison with skeletal muscle: slower onset with a prolonged plateau phase due to calcium influx.
- Calcium-Induced Calcium Release (CICR): Extracellular Ca2+ stimulates further release from the sarcoplasmic reticulum.

Overview:
- X-linked recessive disorder affecting skeletal muscle.
- Early onset (around age 5), results in muscle weakness beginning in the legs and pelvis.
- Leads to wheelchair dependence and reduced life expectancy (death in 30s).
Pathophysiology:
- Caused by mutation in the dystrophin gene (large gene located on X chromosome).
- Absence of dystrophin causes muscle fiber membrane instability, leading to cell death.
- Symptoms include muscle wasting, calf hypertrophy, scoliosis, and impaired mobility.

Definition:
- A condition characterized by the breakdown of skeletal muscle fibers with the release of myoglobin and other substances into circulation.
Common Causes:
- Trauma, immobilization, infections, and certain drugs (statins, alcohol).
Clinical Features:
- Myalgia, muscle weakness, and dark red-brown urine (myoglobinuria).
Complications:
- Can lead to kidney injury due to myoglobinuria, electrolyte imbalances, and muscular damage.

Classes of Antiarrhythmic Agents:
- Class I: Sodium-channel blockers (e.g., quinidine, lidocaine).
- Class II: Beta-blockers (e.g., propranolol).
- Class III: Potassium-channel blockers (e.g., amiodarone).
- Class IV: Calcium-channel blockers (e.g., verapamil).