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pharmacology 12
| Term | Definition |
|---|---|
| occurs as a response to communication between peripheral nerves and muscles | skeletal muscle contaction |
| acetylcholine | transmits messages between nerve and muscle cells |
| ACH filled vesicles | located in the motor neuron endplate |
| calcium increases | the realease ACH - produce cramping spasms ex black widow spider venom |
| drugs that decrease the realse of ACH | CAUSE skeletal muscle relaxation |
| acetylcholine binding causes an inlfuz of:? | sodium, calcium and potasium increasing endplate potential |
| endplate potential must exceed ___? to result in muscle contraction | 15 mv- causing an action potential |
| botulinum toxin, magnesium, high doses of ethanol | natural neuromuscluar blockig agents that decrease's release of ACH |
| central acting muscle relaxants | blind and block calcium channels work in the brain and spinal cord |
| two types of skeletal muscle relaxants | central acting and peripheral acting |
| peripheral acting muscle relaxants | block nerve transmissions between motor endplates and skeletal muscle receptors act directly on muscle) |
| two types of peripheral acting muscle relaxants | nondepolarizing and depolarising |
| nondepolarizing competitive blocking agents | block ach binding antagonists ends in "curonium" an "curium" |
| deploarizing blocking agents | These drugs bind to ACh receptors and initially activate them But they cause sustained depolarization, which forces the receptors into an inactive state. The muscle cannot repolarize, so contraction cannot be repeated → paralysis. |
| succinylcholine | a depolarizing blocking agent improper use can cause death |
| when is Peripheral acting mucscle relaxants used ??? | surgery, general anesthesia |
| botulinum toxin type a uses | temporarily removes wrinkles excessive sweating spasticity migranes uncontrolled blinking |
| botlulinum toxin type a adverse reactions | droopy eyelids (bleoharptosis) headache nasuesea flu redness |
| reversal neuromusclar drugs | Anticholinesterase drugs work by inhibiting acetylcholinesterase (AChE), When AChE is blocked, ACh levels increase They counteract paralysis caused by nondepolarizing blockers |
| Neostigmine and Pyridostigmine (Mestinon®) (tablet only in Canada) | Anticholinesterase drugs- Commonly used in hospitals to reverse nondepolarizing neuromuscular blockade after surgery. By increasing ACh, it restores muscle contraction and breathing function. |
| Anticholinesterase drugs adverse reactions (given USP/high alert) | salivation, muscle twitching, abdominal cramping, nausea, increased bronchial secretions, and difficulty breathing |
| Spasticity | A debilitating motor disorder affects 12 million people worldwide, interfering with daily activities and making effective walking difficult. It often causes fatigue, stiffness, and can also disturb sleep. |
| spasticity positive symptoms | increased muscle tone exaggerated tendon jerks hyperexcitable stretch reflex |
| spacicity negative symptoms | muscle weakness decreased endurance - reduced ability to make voluntary muscle movements |
| 4 phases of spacicity | 1. muscles begin to lose ability to contract 2. excessive muscle tone and increased reflec activity lasting days to years 3. decreased reflex excitability 4. stiff contracted muscles |
| Conditions that produce spasticity | Spinal cord injury, stroke, cerebral palsy, amyotrophic lateral sclerosis (Lou Gehrig’s disease), multiple sclerosis, and muscle strain. |
| Amyotrophic Lateral Sclerosis (ALS), also known as Lou Gehrig’s Disease. | Damage to upper motor neurons leads to the release of acetylcholine, which in turn causes desensitization of motor nerves, muscle weakness, and cell death. |
| role of ASH | transmits messages between nerve and muscle cells binds to nictinic receptor to open sodium, cakcium potassium channels increased enplate potential produces muscle contraction |
| ɣ-Aminobutyric Acid GABA | major inhibitory neurotransmitter GABA 𝐴 receptor binding → chloride channels open |
| Glycine | inhibitory neurotransmitter |
| Hyperekplexia | rare genetic disorder characterized by exaggerated startle responses and muscle stiffness. •Defective glycine receptors are associated with this |
| hypertonia | increased muscle tone) can be caused by glycine |
| Drugs used to treat spasticity | Peripheral-acting drugs: • Act directly on the contractile mechanisms in muscle • Botulinum toxins • Dantrolene |
| dantrolene | peripheral muscle relaxant. Mechanism: blocks calcium release from sarcoplasmic reticulum → weakens hyperexcited muscles. Clinical use: emergency treatment of malignant hyperthermia triggered by succinylcholine or anesthetic gases. |
| Baclofen (Lioresal®)- central acting drug to treat spasticity | an agonist at GABA𝐵 receptors, decreasing release of excitatory neurotransmitters and substance P. This reduces muscle contractions and spasticity. |
| Diazepam)- central acting drug to treat spasticity | Enhances GABA binding at GABA 𝐴 receptors, increasing chloride influx, hyperpolarizing neurons, and reducing excitability. Also improves range of motion and reduces anxiety/insomnia. |
| Tizanidine central acting drug to treat spasticity | Alpha2-adrenergic drugs/ reduced motor neuron firing and less spasticity. Act like naturally occurring neurotransmitters, enhancing the actions of the inhibitory neurotransmitter glycine. |
| •Skeletal muscle relaxants | Treat muscle stiffness, pain, and spasms linked to muscle tension, strain, sprains, or injury. Drugs in this category are centrally acting. |
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