2-14oct Flashcards
What are the two main types of specialized cells in the nervous system?
Neurons and Glia (Neuroglia).
What is the primary function of the nervous system?
It serves as a communications network, receiving information and initiating actions.
What are the divisions of the nervous system?
Central Nervous System (CNS) and Peripheral Nervous System (PNS), which includes the Somatic and Autonomic Nervous Systems.
What is the role of the Sodium-Potassium pump (Na-K ATP-ase)?
It helps maintain ionic gradients by pumping 2 potassium ions in and 3 sodium ions out of the cell.
What is the equilibrium potential for potassium (K+)?
Approximately -70 mV.
What is saltatory conduction?
It is the process by which action potentials jump from one node of Ranvier to another in myelinated axons, speeding up signal transmission.
How do local anesthetics block conduction of action potentials?
They block sodium channels from inside of the cell , preventing the initiation and propagation of action potentials.
What are the routes of administration for local anesthetics?
The routes of administration include topical, infiltration, nerve block, and epidural.
Which local anaesthetics contain ester linkage?
Cocaine, procaine, amethociane(tetraciane), benzocaine
Which of them are amide linkage
Lignocaine(lidocaine), prilocaine, Bupivacaine
The uses and duration of these anaesthetics: cocaine, procaine, lignocaine(lidocaine), prilocaine, amethocaine(tetracaine), bupivacaine, benzocaine
a-topical, b- infiltration, c-peripheral block, d-central block
cocaine-none, <30mins, procaine-b-d,short, lignocaine(lidocaine)-a-d, intermediate , prilocaine-a-d, intermediate(2-3hrs), amethocaine(tetracaine)-a, long, bupivacaine-c,d, long, benzocaine-a, long.
What is epidural anaesthesia injection
Anaesthetics used to anaesthetise the specific nerve root in the lumber region in vertebral column
Administration of topical anesthetics
Skin, cornea, oropharynx
Administration of infiltration anesthetics
Injection around the nerve ends-dentistry
Administration of peripheral nerve block anesthetics
Injection close to major sensory nerve trunks in large proportion of the body. No general anesthetic but local anesthetic
Administration of central nerve block anaesthetics
Infected into:
Subarachnoid space, produce spinal anesthesia.
Epidural anesthesia
Chemical structure of local anesthesia
Aromatic group+ ester(short)/amide(long lasting, only broken in liver+ basic side chain
What does local anesthesia+adrenaline do
Stimulate vasoconstriction to prolong LA’s work
Ache can be inhibited by what so that ach can last longer in the synapse
Edrophonium, neostigmine, physostugmine,
What happened is there antibodies binding to the ach receptors
No enough membrane depolarized to reach threshold so difficulty in breathing and muscle weakness happen
What does hemicholinium do
Affect the neurotransmitter by occupying choline uptake carrier therefore less choline.
What does the triethylcholine(tec) do
Gets taken up into the terminal instead of choline forming ATEC vesicles and released forming false binding therefore false transmission .
Choline acetyltransferase is used to add TEC to acetate
Site of action of Drugs affecting neurotransmission
- Affecting neurotransmitter synthesis (presynaptic)
- Inhibiting neurotransmitter release (presynaptic)
- Affecting nicotinic acetylcholine receptors (postsynaptic)
Drugs affecting neurotranmitters synthesis
Triethylcholine( TEC)-false transmitter, hemicholinium-less ach receptors.
Drugs affecting transmitter release- presynaptic site
Inhibitors of release: local anaesthetics, divalent cations- mg, cd,co, mn, toxins- botulinum toxin, beta-bungarotoxin, tetrodotoxin, antibiotics-Aminoglycoside antibiotics:
streptomycin, neomycin, kanamycin
Potentiators of release: k+ channel blockers- tetraethylammonium, 4- aminopyridine
Drugs affecting neurotransmission – postsynaptic site(s)
Neuromuscular blockers / muscle relaxants
- Non-Depolarizing, Competitive blockers
- Depolarizing, Non-Competitive blockers
Non-Depolarizing, Competitive blockers (B)
Blockers block the site thus closing the channel for na+ and k+ exchange
Depolarizing, Non-Competitive blockers (D)
D first bind inplace of ach still allowing na+ and k+ to bust in the initial stage of block, later D enters the channel and clocks it. The receptors is then desensitized( receptor desensitization) in the later stage
