Task 2

Task 2

Fact	Idea	Learning issue	Action plan
Illness - Types of medicine - Duration recover Headache - Panadol activefast - 30 minutes Headache - Ponstan (200 mg) - 15 minutes Sedative - Diazepam (1 mg) - 2 minute Sedative - Propofol - 5 minute Back pain - Voltaren SR 100 - 15 minutes Back pain - Ponston (200 mg) - 15 minutes	1. As we know, sedative is one type of medicine. 2. Diazepam is one type of sedative.	1. What is sedative? 2. What is the content of Panadol activefast, Postan, Diazepam, Propofol, Voltaren SR 100,Poston? 3. Why Diazepam work fastest than other type of medicine? 4. Why does sedative types of medicine have shorter duration compared to others type of medicine? 5. How would medicine affect the function of neurotransmitter?	1. Refer reference books 2. Search in the internet 3. Discuss with other group members

1. What is sedative?

- An agent or drug that sedates; Calming, soothing, inducing sleep, tranquilizing
en.wiktionary.org/wiki/sedative. A sedative  is a substance that induces sedation by reducing irritability or excitement ( from Wikipedia).

- Sedatives are drugs that decrease activity and have a calming, relaxing effect. People use these drugs mainly to reduce anxiety. At higherdoses, sedatives usually cause sleep. 

2. What is the content of Panadol activefast, Postan, Diazepam, Propofol, Voltaren SR 100,Poston?

Type of medicine	Ingredient
Panadol activefast	Active ingredients - paracetamol 500mg per tablet. (plus sodium 173mg, and potassium sorbate E202)
Postan	Ponstan Forte tablets contain the active ingredient mefenamic acid, which is a type of medicine called a non-steroidal anti-inflammatory drug (NSAID). NSAIDs are used to relieve pain and inflammation
Diazepam	ingredient of diazepam rectal gel, is a benzodiazepine anticonvulsant with the chemical name 7-chloro-1,3-dihydro-1 -methyl-5-phenyl-2H-1,4-benzodiazepin-2-one.
Propofol	The active ingredient is 2,6-di-isopropylphenol.
Voltaren SR 100,	hydroxypropyl methylcellulose, iron oxide, lactose, magnesium stearate, methacrylic acid copolymer, microcrystalline cellulose, polyethylene glycol, povidone, propylene glycol, sodium hydroxide, sodium starch glycolate, talc, titanium dioxide.

3. Why Diazepam work fastest than other type of medicine?

Diazepam is a type of benzodiazepines and a type of tranquilliser, benzodiazepines can make you less worried and more relaxed. They can also help some patients sleep better. They work faster than other treatments for anxiety, but they can have serious side effects. You may feel sleepy or doped up. You may have trouble remembering things or concentrating, benzodiazepines can make you feel better quickly. Benzodiazepines generally work faster than other drug treatments for anxiety disorder, usually within a week. How it’s work? Benzodiazepines change the way a chemical called gamma-aminobutyric acid (GABA) works in your brain. GABA stops some cells in your brain communicating with each other, slowing down your brain. Benzodiazepines help GABA work harder, slowing down your brain even more. As a result, you feel calmer. Benzodiazepines also help you sleep.

4. Why does sedatives types of medicine have shorter duration compared to others type of medicine?

Barbiturates are types of sedatives. Barbiturates are drugs that act as central nervous system depressants, and, by virtue of this, they produce a wide spectrum of effects, from mild sedation to total anesthesia.  Ultrashort-acting barbiturates are commonly used for anesthesia because their extremely short duration of action allows for greater control. These properties allow doctors to rapidly put a patient "under" in emergency surgery situations. Doctors can also bring a patient out of anesthesia just as quickly should complications arise during surgery. The middle two classes of barbiturates are often combined under the title "short/intermediate-acting." These barbiturates are also employed for anesthetic purposes, and are also sometimes prescribed for anxiety or insomnia.

The principal mechanism of action of barbiturates is believed to be their affinity for the GABA_A receptor. GABA is the principal inhibitory neurotransmitter in the mammalian central nervous system (CNS). It plays a role in regulating neuronal excitability throughout the nervous system. Barbiturates bind to the GABA_A receptor at the alpha subunit, which are binding sites distinct from GABA itself and also distinct from the benzodiazepine binding site. Like benzodiazepines, barbiturates potentiate the effect of GABA at this receptor.

 In addition to this GABA-ergic effect, barbiturates also block the AMPA receptor, a subtype of glutamate receptor. Glutamate is the principal excitatory neurotransmitter in the mammalian CNS. Taken together, the findings that barbiturates potentiate inhibitory GABA_A receptors and inhibit excitatory AMPA receptors can explain the CNS-depressant effects of these agents. At higher concentration they inhibit the Ca²⁺-dependent release of neurotransmitters. Barbiturates produce their pharmacological effects by increasing the duration  of chloride ion channel opening at the GABA_A receptor (pharmacodynamics: this increases the efficacy of GABA), whereas benzodiazepines increase the frequency of the chloride ion channel opening at the GABA_A receptor (pharmacodynamics: this increases the potency of GABA). The direct gating or opening of the chloride ion channel is the reason for the increased toxicity of barbiturates compared to benzodiazepines in overdose.^[14][15]

Further, barbiturates are relatively "promiscious" (i.e. non-selective) compounds that bind to an entire superfamily of ligand-gated ion channels, of which the GABA_A receptor channel is only one of several representatives. Surprisingly, while GABA_A receptor currents are increased by barbiturates, ligand-gated ion channels that are predominantly permeable for cationic ions are blocked by these compounds. For example, neuronal nACHR channels are blocked by clinically relevant anaesthetic concentrations of both thiopental and pentobarbital. Such findings implicate (non-GABA-ergic) ligand-gated ion channels,  the neuronal nAChR channel, in mediating some of the (side) effects of barbiturates.

5. How would medicine affect the function of neurotransmitter?

Drugs interfere with neurotransmission. More specifically, drugs of abuse produce feelings of pleasure by altering neurotransmission by neurons in the reward system that release the neurotransmitter dopamine. Thus, drugs of abuse alter the communication between neurons that is mediated by dopamine. Because the synapse is so complex, there is a variety of sites at which drugs may affect synaptic transmission. One way to affect synaptic transmission is to increase the amount of neurotransmitter that is released into the synaptic space. Drugs like alcohol, heroin, and nicotine excite the dopamine-containing neurons in the ventral tegmental area (VTA) so that they produce more action potentials.  As the number of action potentials increases, so does the amount of dopamine released into the synapse. Amphetamines (e.g., methamphetamine, crystal, crank) actually cause the release of dopamine from the vesicles. This is independent of the rate of action potentials and, depending on dose, can cause a relatively quick and prolonged rise of extracellular dopamine levels.

Figure 3.1: Methamphetamine alters dopamine neurotransmission in two ways. Methamphetamine enters the neuron by passing directly through nerve cell membranes. It is carried to the nerve cell terminals by transporter molecules that normally carry dopamine. In the nerve terminal, methamphetamine enters the dopamine causes  the release of neurotransmitter. Methamphetamine also blocks the dopamine transporter from pumping dopamine back into the transmitting neuron. Methamphetamine acts similarly to cocaine in this way.