Lorazepam: The Liver’s BFF
Pharmacodynamics
Lorazepam or better know as Ativan belongs to the benzodiazepine family and produces inhibitory effects in the central nervous system. The therapeutic action of Lorazepam happens with the interaction at the benzodiazepine binding sites. These binding sites are located on the inotropic gamma-amino butyric acid-A (GABAA) receptors. The neurotransmitter used by Lorazepam is the inhibitory neurotransmitter GABA. Lorazepam and other benzodiazepines do not bind directly to the same receptor site as the endogenous GABA neurotransmitter does. As you can see from Figure 1 they bind to the benzodiazepine binding sites located in between the alpha and gamma subunits on the GABAA receptors. Once the benzodiazepine locks into the GABAA receptor it alters it, so the neurotransmitter GABA has a much higher affinity for it. Lorazepam doesn’t mimic the effects of GABA, but instead enhances GABA’s affinity for the GABAA receptor. Lorazepam doesn’t directly open the chloride gates itself. The GABA neurotransmitter is what opens the gates. With the higher affinity is becomes a pulsing motion of the gate opening and closing rendering its effects of more chloride being let in.
When GABA normally binds to the GABAA receptor it opens a chloride channel allowing chloride to rush in. When Lorazepam binds to the benzodiazepine site on the GABAA receptor it increases the rate at which the chloride channel opens when GABA attaches to them. This allows an increase in the concentration of chloride ions in the cell. This effect results in hyper-polarizing the cell making it highly negative inside, which makes it less excitable. This reversal potential of the chloride ions inhibits the firing of any new action potent...
... middle of paper ...
...
When the patient suffers from anxiety or alcohol withdrawals they receive the same dose. It is given sublingually at the dose of 2-6 mg. If the patient is in status epilepticcus then the recommend dose is 0.05 mg/kg to a max of 4 mg by a slow intravenous push. This dose is able to be repeated once in a 12 hour period. (Wyeth & Ayerst)
Local protocols may differ from this does and medical directors can decide which dose of the medication they prefer to be given. As you can see from Table 1 the dose recommend by Alberta Health Services is 1 mg sublingually and may be repeated once. More can be administered but consultation with on-line medical control would have to be done.
Lorazepam - Alcohol Withdrawal and Non-Aggressive Psychiatric
Table 1: AHS Protocols
(https://www.ahsems.com/secure/protocols/1#view/5042/Notes)
(Saari, Uusi-Oukari, Ahonen & Olkkola , 2011)
As previously stated, Lexapro is a Selective serotonin reuptake inhibitor. Selective serotonin reuptake inhibitors are by far, the most frequently prescribed antidepressants ("Selective serotonin reuptake," 2013). SSRI’s work by increasing the levels of serotonin, which is a neurotransmitter in the brain (Mandal, n.d.). Serotonin regulates some aspects of the brain including mood, sleep and emotion (Mandal, n.d.). People with depression have low levels of serotonin so the SSRIs block the reuptake of serotonin, which means a greater amount of serotonin than usual remains available in the synaptic space between the two nerves (Mandal, n.d.). SSRIs relieve symptoms of depression and anxiety, are rather safe and generally cause less side effects than other types of antidepressants ("Selective serotonin reuptake," 2013). Lexapro tablets are film coated, round tablets containing esxitalopram oxalate in strengths equal to 5mg, 10mg, and 20 mg ("Lexapro," 2004).
Synaptic Transmitters Involved in LSD Administration The nearly concurrent discovery of serotonin (5-HT) and LSD-25 in the 1950 's encouraged a lot of research to be done on the relationship between LSD and serotonin, which helped to develop a greater understanding of the role serotonin plays as a neurotransmitter in the brain (Nichols, 2004). Today it is believed that LSD (and other hallucinogens) stimulate 5-HT2A receptors (Kalat, 2004). Activation of these receptors causes cortical glutamate levels to increase. This is presumed to be a result of a "presynaptic receptor-mediated release" from neurons in the thalumus (Nichols, 2004).
Flonase 50 mcg spray OTC - instruct patient to use to use one spray per nostril daily and increase to two sprays per nostril daily if no improvement. Instructed patient on proper use of the nasal spray and to avoid spraying medication directly into nostril.
There are also explanations dealing with clozapine's interaction with the serotonin 5HT2 receptors and the glutamate receptors. ... ... middle of paper ... ... hin a week levels will increase with treatment of colazopine.(Naheed & Green, 2000) Andreasen, N.C. (1994).
Reserpine is called a vesicular monoamine transporter (VMAT) ligand because it binds to the amine substrate site of the VMAT and permanently stops the acceptance of monoamines into the secretory vesicles. Reserpine is used as an antihypertensive and an antipsychotic agent.
Its ability to inhibit sodium channels within brain cells thereby protecting the cells from hypoxia (lack of oxygen)
Over the years, my sister has been through various different medications whose intent was to control her seizure activity. A new type of treatment that her neurologist suggested trying is Valium (Diazepam). Valium is a drug that effects the limbic, thalamic and hypothalamic regions of the central nervous system. ((3).) Valium slows the central nervous system and is used to treat anxiety related disorders and conditions that cause severe muscle spasms and convulsions. ((4).) Valium is administered rectally. Liquid Valium is absorbed fast from the rectum. The effect should take place 5-15 minutes after the injection.((3).) Valium should not be used on a daily basis because it can cause withdraw and it also has many other side effects.
γ-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the CNS. GABAA is a ligand gated ion channel composed of five subunits. Through positive allosteric modulation ethanol binds to the δ subunit of the receptor and enhances the inhibitory effect of GABA. Once ethanol has bound to the GABAA receptor, chloride ions enter the post-synaptic neuron. This cascade of ions hyperpolarises the neuron, thus increasing inhibitory effects and makes the neuron less excitable. Ethanol alters the enzyme kinetics enabling the ion...
There are many options for substance addiction treatment and utilizing medication as a means of eliminating substance use is one that has been called a double edge sword. There are two schools of thought with medically assisted treatment. First, let 's define medication assisted treatment (MAT): “it is the use of pharmacological medications, in combination with counseling and behavioral therapies, to provide a “whole patient” approach to the treatment of substance use disorders. Research indicates that a combination of medication and behavioral therapies can successfully treat substance use disorders, and for some people struggling with addiction, MAT can help sustain recovery” (Watkins, 2016). One side of this treatment option is that it provides that extra little nudge to start recovery with less or more withdrawal symptoms. For example, disulfiram is an alcohol aversion agent, that when taken with alcohol the person becomes very ill (Watkins, 2016). There are also other medications that help with reducing symptoms of withdrawal, such as methadone.
Arias, M.D., A. J., & Kranzler, M.D, H. R. (n.d). Treatment of co-occurring alcohol and other drug Use disorders. Retrieved from http://pubs.niaaa.nih.gov/publications/arh312/155-167.htm
This raises an interesting question: What and/or where is the mechanism of action of clonazepam in the reduction of the
Benzodiazepine or know as benzo on the street. Benzos effect the central nervous system by slowing down the ...
Therapy can mean many different things from relaxation therapy to group therapy or even seeing a psychologist. Cognitive-behavioral therapy is one of the most effective treatment plans for patients dealing with anxiety. Cognitive-behavioral therapy deals with the patient’s problems, and helping them find different ways to cope with their situations. They help change negative thoughts into more supportive thoughts and answers. If a patient can realize what activates their anxiety they will be able to recognize when they need to talk to someone or even take their medications as prescribed. Promoting resilience is another way to help with patients cope with anxiety. “Resilience is the quality of being hardy or stress resistant.” (Karen M. Burke, 2011) Nurses or even family members can help older patients with anxiety by supporting their ADL’s, and that is encouraging resilience. The most common medications used to treat anxiety are benzodiazepines and sedative hypnotics. Benzodiazepines have a rapid onset and help react to the central nervous system. The most common side effects of benzodiazepines are sedation, weakness, lethargy, dizziness, and a decreased in organization. The most common benzodiazepines prescribed are Xanax, klonopin, valium, and Ativan. Sedative-hypnotic agents have a more sedative effect on the mind and help treat insomnia. Side effects include sedation, drowsiness, and dizziness. Most
Furosemide is available in tablets, sublingual tablets, oral suspension, and intravenously. (2) The recommended schedule dose for adults for an initial dose is 20 to 80mg. (3) The same dose as well as higher doses may be administered 6 to 8 hours following the previous dose if needed. (2) When titrating doses it may be raised by 20 to 40mg but not within 6 to 8 hours after the initial dose, and this may continue until the desi...
Due to my uncertainty, I asked the pharmacist for some tips on how to proceed. He said to use simple language and tell the patient the medication’s dose and frequency, as well as how long to take it for. He also said to mention the cautions and side effects, and which side effects would require coming back to see the pharmacist or the patient’s GP. I was also told to mention any interactions (i.e. if alcohol interacts with the drug to cause drowsiness then avoid driving). These points are in accordance with the NHS’s Patient Counselling and Consultation Skills (2014). Having a mental checklist of what to do improved my confidence when it came to talking to the patient, therefore making me feel less