DAP,Fellow

Which mental health disorder is associated with HIV?

One of the most common mental health conditions that people with HIV face is depression. Depression can range from mild to severe, and the symptoms of depression can affect your day-to-day life. Both HIV-related medical conditions and HIV medications can contribute to depression.

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The most common risks are:

Having Unprotected Sex. Most people get HIV by having sex. ...

Drug Use. Using needles to inject drugs raises the risk of HIV. ...

Having Certain Health Problems. Having a sexually transmitted infection (STI) makes a person's risk of HIV higher. ...

Blood Products. ...

Having Certain Jobs.

Is HIV a risk factor for alcohol abuse?

However, drinking alcohol and ingesting, smoking, or inhaling drugs are also associated with increased risk for HIV. These substances alter judgment, which can lead to risky sexual behaviors (e.g., having sex without a condom, having multiple partners) that can make people more likely to get and transmit HIV

Medication Naloxone in OUD,overdose :

Naloxone, sold under the brand names Narcan and Kloxxado among others, is a medication used to reverse the effects of opioids. It is commonly used to counter decreased breathing in opioid overdose. Effects begin within two minutes when given intravenously, and within five minutes when injected into a muscle

Symptoms of OUD,overdose:

The symptoms of a drug overdose may vary depending on the person, drug, and amount taken. However, universal symptoms include:

nausea and vomiting

drowsiness

loss of consciousness

trouble breathing

difficulty walking

agitation

aggression or violence

enlarged pupils

tremors

convulsions

hallucinations or delusions

You should seek medical help immediately if you have these symptoms or witness them in someone else and suspect they may have overdosed. The most obvious way to tell if these symptoms indicate overdose is if you know you have taken drugs or have seen someone else take drugs. Getting medical help quickly can make a big difference in the effectiveness of drug overdose treatment

Treatment OUD,overdose:

Treatment for a drug overdose varies depending on the situation. Knowing how much of what drug was ingested can be extremely helpful during treatment. However, this information is not always available. General treatment strategies that healthcare providers may use include:

clearing the airway or inserting a breathing tube when there is a problem with breathing

giving activated charcoal, which acts in the digestive tract to absorb the drug

inducing vomiting to remove the substance from the stomach

pumping the stomach to remove the substance from the stomach

giving intravenous fluids to help speed up the body’s removal of the substance

The healthcare provider may be able to use an antidote for certain drug overdoses. For example, the drug naloxone can help reverse the effects of a heroin overdose.

Transcriptomic and genetic studies identify NFAT5 as a candidate gene for cocaine dependence :

Cocaine reward and reinforcing effects are mediated mainly by dopaminergic neurotransmission. In this study, we aimed at evaluating gene expression changes induced by acute cocaine exposure on SH-SY5Y-differentiated cells, which have been widely used as a dopaminergic neuronal model. Expression changes and a concomitant increase in neuronal activity were observed after a 5 μM cocaine exposure, whereas no changes in gene expression or in neuronal activity took place at 1 μM cocaine. Changes in gene expression were identified in a total of 756 genes, mainly related to regulation of transcription and gene expression, cell cycle, adhesion and cell projection, as well as mitogen-activeated protein kinase (MAPK), CREB, neurotrophin and neuregulin signaling pathways. Some genes displaying altered expression were subsequently targeted with predicted functional single-nucleotide polymorphisms (SNPs) in a case–control association study in a sample of 806 cocaine-dependent patients and 817 controls. This study highlighted associations between cocaine dependence and five SNPs predicted to alter microRNA binding at the 3′-untranslated region of the NFAT5 gene. The association of SNP rs1437134 with cocaine dependence survived the Bonferroni correction for multiple testing. A functional effect was confirmed for this variant by a luciferase reporter assay, with lower expression observed for the rs1437134G allele, which was more pronounced in the presence of hsa-miR-509. However, brain volumes in regions of relevance to addiction, as assessed with magnetic resonance imaging, did not correlate with NFAT5 variation. These results suggest that the NFAT5 gene, which is upregulated a few hours after cocaine exposure, may be involved in the genetic predisposition to cocaine dependence

Introduction of Cocaine :

 Cocaine is a psychostimulant drug of abuse and its use has become a public health problem worldwide. Cocaine's pleasurable and addictive effects are thought to be mediated mainly through dopamine (DA), which is a key neurotransmitter in reward pathways.1 Cocaine binds the DA transporter producing an increase in DA concentration at the synapses and thus stimulating neurons in brain regions involved in reward and reinforcement behavior.1, 2, 3

 Cocaine's chronic and acute effects on gene expression have been studied using a broad range of animal models and experimental paradigms and procedures, including human post-mortem samples.4, 5 These studies have identified gene expression changes in the brain related to diverse functional categories including synaptic communication and neuroplasticity, receptors, ion channels and transporters, cytoskeleton, extracellular matrix, oligodentrocytes and myelin, mitochondrial function, apoptosis and cell death, transcription factors and signal transduction. Moreover, two important pathways have been found affected by changes in gene expression: the mitogen-activated protein kinase (MAPK) and the synaptic long-term potentiation signal transduction pathways.4, 5

 The repeated use of cocaine induces molecular and cellular adaptations in the central nervous system, such as synaptic changes and neuronal remodeling, and as the consumption becomes chronic those adaptations become stable.6 Individual's genetic background and environment determine the initial sensitivity to first drug exposure and how individual nerve cells and circuits adapt to chronic drug exposure, which could establish the development of addiction in some individuals but not others.7 Around 15–16% of cocaine users develop dependence, and heritability for cocaine addiction has been estimated around 60–70 %.8, 9, 10 Some of those genetic factors may lie in genes that mediate acute and chronic cocaine's effects, conferring initial vulnerability to the establishment of drug-induced adaptations.

 Compared with other drugs of abuse, relatively few association studies have been performed on cocaine dependence, and little is known about the genetic susceptibility to this psychiatric disorder.11 Some association studies have focused on candidate genes, especially on DA-related genes, the majority failing to detect associations or showing controversial results. Only associations with two genes, CNR1 (cannabinoid receptor 1, brain) and CHRNA5 (cholinergic receptor, nicotinic, alpha 5, neuronal) have been replicated so far.11, 12, 13 Other studies have assessed hundreds of single-nucleotide polymorphisms (SNPs ) in multiple genes within candidate systems, and two genome-wide association studies have been reported in cocaine dependence, identifying shared as well as specific associations in European Americans and in African American populations.14, 15, 16, 17

 We aimed at discovering novel genes involved in the susceptibility to cocaine dependence that could mediate its effects. Under the hypothesis that sequence variants in genes showing differential expression induced by cocaine may contribute to cocaine dependence, and considering the essential role that DA has in cocaine's effects and addiction, we designed a two-stage study by (i) identifying cocaine-induced changes in gene expression in a dopaminergic neuron-like model (SH-SY5Y) using microarray technology and (ii) subsequently considering differentially expressed genes as potential candidates for cocaine dependence, by assessing predicted functional SNPs in these genes through a case–control association study.

 How does the brain's reward system work in addiction ?

 Scientists now think that the brain changes associated with addiction go beyond the withdrawal phase. Addiction is characterized by a strong craving for a drug (or behavior) that dominates the addict's life and almost nothing can stop the person from engaging in the addictive activity. Addicts want everything in their lives because of their addiction. did They lose all their money on cocaine, abandon their loved ones to feed their craving for alcohol, and sometimes abandon their lives. A perplexing question for neuroscientists studying addiction is how does the brain learn to crave something so strongly, and how to reverse that craving? With new imaging techniques, we can see brain activity in real time, and we now know that addictive drugs activate a special set of neural circuits called the brain's reward system. This system controls most of our motivated behavior. But most people are hardly familiar with it.

 The brain's reward system motivates us to behave in ways like eating food and having sex that help us survive as individuals and as a species. This system organizes the behaviors that contribute to our sustainable existence, provides some of the tools necessary to perform desirable actions, and then rewards us with pleasure. Research shows that almost any normal activity, from listening to music to seeing a beautiful face that we enjoy, can activate the reward system. When this happens, not only are we stimulated, but these circuits enable our brains to encode and remember the conditions that lead to pleasure so that we can repeat the behavior and receive rewards in the future. A critical component of this system is the chemical dopamine, which is released from neurons in the circuits of the reward system and acts as a neurotransmitter. Through a combination of biochemical, electrophysiological and imaging experiments, scientists have found that all addictive drugs increase the release of dopamine in the brain. Some of them increase dopamine much more than any natural stimulant.

Reward systems:

  It is the brain's special messaging system that informs the body that its needs are met.

The reward system refers to a group of brain structures that are activated in response to reinforcing or pleasurable stimuli such as drugs and addictive drugs.

Brain Reward Circuit:

 The expression of a set of factors that increase the desired frequency or any pleasant and satisfying factor that increases the rate of response (behavior) in a person is called reward.

Dopamine:

Dopamine is a neuromodulatory molecule that plays several important roles in cells. It is an organic chemical of the catecholamine and phenethylamine families. Dopamine constitutes about 80% of the catecholamine content in the 🧠.

What type of therapy is best for addicts?

Behavioral therapy is perhaps the most commonly utilized types of treatment for addiction that is frequently used during substance rehabilitation.

A general behavioral therapeutic approach has been adapted into a variety of effective techniques

What are five types of therapy that can be used to treat alcoholism?

There are many effective, evidence-based treatment therapy options for alcoholism. Most rehab facilities will utilize some or all of following treatment methods.

@Motivational Interviewing

@Expressing empathy.

@Rolling with resistance.

@Developing self-efficacy.

@Developing discrepancy

Is CBT or DBT better for addiction?

If you experience factors that trigger addiction, such as stress, boredom, or old friends, CBT might work best for you. DBT is ideal for individuals with a dual diagnosis. However, the therapist can combine both methods or use them one after the other, depending on how you respond to treatment

Dialectical behaviour therapy:

Dialectical behaviour therapy (DBT) is a type of talking therapy. It's based on cognitive behavioural therapy (CBT), but it's specially adapted for people who feel emotions very intensely. The aim of DBT is to help you: Understand and accept your difficult feelings. Learn skills to manage them

Which is better empathy or sympathy,with addicted clients:

Sympathy is observation and acceptance of what someone else is going through. Empathy involves taking on someone else's feelings. Empathy is better than sympathy, so it is considered better

Cultural competence is comprised of four components:

(a) Awareness of one's own cultural worldview,

(b) Attitude towards cultural differences,

(c) Knowledge of different cultural practices and worldviews, and;

(d) Cross cultural Skills

The Neurobiological Basis of Opioid Addiction :

 It has been known for a long time that opioids such as morphine, heroin, and derivatives induce numerous pharmacological responses, including analgesia, dependence, respiratory depression or euphoria (4, 5). From these observations, evidence that different opioid drug effects could only be explained by the existence of stereospecific receptors has emerged. In the 1970s, the endogenous opioid receptors were discovered (6–8), followed by the characterization of the endogenous opioid peptides (9). Since these identifications numerous studies have been conducted in the opioid field.

 Historically, three opioid receptors have been characterized, mu (MOPr), delta (DOPr), and kappa (KOPr). Additional receptor types have been identified, but are no longer considered as “classical” opioid receptors (e.g., sigma, nociceptin/orphanin receptor, NOPr) (10). The three opioid receptors were cloned in the early nineties (11–14). Since this period, several knockout mice lines, each harboring deletions of the genes encoding a particular opioid receptor, have been used to clarify the specific role of the different receptors in vivo and in many physiopathological conditions (15). In this review the focus will be on reward and addiction.

 It is well-known that all drugs of abuse increase extracellular dopamine levels in the nucleus accumbens (Nac), either directly (e.g., cocaine and amphetamine directly target dopamine transporters), or indirectly (e.g., opioids decrease GABA release in the ventral tegmental area , leading to an activation of dopamine neurons). Several lines of evidence indicate that MOPr play a key role in mediating the rewarding effects of opioids, while the role of DOPr remains debatable, and KOPr are considered to have opposite functions to those of MOPr in the regulation of reward and addiction. KOPr agonists have dysphoric and aversive effects in humans and rodents (16, 17), in good agreement with decreases in dopamine release in the Nac observed following injection of selective agonists in this brain structure (18).

 The pharmacological responses induced by opioids (e.g., conditioned place preference, intravenous self-administration, locomotor activity, analgesia) are abolished in MOPr knockout mice, demonstrating that MOPr represent the primary in vivo molecular target for these ligands (15). Morphine-induced conditioned place preference in an unbiased procedure is also reduced in DOPr knockout mice (19, 20), but these animals show normal motivation to obtain morphine in intravenous self-administration paradigm (20). These results, combined with other data obtained from other experimental approaches suggest that morphine reward and motivation to obtain opioids are intact in DOPr knockout mice, however drug-context association is more certainly impaired.

 mice (19, 20), but these animals show normal motivation to obtain morphine in intravenous self-administration paradigm (20). These results, combined with other data obtained from other experimental approaches suggest that morphine reward and motivation to obtain opioids are intact in DOPr knockout mice, however drug-context association is more certainly impaired.

 Both with most clinically useful (e.g., morphine, fentanyl, oxycodone) and most largely abused (heroin) opioids, opioid-use disorder is a public health problem. The number of opioid prescriptions sharply increased in the past two decades, increasing risks for addiction and overdoses. Addiction to prescribed opioids is associated with transition to illicit opioid use like heroin (21), and overdoses have strongly risen since the 1990s (22). As mentioned earlier the notion of “opioid crisis” or “opioid epidemic” has emerged in North America, and to a lesser extent in Australia (23). European countries appear to be less affected (24), but even if the risk in Europe appears relatively limited, vigilance is needed (25).

 Opioid addiction is a brain disorder, involving alterations in neuronal circuits with complex neuroadaptative mechanisms that lead to dependence, craving, and relapse; thus contributing to the maintenance of drug use. Until now, no medication can reverse the drug-induced changes observed in the brain that are involved in the relapsing nature of opioid-use disorders, even after a protracted abstinence. Currently, the therapeutic approach using an agonist strategy with methadone and buprenorphine, has shown physical and psychosocial improvements in drug users, but these molecules possess MOPr agonist properties which limit their clinical usefulness, as described below.

 Techniques of crisis intervention :

SUSTAINMENT:

Sustainment techniques are used primarily during the initial stages of crisis intervention; the goals of sustainment are to lower the individual's anxiety, guilt, and tension and to provide emotional support.

Examples include catharsis, reassurance, encouragement, and sympathetic listening

Three steps in crisis intervention :

pre- intervention, assessment, and disposition. 

Before responding to a community or individual in crisis, find out as much as possible.