Signs and symptoms of opioid overdose include, but are not limited to:

- Pin-point pupils may occur. Patient presenting with dilated pupils may still be suffering an opioid overdose.

- Decreased heart rate

- Decreased body temperature

- Decreased breathing

- Altered level of consciousness. People may be unresponsive or unconscious.

- Pulmonary edema (fluid accumulation in the lungs)

- Shock

- Death

The signs and symptoms of benzodiazepine dependence include feeling unable to cope without the drug, unsuccessful

attempts to cut down or stop benzodiazepine use, tolerance to the effects of benzodiazepines, and withdrawal symptoms when not taking the drug. Some withdrawal symptoms that may appear include anxiety, depressed mood, depersonalisation, derealisation, sleep disturbance, hypersensitivity to touch and pain, tremor, shakiness, muscular aches, pains, twitches, and headache. Benzodiazepine dependence and withdrawal have been associated with suicide and self-harming behaviors, especially in young people. The Department of Health substance misuse guidelines recommend monitoring for mood disorder in those dependent on or withdrawing from benzodiazepines.

Benzodiazepine dependence is a frequent complication for those prescribed for or using for longer than four weeks, with physical dependence and withdrawal symptoms being the most common problem, but also occasionally drug-seeking behavior. Withdrawal symptoms include anxiety, perceptual disturbances, distortion of all the senses, dysphoria, and, in rare cases, psychosis and epileptic seizures.

Signs and symptoms of opioid intoxication include:

- Decreased perception of pain

- Euphoria

- Confusion

- Desire to sleep

- Nausea

- Constipation

- Miosis

Drug tolerance is a pharmacological concept describing subjects' reduced reaction to a drug following its repeated use. Increasing its dosage may re-amplify the drug's effects, however this may accelerate tolerance, further reducing the drug's effects. Drug tolerance is indicative of drug use but is not necessarily associated with drug dependence or addiction. The process of tolerance development is reversible (e.g., through a drug holiday) and can involve both physiological factors and psychological factors.

One may also develop drug tolerance to side effects, in which case tolerance is a desirable characteristic. A medical intervention that has for objective to increase tolerance (e.g., allergen immunotherapy, in which one is exposed to larger and larger amounts of allergen to decrease one's allergic reactions) is called drug desensitization.

The opposite concept to drug tolerance is drug reverse tolerance (or drug sensitization), in which case the subject's reaction or effect will increase following its repeated use. The two notions are not incompatible and tolerance may sometimes lead to reverse tolerance. For example, heavy drinkers initially develop tolerance to alcohol (requiring them to drink larger amounts to achieve a similar effect) but excessive drinking can cause liver damage, which then puts them at risk of intoxication when drinking even very small amounts of alcohol.

Drug tolerance should not be confused with drug tolerability, which refers to the degree to which overt adverse effects of a drug can be tolerated by a patient.

Typically the severity of the symptoms experienced will depend on the amount and duration of prior alcohol consumption, as well as the number and severity of previous withdrawals. Even the most severe of these symptoms can occur in as little as 2 hours after cessation; therefore, the overall unpredictability necessitates either pre-planned hospitalization, treatment coordinated with a doctor, or at the very least rapid access to medical care, and a supporting system of friends or family should be introduced prior to addressing detoxification. In many cases, however, symptoms follow a reasonably predictable time frame as exampled below:

Six to 12 hours after the ingestion of the last drink, withdrawal symptoms such as shaking, headache, sweating, anxiety, nausea or vomiting occur. Other comparable symptoms may also exist in this period. Twelve to 24 hours after cessation, the condition may progress to such major symptoms as confusion, hallucinations (with awareness of reality), tremor, agitation, and similar ailments.

At 24 to 48 hours following the last ethanol ingestion, the possibility of seizures should be anticipated. Meanwhile, none of the earlier withdrawal symptoms will have abated. Seizures carry the risk of death for the alcoholic.

Although, most often, the patient's condition begins to improve past the 48-hour mark, it can sometimes continue to increase in severity to delirium tremens, characterized by hallucinations that are indistinguishable from reality, severe confusion, more seizures, high blood pressure and fever which can persist anywhere from 4 to 12 days.

Benzodiazepine dependence is the condition resulting from repeated use of benzodiazepine drugs. It can include both a physical dependence as well as a psychological dependence and is typified by a withdrawal syndrome upon a fall in blood plasma levels of benzodiazepines, e.g., during dose reduction or abrupt withdrawal.

Signs and symptoms of alcohol withdrawal occur primarily in the central nervous system. The severity of withdrawal can vary from mild symptoms such as sleep disturbances and anxiety to severe and life-threatening symptoms such as delirium, hallucinations, and autonomic instability.

Withdrawal usually begins 6 to 24 hours after the last drink. It can last for up to one week. To be classified as alcohol withdrawal syndrome, patients must exhibit at least two of the following symptoms: increased hand tremor, insomnia, nausea or vomiting, transient hallucinations (auditory, visual or tactile), psychomotor agitation, anxiety, tonic-clonic seizures, and autonomic instability.

The severity of symptoms is dictated by a number of factors, the most important of which are degree of alcohol intake, length of time the individual has been using alcohol, and previous history of alcohol withdrawal. Symptoms are also grouped together and classified:

- Alcohol hallucinosis: patients have transient visual, auditory, or tactile hallucinations, but are otherwise clear.

- Withdrawal seizures: seizures occur within 48 hours of alcohol cessations and occur either as a single generalized tonic-clonic seizure or as a brief episode of multiple seizures.

- Delirium tremens: hyperadrenergic state, disorientation, tremors, diaphoresis, impaired attention/consciousness, and visual and auditory hallucinations. This usually occurs 24 to 72 hours after alcohol cessation. Delirium tremens is the most severe form of withdrawal and occurs in 5 to 20% of patients experiencing detoxification and 1/3 of patients experiencing withdrawal seizures.

Include the following:

- Depression

- Shaking

- Feeling unreal

- Appetite loss

- Muscle twitching

- Memory loss

- Motor impairment

- Nausea

- Muscle pains

- Dizziness

- Apparent movement of still objects

- Feeling faint

- Noise sensitivity

- Light sensitivity

- Peculiar taste

- Pins and needles

- Touch sensitivity

- Sore eyes

- Hallucinations

- Smell sensitivity

All sedative-hypnotics, e.g. alcohol, barbiturates, benzodiazepines and the nonbenzodiazepine Z-drugs have a similar mechanism of action, working on the GABA receptor complex and are cross tolerant with each other and also have abuse potential. Use of prescription sedative-hypnotics; for example the nonbenzodiazepine Z-drugs often leads to a relapse back into substance misuse with one author stating this occurs in over a quarter of those who have achieved abstinence.

Tachyphylaxis is a subcategory of drug tolerance referring to cases of sudden, short-term onset of tolerance following the administration of a drug.

Following an acute overdose of a benzodiazepine the onset of symptoms is typically rapid with most developing symptoms within 4 hours. Patients initially present with mild to moderate impairment of central nervous system function. Initial signs and symptoms include intoxication, somnolence, diplopia, impaired balance, impaired motor function, anterograde amnesia, ataxia, and slurred speech. Most patients with pure benzodiazepine overdose will usually only exhibit these mild CNS symptoms. Paradoxical reactions such as anxiety, delirium, combativeness, hallucinations, and aggression can also occur following benzodiazepine overdose. Gastrointestinal symptoms such as nausea and vomiting have also been occasionally reported.

Cases of severe overdose have been reported and symptoms displayed may include prolonged deep coma or deep cyclic coma, apnea, respiratory depression, hypoxemia, hypothermia, hypotension, bradycardia, cardiac arrest, and pulmonary aspiration, with the possibility of death. Severe consequences are rare following overdose of benzodiazepines alone but the severity of overdose is increased significantly if benzodiazepines are taken in overdose in combination with other medications. Significant toxicity may result following recreation drug misuse in conjunction with other CNS depressants such as opioids or ethanol. The duration of symptoms following overdose is usually between 12 and 36 hours in the majority of cases. The majority of drug-related deaths involve misuse of heroin or other opioids in combination with benzodiazepines or other CNS depressant drugs. In most cases of fatal overdose it is likely that lack of opioid tolerance combined with the depressant effects of benzodiazepines is the cause of death.

The symptoms of an overdose such as sleepiness, agitation and ataxia occur much more frequently and severely in children. Hypotonia may also occur in severe cases.

Sedative-hypnotics such as alcohol, benzodiazepines, and the barbiturates are known for the severe physical dependence that they are capable of inducing which can result in severe withdrawal effects. This severe neuroadaptation is even more profound in high dose drug users and misusers. A high degree of tolerance often occurs in chronic benzodiazepine abusers due to the typically high doses they consume which can lead to a severe benzodiazepine dependence. The benzodiazepine withdrawal syndrome seen in chronic high dose benzodiazepine abusers is similar to that seen in therapeutic low dose users but of a more severe nature. Extreme antisocial behaviors in obtaining continued supplies and severe drug-seeking behavior when withdrawals occur. The severity of the benzodiazepine withdrawal syndrome has been described by one benzodiazepine drug misuser who stated that I'd rather withdraw off heroin any day. If I was withdrawing from benzos you could offer me a gram of heroin or just 20mg of diazepam and I'd take the diazepam every time – I've never been so frightened in my life. Those who use benzodiazepines intermittently are less likely to develop a dependence and withdrawal symptoms upon dose reduction or cessation of benzodiazepines than those who use benzodiazepines on a daily basis.

Misuse of benzodiazepines is widespread amongst drug misusers; however, many of these people will not require withdrawal management as their use is often restricted to binges or occasional misuse. Benzodiazepine dependence when it occurs requires withdrawal treatment. There is little evidence of benefit from long-term substitution therapy of benzodiazepines, and conversely, there is growing evidence of the harm of long-term use of benzodiazepines, especially higher doses. Therefore, gradual reduction is recommended, titrated against withdrawal symptoms. For withdrawal purposes, stabilisation with a long-acting agent such as diazepam is recommended before commencing withdrawal. Chlordiazepoxide (Librium), a long-acting benzodiazepine, is gaining attention as an alternative to diazepam in substance abusers dependent on benzodiazepines due to its decreased abuse potential. In individuals dependent on benzodiazepines who have been using benzodiazepines long-term, taper regimens of 6–12 months have been recommended and found to be more successful. More rapid detoxifications e.g. of a month are not recommended as they lead to more severe withdrawal symptoms.

Tolerance leads to a reduction in GABA receptors and function; when benzodiazepines are reduced or stopped this leads to an unmasking of these compensatory changes in the nervous system with the appearance of physical and mental withdrawal effects such as anxiety, insomnia, autonomic hyperactivity and possibly seizures.

Overmedication is an inappropriate medical treatment that occurs when a patient takes unnecessary or excessive medications. This may happen because the prescriber is unaware of other medications the patient is already taking, because of drug interactions with another chemical or target population, because of human error, because of undiagnosed medical conditions or because of conflicts of interest in the pharmaceutical industry, creating-over promotion (via advertising campaigns, sales to private practice Doctors, or biased or altered medical studies) causing widespread unnecessary use of a specific medicine, or unnecessary dosage of a medicine, due to excessive profit motives in the pharmaceutical industry. This is also sometimes described as the "commercialization of medicine".

Overmedication can also occur when consumers take more medication than is prescribed or as labeled on over-the-counter (OTC) products—either intentionally or unintentionally—or when consumers unknowingly take both prescription and nonprescription drug products containing the same active ingredients. For example, overmedication (in the form of acute overdose) can occur when a prescription drug like Vicodin, which contains both hydrocodone and acetaminophen, is taken along with the nonprescription product Tylenol, which contains acetaminophen as the active ingredient. In other words, overmedication can be caused by both prescribers and consumers or their caretakers.

Another important instance of overmedication occurs when consumers are either prescribed or take additional prescribed or OTC drugs which produce the same or similar therapeutic effects. For instance, if a patient is taking a prescription strength ibuprofen product and also uses a naprosyn product—whether prescription or OTC strength—this, too, can constitute overmedication, can be dangerous, and can be costly to the patient in overall health care costs. Often consumers/patients overmedicate themselves by taking their medications at shorter intervals than prescribed or than container labels specify. As a result, medications may accumulate at higher levels, causing undesired side effects, sometimes serious, or even fatal. Such situations are often reversed through targeted deprescribing by members of the medical team.

Persons who feel that they are overmedicated tend to not to follow their physician's instructions for taking their medication.

Benzodiazepine overdose describes the ingestion of one of the drugs in the benzodiazepine class in quantities greater than are recommended or generally practiced. The most common symptoms of overdose include central nervous system (CNS) depression, impaired balance, ataxia, and slurred speech. Severe symptoms include coma and respiratory depression. Supportive care is the mainstay of treatment of benzodiazepine overdose. There is an antidote, flumazenil, but its use is controversial.

Death from single-drug benzodiazepine overdoses occur infrequently, particularly after the point of hospital admission. However, combinations of high doses of benzodiazepines with alcohol, barbiturates, opioids or tricyclic antidepressants are particularly dangerous, and may lead to severe complications such as coma or death. In 2013, benzodiazepines were involved in 31% of the estimated 22,767 deaths from prescription drug overdose in the United States. The US Food and Drug Administration (FDA) has subsequently issued a black box warning regarding concurrent use of benzodiazepines and opioids. Benzodiazepines are one of the most highly prescribed classes of drugs, and they are commonly used in self-poisoning.

The U.S Food and Drug Administration defines a serious adverse event as one when the patient outcome is one of the following:

- Death

- Life-threatening

- Hospitalization (initial or prolonged)

- Disability - significant, persistent, or permanent change, impairment, damage or disruption in the patient's body function/structure, physical activities or quality of life.

- Congenital anomaly

- Requires intervention to prevent permanent impairment or damage

Severity is a point on an arbitrary scale of intensity of the adverse event in question. The terms "severe" and "serious" when applied to adverse events are technically very different. They are easily confused but can not be used interchangeably, requiring care in usage.

A headache is severe, if it causes intense pain. There are scales like "visual analog scale" that help clinicians assess the severity. On the other hand, a headache is not usually serious (but may be in case of subarachnoid haemorrhage, subdural bleed, even a migraine may temporally fit criteria), unless it also satisfies the criteria for seriousness listed above.

Types A and B were proposed in the 1970s, and the other types were proposed subsequently when the first two proved insufficient to classify ADRs.

Medication phobia, also known as pharmacophobia, is a fear of the use of pharmacological treatments. In severe, excessive and irrational, cases it may be a type of specific phobia.

While lack of awareness by patient or doctor of adverse drug reactions can have serious consequences, having a phobia of medications can also have serious detrimental effects on patient health, for example refusal of necessary pharmacological interventions. Medication phobia can also lead to problems with medication compliance. Medication phobia can also present in parents who are concerned about giving medications to their children, fearing that the medications will do more harm than good. Medication phobia can be triggered by unpleasant adverse reactions to medications which are sometimes prescribed inappropriately or at excessive doses. Lack of awareness of the patient's predisposition to adverse effects (e.g. anxious patients and the elderly) and failure to attribute the adverse effects to the drug serves to compound the phobia. Starting at low doses and slowly increasing the medication dosage can avoid medication phobia secondary to adverse effects from developing.

Fears of medication use is also prevalent in people who have experienced unpleasant withdrawal effects from psychotropic drugs. Sometimes patients wrongly associate symptoms of an acute disease or illness with medications used to treat the disease or illness. This form of pharmacophobia can be treated by attempting to convince the patient to take test doses of the drug or another drug in the same drug class to prove to the patient that the symptoms were not due to the drug but due to the illness the drug was taken to treat.

The overmedication of children has dramatically risen with those between the ages of 2 and 5 years old who are being prescribed atypical antipsychotics for bipolar disorders, developmental disabilities, ADHD, and behavior disorders. Drug companies have benefited considerably with profits made in sales for drugs such as stimulants for hyperactive children, with half a million children in the United States receiving medication. Children have become more involved with technology resulting in less play time outside and less time spent with parents. The long hours children spend with technology has impacted their attachment development, sensory and motor development, along with socialization skills, in return causing behavioral and psychological disorders and learning disabilities being diagnosed by psychotropic medication.

According to recent data from IMS health one of the leading services for data distribution in health care, 274,000 infants (0 to 1) are on anti-anxiety drugs, and 26,000 under a year old are on antidepressants. This is only a fraction of the millions of children 5 to 12 being prescribed these same drugs.

While these drugs can provide relief from some symptoms the children may suffer, psychiatric drugs have been shown in some instances to worsen the symptoms of mental illness and can cause adverse physical effects such as liver damage, weight gain, decreased cognitive function and dependency on the drug. (1) Antidepressants have side effects that can include suicidal thoughts and worsening depression. These medications can have long lasting effects on the children and these risks need to be taken into consideration.

It's important for parents to monitor their child's behavior and regulate their environment in order to help prevent any future affective disorders. Medication is often prescribed to these children however, it alone will not teach a child to create more valuable relationships at home or in the community. Other forms of intervention can be applied to supplement the effects of medication therapy and teach the child self-regulatory behaviors and healthy coping skills. The increase of psychiatric medication of children may be a result of the declining support for caregiving, leading to psychopathology in which drugs are oftentimes the go to method of treatment. Families do not always have knowledge regarding or the means to pursue other methods of intervention such as one-on-one therapy with the child, family therapy and parenting counseling that can teach effective parenting strategies to meet their child's specific needs. There is debate that healthcare professionals have been put under pressure to perform proficiently causing the influence of piecemeal polypharmacy.

A drug interaction is a situation in which a substance (usually another drug) affects the activity of a drug when both are administered together. This action can be synergistic (when the drug's effect is increased) or antagonistic (when the drug's effect is decreased) or a new effect can be produced that neither produces on its own. Typically, interactions between drugs come to mind (drug-drug interaction). However, interactions may also exist between drugs and foods (drug-food interactions), as well as drugs and medicinal plants or herbs (drug-plant interactions). People taking antidepressant drugs such as monoamine oxidase inhibitors should not take food containing tyramine as hypertensive crisis may occur (an example of a drug-food interaction). These interactions may occur out of accidental misuse or due to lack of knowledge about the active ingredients involved in the relevant substances.

It is therefore easy to see the importance of these pharmacological interactions in the practice of medicine. If a patient is taking two drugs and one of them increases the effect of the other it is possible that an overdose may occur. The interaction of the two drugs may also increase the risk that side effects will occur. On the other hand, if the action of a drug is reduced it may cease to have any therapeutic use because of under dosage. Notwithstanding the above, on occasion these interactions may be sought in order to obtain an improved therapeutic effect. Examples of this include the use of codeine with paracetamol to increase its analgesic effect. Or the combination of clavulanic acid with amoxicillin in order to overcome bacterial resistance to the antibiotic. It should also be remembered that there are interactions that, from a theoretical standpoint, may occur but in clinical practice have no important repercussions.

The pharmaceutical interactions that are of special interest to the practice of medicine are primarily those that have negative effects for an organism. The risk that a pharmacological interaction will appear increases as a function of the number of drugs administered to a patient at the same time. Over a third (36%) of older adults in the U.S. regularly use 5 or more medications or supplements and 15% are potentially at risk for a major drug-drug interaction. Both the use of medications and subsequent adverse drug interactions have increased significantly between 2005-2011.

It is possible that an interaction will occur between a drug and another substance present in the organism (i.e. foods or alcohol). Or in certain specific situations a drug may even react with itself, such as occurs with dehydration. In other situations, the interaction does not involve any effect on the drug. In certain cases, the presence of a drug in an individual's blood may affect certain types of laboratory analysis (analytical interference).

It is also possible for interactions to occur outside an organism before administration of the drugs has taken place. This can occur when two drugs are mixed, for example, in a saline solution prior to intravenous injection. Some classic examples of this type of interaction include that thiopentone and suxamethonium should not be placed in the same syringe and same is true for benzylpenicillin and heparin. These situations will all be discussed under the same heading due to their conceptual similarity.

Drug interactions may be the result of various processes. These processes may include alterations in the pharmacokinetics of the drug, such as alterations in the absorption, distribution, metabolism, and excretion (ADME) of a drug. Alternatively, drug interactions may be the result of the pharmacodynamic properties of the drug, e.g. the co-administration of a receptor antagonist and an agonist for the same receptor.

Drug intolerance or drug sensitivity refers to an inability to tolerate the adverse effects of a medication, generally at therapeutic or subtherapeutic doses. Conversely, a patient is said to be "tolerating" a drug when they can tolerate its adverse effects. It is not to be confused with a drug allergy, which is a form of drug intolerance, but requires an immune-mediated component. It is also not to be confused with drug tolerance ("drug resistance," or tachyphylaxis) which refers to a "lack" of adverse effects even at higher than average doses. Some instances of drug intolerance are known to result from genetic variations in drug metabolism.

Intolerance to analgesics, particularly NSAIDs, is relatively common. It is thought that a variation in the metabolism of arachidonic acid is responsible for the intolerance. Symptoms include chronic rhinosinusitis with nasal polyps, asthma, gastrointestinal ulcers, angioedema, and urticaria.

Nicotine poisoning describes the symptoms of the toxic effects of nicotine following ingestion, inhalation, or skin contact. Nicotine poisoning can potentially be deadly, though serious or fatal overdoses are rare. Historically, most cases of nicotine poisoning have been the result of use of nicotine as an insecticide. More recent cases of poisoning typically appear to be in the form of Green Tobacco Sickness, or due to unintended ingestion of tobacco or tobacco products or consumption of nicotine-containing plants.

The estimated lower limit of a lethal dose of nicotine has been reported as between 500 and 1000 mg. Children may become ill following ingestion of one cigarette; ingestion of more than this may cause a child to become severely ill. The nicotine in the e-liquid of an electronic cigarette can be hazardous to infants and children, through accidental ingestion or skin contact. In some cases children have become poisoned by topical medicinal creams which contain nicotine.

People who harvest or cultivate tobacco may experience Green Tobacco Sickness (GTS), a type of nicotine poisoning caused by skin contact with wet tobacco leaves. This occurs most commonly in young, inexperienced tobacco harvesters who do not consume tobacco.

A multitude of reactions can occur during a psychedelic crisis. Some users may experience a general sense of fear or an anxiety attack. A user may be overwhelmed with the disconnection many psychedelics cause, and fear that they are going insane or will never return to reality. This can cause the user to fall into a depressive mood. Other reactions include an amplification of nameless fears; that is, fears that are unfounded and are usually not encountered in normality.

A person having a bad trip might try to harm themselves or others around them. This harm could take the form of suicidal ideation, or full-blown suicide attempts. Because of the magnification of emotions many psychedelics could possibly cause thoughts of death and intensely adverse reactions in some users. Users can believe that their death is imminent or that the very universe itself is collapsing. Rapidly accelerated aging of other people may be experienced, perpetuating the aforementioned fears to an even greater degree.

Some users may experience disorientation. The normal views of time, space and person can be substantially altered, causing fear. Some can worsen their condition by trying to fight the psychedelic experience after embarkment. There can be illusions of insects crawling over or into one's self, or of being in dirty places such as sewers. Some users may experience losing the control of their mind in form of racing thoughts.

In rare cases, an apparent complete loss of control can be observed, and the behavior a person tends to exhibit reflects a lack of normal understanding about navigation of a physical environment. This can cause accidental harm to themselves and others, including running into traffic, flailing around, or, as it may not necessarily involve physical movement, inducing a catatonic state, or causing seemingly random vocalizations, not limited to speech. This may be caused by a failure to recognize external stimuli for what it is. Stanislav Grof explains this feature:

A bad trip (drug-induced temporary psychosis or psychedelic crisis) is a disturbing experience typically associated with use of one or more of various hallucinogens of types including psychedelics, such as LSD, mescaline, psilocybin, and DMT, dissociatives, such as dextromethorphan, and phencyclidine, and deliriants, such as Salvinorin A (the active chemical of "Salvia divinorum").

The manifestations can range from feelings of vague anxiety and alienation to profoundly disturbing states of unrelieved terror, ultimate entrapment, or complete loss of self-identity. Psychedelic specialists in the therapeutic community do not necessarily consider unpleasant experiences as threatening or negative, instead focusing on their potential to greatly benefit the user when properly resolved. Bad trips can be exacerbated by the inexperience or irresponsibility of the user or the lack of proper preparation and environment for the trip, and are reflective of unresolved psychological tensions triggered during the course of the experience.

It is suggested that, at a minimum, such crises be managed by preventing the individual from harming oneself or others by whatever means necessary up to and including physical restraint, providing the patient with a safe and comfortable space, and supervising the intake until all effects of the drug have completely worn off.

Nicotine poisoning tends to produce symptoms that follow a biphasic pattern. The initial symptoms are mainly due to stimulatory effects and include nausea and vomiting, excessive salivation, abdominal pain, pallor, sweating, hypertension, tachycardia, ataxia, tremor, headache, dizziness, muscle fasciculations, and seizures. After the initial stimulatory phase, a later period of depressor effects can occur and may include symptoms of hypotension and bradycardia, central nervous system depression, coma, muscular weakness and/or paralysis, with difficulty breathing or respiratory failure.

From September 1, 2010 to December 31, 2014, there were at least 21,106 traditional cigarette calls to US poison control centers. During the same period, the ten most frequent adverse effects to traditional cigarettes reported to US poison control centers were vomiting (80.0%), nausea (9.2%), drowsiness (7.8%), cough (7.2%), agitation (6.6%), pallor (3.0%), tachycardia (2.5%), diaphoresis (1.5%), dizziness (1.5%), and diarrhea (1.4%). 95% of traditional cigarette calls were related to children 5 years old or less. Most of the traditional cigarette calls were a minor effect.

Calls to US poison control centers related to e-cigarette exposures involved inhalations, eye exposures, skin exposures, and ingestion, in both adults and young children. Minor, moderate, and serious adverse effects involved adults and young children. Minor effects correlated with e-cigarette liquid poisoning were tachycardia, tremor, chest pain and hypertension. More serious effects were bradycardia, hypotension, nausea, respiratory paralysis, atrial fibrillation and dyspnea. The exact correlation is not fully known between these effects and e-cigarettes. 58% of e-cigarette calls to US poison control centers were related to children 5 years old or less. E-cigarette calls had a greater chance to report an adverse effect and a greater chance to report a moderate or major adverse effect than traditional cigarette calls. Most of the e-cigarette calls were a minor effect.

From September 1, 2010 to December 31, 2014, there were at least 5,970 e-cigarette calls to US poison control centers. During the same period, the ten most frequent adverse effects to e-cigarettes and e-liquid reported to US poison control centers were vomiting (40.4%), eye irritation or pain (20.3%), nausea (16.8%), red eye or conjunctivitis (10.5%), dizziness (7.5%), tachycardia (7.1%), drowsiness (7.1%), agitation (6.3%), headache (4.8%), and cough (4.5%).

Anticonvulsant/sulfonamide hypersensitivity syndrome is a potentially serious hypersensitivity reaction that can be seen with drugs with an aromatic amine chemical structure, such as aromatic anticonvulsants (e.g. diphenylhydantoin, phenobarbital, phenytoin, carbamazepine, lamotrigine), sulfonamides, or other drugs with an aromatic amine (procainamide). Cross-reactivity should not occur between drugs with an aromatic amine and drugs without an aromatic amine (e.g., sulfonylureas, thiazide diuretics, furosemide, and acetazolamide); therefore, these drugs can be safely used in the future.

The hypersensitivity syndrome is characterized by a skin eruption that is initially morbilliform. The rash may also be a severe Stevens-Johnson syndrome or toxic epidermal necrolysis. Systemic manifestations occur at the time of skin manifestations and include eosinophilia, hepatitis, and interstitial nephritis. However, a subgroup of patients may become hypothyroid as part of an autoimmune thyroiditis up to 2 months after the initiation of symptoms.

This kind of adverse drug reaction is caused by the accumulation of toxic metabolites; it is not the result of an IgE-mediated reaction. The risk of first-degree relatives’ developing the same hypersensitivity reaction is higher than in the general population.

As this syndrome can present secondary to multiple anticonvulsants, the general term "anticonvulsant hypersensitivity syndrome" is favored over the original descriptive term "dilantin hypersensitivity syndrome."