Chemotherapy-induced nausea and vomiting (CINV) is a common side-effect of many cancer treatments. Nausea and vomiting are two of the most feared cancer treatment-related side effects for cancer patients and their families. In 1983, Coates et al. found that patients receiving chemotherapy ranked nausea and vomiting as the first and second most severe side effects, respectively. Up to 20% of patients receiving highly emetogenic agents in this era postponed, or even refused, potentially curative treatments. Since the 1990s, several novel classes of antiemetics have been developed and commercialized, becoming a nearly universal standard in chemotherapy regimens, and helping to better manage these symptoms in a large portion of patients. Efficient mediation of these unpleasant and sometimes crippling symptoms results in increased quality of life for the patient, and better overall health of the patient, and, due to better patient tolerance, more effective treatment cycles.

There are several subtypes of CINV. The classifications of nausea and vomiting are:

- Acute: occurring within 24 hours of chemotherapy

- Delayed: occurring between 24 hours and 5 days after treatment

- Breakthrough: occurring despite prophylactic treatment

- Anticipatory: triggered by taste, odor, memories, visions, or anxiety related to chemotherapy

- Refractory: occurring during subsequent cycles when antiemetics have failed in earlier cycles

The signs and symptoms of paracetamol toxicity occur in three phases. The first phase begins within hours of overdose, and consists of nausea, vomiting, a pale appearance, and sweating. However, patients often have no specific symptoms or only mild symptoms in the first 24 hours of poisoning. Rarely, after massive overdoses, patients may develop symptoms of metabolic acidosis and coma early in the course of poisoning.

The second phase occurs between 24 h and 72 h following overdose and consists of signs of increasing liver damage. In general, damage occurs in liver cells as they metabolize the paracetamol. The individual may experience right upper quadrant abdominal pain. The increasing liver damage also changes biochemical markers of liver function; International normalized ratio (INR) and the liver transaminases ALT and AST rise to abnormal levels. Acute kidney failure may also occur during this phase, typically caused by either hepatorenal syndrome or multiple organ dysfunction syndrome. In some cases, acute kidney failure may be the primary clinical manifestation of toxicity. In these cases, it has been suggested that the toxic metabolite is produced more in the kidneys than in the liver.

The third phase follows at 3 to 5 days, and is marked by complications of massive liver necrosis leading to fulminant liver failure with complications of coagulation defects, low blood sugar, kidney failure, hepatic encephalopathy, brain swelling, sepsis, multiple organ failure, and death. If the third phase is survived, the liver necrosis runs its course, and liver and kidney function typically return to normal in a few weeks. The severity of paracetamol toxicity varies depending on the dose and whether appropriate treatment is received.

Aspirin overdose has potentially serious consequences, sometimes leading to significant morbidity and death. Patients with mild intoxication frequently have nausea and vomiting, abdominal pain, lethargy, ringing in the ears, and dizziness. More significant signs and symptoms occur in more severe poisonings and include high body temperature, fast breathing rate, respiratory alkalosis, metabolic acidosis, low blood potassium, low blood glucose, hallucinations, confusion, seizure, cerebral edema, and coma. The most common cause of death following an aspirin overdose is cardiopulmonary arrest usually due to pulmonary edema.

Paracetamol poisoning, also known as acetaminophen poisoning, is caused by excessive use of the medication paracetamol (acetaminophen). Most people have few or non-specific symptoms in the first 24 hours following overdose. This may include feeling tired, abdominal pain, or nausea. This is typically followed by a couple of days without any symptoms after which yellowish skin, blood clotting problems, and confusion occurs. Additional complications may include kidney failure, pancreatitis, low blood sugar, and lactic acidosis. If death does not occur, people tend to recover fully over a couple of weeks. Without treatment some cases will resolve while others will result in death.

Paracetamol poisoning can occur accidentally or as an attempt to end one's life. Risk factors for toxicity include alcoholism, malnutrition, and the taking of certain other medications. Liver damage results not from paracetamol itself, but from one of its metabolites, "N"-acetyl-"p"-benzoquinone imine (NAPQI). NAPQI decreases the liver's glutathione and directly damages cells in the liver. Diagnosis is based on the blood level of paracetamol at specific times after the medication was taken. These values are often plotted on the Rumack-Matthew nomogram to determine level of concern.

Treatment may include activated charcoal if the person presents soon after the overdose. Attempting to force the person to vomit is not recommended. If there is a potential for toxicity, the antidote acetylcysteine is recommended. The medication is generally given for at least 24 hours. Psychiatric care may be required following recovery. A liver transplant may be required if damage to the liver becomes severe. The need for transplant is often based on low blood pH, high blood lactate, poor blood clotting, or significant hepatic encephalopathy. With early treatment liver failure is rare. Death occurs in about 0.1% of cases.

Paracetamol poisoning was first described in the 1960s. Rates of poisoning vary significantly between regions of the world. In the United States more than 100,000 cases occur a year. In the United Kingdom it is the medication responsible for the greatest number of overdoses. Young children are most commonly affected. In the United States and the United Kingdom paracetamol is the most common cause of acute liver failure.

Salicylate poisoning, also known as aspirin poisoning, is the acute or chronic poisoning with a salicylate such as aspirin. The classic symptoms are ringing in the ears, nausea, abdominal pain, and a fast breathing rate. Early on these may be subtle while larger doses may result in fever. Complications can include swelling of the brain or lungs, seizures, low blood sugar, or cardiac arrest.

While usually due to aspirin, other possible causes include oil of wintergreen and bismuth subsalicylate. Excess doses can be either on purpose or accidental. Small amounts of oil of wintergreen can be toxic. Diagnosis is generally based on repeated blood tests measuring aspirin levels and blood gases. While a type of graph has been created to try to assist with diagnosis, its general use is not recommended. In overdose maximum blood levels may not occur for more than 12 hours.

Efforts to prevent poisoning include child-resistant packaging and a lower number of pills per package. Treatment may include activated charcoal, intravenous sodium bicarbonate with dextrose and potassium chloride, and dialysis. Giving dextrose may be useful even if the blood sugar is normal. Dialysis is recommended in those with kidney failure, decreased level of consciousness, blood pH less than 7.2, or high blood salicylate levels. If a person requires intubation a fast respiratory rate may be required.

The toxic effects of salicylates have been described since at least 1877. In 2004 more than 20,000 cases with 43 deaths were reported in the United States. About 1% of those with an acute overdose die while chronic overdoses may have worse outcomes. Older people are at higher risks of toxicity for any given dose.

Invasive candidiasis can manifest as serious diseases including as fungemia, endocarditis, endophthalmitis, osteomyelitis, and central nervous system infections.

Symptoms of invasive candidiasis can be confused with other medical conditions, however, the most common symptoms are fever and chills that do not improve with antibiotic treatment. Other symptoms develop as the infection spreads, depending on which parts of the body are involved.

Zinc toxicity is a medical condition involving an overdose on, or toxic overexposure to, zinc. Such toxicity levels have been seen to occur at ingestion of greater than 225 mg of zinc. Excessive absorption of zinc can suppress copper and iron absorption. The free zinc ion in solution is highly toxic to bacteria, plants, invertebrates, and even vertebrate fish. Zinc is an essential trace metal with very low toxicity in humans.

Following an oral intake of extremely high doses of zinc (where 300 mg Zn/d – 20 times the US RDA – is a "low intake" overdose), nausea, vomiting, pain, cramps and diarrhea may occur. There is evidence of induced copper deficiency, alterations of blood lipoprotein levels, increased levels of LDL, and decreased levels of HDL at long-term intakes of 100 mg Zn/d. The USDA RDA is 15 mg Zn/d.

There is also a condition called the "zinc shakes" or "zinc chills" or metal fume fever that can be induced by the inhalation of freshly formed zinc oxide formed during the welding of galvanized materials.

The primary symptoms of hypotension are lightheadedness or dizziness.

If the blood pressure is sufficiently low, fainting may occur.

Low blood pressure is sometimes associated with certain symptoms, many of which are related to causes rather than effects of hypotension:

- chest pain

- shortness of breath

- irregular heartbeat

- fever higher than 38.3 °C (101 °F)

- headache

- stiff neck

- severe upper back pain

- cough with sputum

- Prolonged diarrhea or vomiting

- dyspepsia (indigestion)

- dysuria (painful urination)

- adverse effect of medications

- acute, life-threatening allergic reaction

- seizures

- loss of consciousness

- profound fatigue

- temporary blurring or loss of vision

- Black tarry stools

Cobalt poisoning is intoxication caused by excessive levels of cobalt in the body. Cobalt is an essential element for health in animals in minute amounts as a component of Vitamin B. A deficiency of cobalt, which is very rare, is also potentially lethal, leading to pernicious anemia.

Hypokalemic periodic paralysis (hypoKPP) is a rare, autosomal dominant channelopathy characterized by muscle weakness or paralysis when there is a fall in potassium levels in the blood. In individuals with this mutation, attacks often begin in adolescence and most commonly occur on awakening or after sleep or rest following strenuous exercise (attacks during exercise are rare), high carbohydrate meals, meals with high sodium content, sudden changes in temperature, and even excitement, noise, flashing lights and cold temperatures. Weakness may be mild and limited to certain muscle groups, or more severe full-body paralysis. During an attack reflexes may be decreased or absent. Attacks may last for a few hours or persist for several days. Recovery is usually sudden when it occurs, due to release of potassium from swollen muscles as they recover. Some patients may fall into an abortive attack or develop chronic muscle weakness later in life.

Some people only develop symptoms of periodic paralysis due to hyperthyroidism (overactive thyroid). This entity is distinguished with thyroid function tests, and the diagnosis is instead called thyrotoxic periodic paralysis.

Individuals with CPH suffer multiple short, severe headaches a day, often more than five, with most lasting between 5 and 30 minutes each. When compared to cluster headaches, CPH attacks are typically shorter. Each headache is centered around the eye, temple and forehead and is localized to one side of the head. While redness and watering of the eye are associated with CPH, patients typically do not experience nausea or vomiting.

Hypernatremia, also spelled hypernatraemia, is a high sodium ion level in the blood. Early symptoms may include a strong feeling of thirst, weakness, nausea, and loss of appetite. Severe symptoms include confusion, muscle twitching, and bleeding in or around the brain. Normal serum sodium levels are 135 – 145 mmol/L (135 – 145 mEq/L). Hypernatremia is generally defined as a serum sodium level of more than 145 mmol/L. Severe symptoms typically only occur when levels are above 160 mmol/L.

Hypernatremia is typically classified by a person's fluid status into low volume, normal volume, and high volume. Low volume hypernatremia can occur from sweating, vomiting, diarrhea, diuretic medication, or kidney disease. Normal volume hypernatremia can be due to fever, inappropriately decreased thirst, prolonged increased breath rate, diabetes insipidus, and from lithium among other causes. High volume hypernatremia can be due to hyperaldosteronism, be health care caused such as when too much intravenous 3% normal saline or sodium bicarbonate is given, or rarely be from eating too much salt. Low blood protein levels can result in a falsely high sodium measurement. The cause can usually be determined by the history of events. Testing the urine can help if the cause is unclear.

If the onset of hypernatremia was over a few hours, then it can be corrected relatively quickly using intravenous normal saline and 5% dextrose. Otherwise, correction should occur slowly with, for those unable to drink water, half-normal saline. Hypernatremia due to diabetes insipidus as a result of a brain disorder, may be treated with the medication desmopressin. If the diabetes insipidus is due to kidney problems the medication which is causing it may need to be stopped. Hypernatremia affects 0.3–1% of people in hospital. It most often occurs in babies, those with impaired mental status, and the elderly. Hypernatremia is associated with an increased risk of death but it is unclear if it is the cause.

Hypotension is low blood pressure, especially in the arteries of the systemic circulation. Blood pressure is the force of blood pushing against the walls of the arteries as the heart pumps out blood. A systolic blood pressure of less than 90 millimeters of mercury (mm Hg) or diastolic of less than 60 mm Hg is generally considered to be hypotension. However, in practice, blood pressure is considered too low only if noticeable symptoms are present.

Hypotension is the opposite of hypertension, which is high blood pressure. It is best understood as a physiological state, rather than a disease. Severely low blood pressure can deprive the brain and other vital organs of oxygen and nutrients, leading to a life-threatening condition called shock.

For some people who exercise and are in top physical condition, low blood pressure is a sign of good health and fitness.

For many people, excessively low blood pressure can cause dizziness and fainting or indicate serious heart, endocrine or neurological disorders.

Treatment of hypotension may include the use of intravenous fluids or vasopressors. When using vasopressors, trying to achieve a mean arterial pressure (MAP) of greater than 70 mmHg does not appear to result in better outcomes than trying to achieve a MAP of greater than 65 mm Hg in adults.

The major symptom is thirst. The most important signs result from brain cell shrinkage and include confusion, muscle twitching or spasms. With severe elevations, seizures and comas may occur.

Severe symptoms are usually due to acute elevation of the plasma sodium concentration to above 157 mmol/L (normal blood levels are generally about 135–145 mmol/L for adults and elderly). Values above 180 mmol/L are associated with a high mortality rate, particularly in adults. However, such high levels of sodium rarely occur without severe coexisting medical conditions. Serum sodium concentrations have ranged from 150–228 mmol/L in survivors of acute salt overdosage, while levels of 153–255 mmol/L have been observed in fatalities. Vitreous humor is considered to be a better postmortem specimen than postmortem serum for assessing sodium involvement in a death.

Many secondary conditions have been reported to be possible causes of CPH, according to Mehta et al., most of which are arterial abrasions or tumors. These include aneurysms in the circle of Willis, middle cerebral artery infarction, parietal arteriovenous malformation, cavernous sinus and petrous ridge meningiomas, pituitary adenoma, Pancoast tumor, gangliocytoma of the sella turcica, and malignant frontal tumors. This accentuates the urgency for those diagnosed with CPH to receive an MRI head scan.

Microsporidiosis is an opportunistic intestinal infection that causes diarrhea and wasting in immunocompromised individuals (HIV, for example). It results from different species of microsporidia, a group of microbial (unicellular) fungi.

In HIV infected individuals, microsporidiosis generally occurs when CD4+ T cell counts fall below 150.

Substantial numbers of patients with intestinal malabsorption present initially with symptoms or laboratory abnormalities that point to other organ systems in the absence of or overshadowing symptoms referable to the gastrointestinal tract. For example, there is increasing epidemiologic evidence that more patients with coeliac disease present with anemia and osteopenia in the absence of significant classic gastrointestinal symptoms. Microcytic, macrocytic, or dimorphic anemia may reflect impaired iron, folate, or vitamin B12 absorption. Purpura, subconjunctival hemorrhage, or even frank bleeding may reflect hypoprothrombinemia secondary to vitamin K malabsorption. Osteopenia is common, especially in the presence of steatorrhea. Impaired calcium and vitamin D absorption and chelation of calcium by unabsorbed fatty acids resulting in fecal loss of calcium may all contribute. If calcium deficiency is prolonged, secondary hyperparathyroidism may develop. Prolonged malnutrition may induce amenorrhea, infertility, and impotence. Edema and even ascites may reflect hypoproteinemia associated with protein losing enteropathy caused by lymphatic obstruction or extensive mucosal inflammation. Dermatitis and peripheral neuropathy may be caused by malabsorption of specific vitamins or micronutrients and essential fatty acids.

Exposure to cobalt metal dust is most common in the fabrication of tungsten carbide. Another potential source is wear and tear of metal-on-metal hip prostheses; however, this is a relatively uncommon phenomenon with 18 reported cases being documented in the medical literature.

Symptoms may include palpitations, feeling faint, sweating, shortness of breath, and chest pain. Episodes start and end suddenly.

Affected infants present within a few months after birth with failure to thrive and severe folate deficiency manifested as macrocytic anemia and developmental delays. There can be (i) pancytopenia, (ii) diarrhea and/or mucositis and/or (iii) immune deficiency due to T-cell dysfunction and hypoimmunoglobulinemia resulting in pneumonia usually due to Pneumocystis jirovecii. Recently, several infants with the immune deficiency syndrome were described. Untreated, or with inadequate treatment, there are progressive systemic and neurological signs with a spectrum of manifestations including seizures that are often intractable. Females with HFM are fertile and, if folate sufficient during pregnancy, have normal offspring. Subjects that carry one mutated PCFT allele are normal. The genomic and clinical features of HFM were recently reviewed.

Hereditary folate malabsorption (HFM - OMIM #229050) is a rare autosomal recessive disorder caused by loss-of-function mutations in the proton-coupled folate transporter (PCFT) gene, resulting in systemic folate deficiency and impaired delivery of folate to the brain.

Symptoms can manifest in a variety of ways and features might give a clue to the underlying condition. Symptoms can be intestinal or extra-intestinal - the former predominates in severe malabsorption.

- Diarrhoea, often steatorrhoea, is the most common feature. Watery, diurnal and nocturnal, bulky, frequent stools are the clinical hallmark of overt malabsorption. It is due to impaired water, carbohydrate and electrolyte absorption or irritation from unabsorbed fatty acid. The latter also results in bloating, flatulence and abdominal discomfort. Cramping pain usually suggests obstructive intestinal segment e.g. in Crohn's disease, especially if it persists after defecation.

- Weight loss can be significant despite increased oral intake of nutrients.

- Growth retardation, failure to thrive, delayed puberty in children

- Swelling or oedema from loss of protein

- Anaemias, commonly from vitamin B, folic acid and iron deficiency presenting as fatigue and weakness.

- Muscle cramp from decreased vitamin D, calcium absorption. Also lead to osteomalacia and osteoporosis

- Bleeding tendencies from vitamin K and other coagulation factor deficiencies.