Dysmelia can be caused by

- inheritance of abnormal genes, e.g. polydactyly, ectrodactyly or brachydactyly, symptoms of deformed limbs then often occur in combination with other symptoms (syndromes)

- external causes during pregnancy (thus not inherited), e.g. via amniotic band syndrome

- teratogenic drugs (e.g. thalidomide, which causes phocomelia) or environmental chemicals

- ionizing radiation (nuclear weapons, radioiodine, radiation therapy)

- infections

- metabolic imbalance

Dysmelia can refer to

- missing (aplasia) limbs: amelia, oligodactyly, congenital amputation e.g. Tibial or Radial aplasia

- malformation of limbs: shortening (micromelia, rhizomelia or mesomelia), ectrodactyly, phocomelia, meromelia, syndactyly, brachydactyly, club foot

- too many limbs: polymelia, polydactyly, polysyndactyly

- others: Tetraamelia, hemimelia, Symbrachydactyly

Placental site trophoblastic tumor is a form of gestational trophoblastic disease, which is thought to arise from intermediate trophoblast.

It may secrete human placental lactogen (human chorionic somatomammotropin), and result in a false-positive pregnancy test.

Placental site trophoblastic tumor is a monophasic neoplasm of the implantation site intermediate trophoblast, and usually a benign lesion, which comprises less than 2% of all gestational trophoblastic proliferations. Preceding conditions include molar pregnancy (5%). Compared to choriocarcinoma or invasive mole, hemorrhage is less conspicuous and serum β-HCG level is low, making early diagnosis difficult.

Immunohistochemistry: Often stains with hPL, keratin, Mel-CAM, EGFR.

Prognosis: 10–20% of cases metastase leading to death.

Treatment: Because chemotherapy is ineffective; the patient should undergo hysterectomy.

Type 2 DM is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 DM is the most common type of diabetes mellitus.

In the early stage of type 2, the predominant abnormality is reduced insulin sensitivity. At this stage, high blood sugar can be reversed by a variety of measures and medications that improve insulin sensitivity or reduce the liver's glucose production.

Type 2 DM is primarily due to lifestyle factors and genetics. A number of lifestyle factors are known to be important to the development of type 2 DM, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization. Excess body fat is associated with 30% of cases in those of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders. Even those who are not obese often have a high waist–hip ratio.

Dietary factors also influence the risk of developing type 2 DM. Consumption of sugar-sweetened drinks in excess is associated with an increased risk. The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk. Eating lots of white rice also may increase the risk of diabetes. A lack of physical activity is believed to cause 7% of cases.

Prediabetes indicates a condition that occurs when a person's blood glucose levels are higher than normal but not high enough for a diagnosis of type 2 DM.

Many people destined to develop type 2 DM spend many years in a state of prediabetes.

Latent autoimmune diabetes of adults (LADA) is a condition in which type 1 DM develops in adults. Adults with LADA are frequently initially misdiagnosed as having type 2 DM, based on age rather than cause.

Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, "malnutrition-related diabetes mellitus" (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization when the current taxonomy was introduced in 1999.

Other forms of diabetes mellitus include congenital diabetes, which is due to genetic defects of insulin secretion, cystic fibrosis-related diabetes, steroid diabetes induced by high doses of glucocorticoids, and several forms of monogenic diabetes.

"Type 3 diabetes" has been suggested as a term for Alzheimer's disease as the underlying processes may involve insulin resistance by the brain.

The following is a comprehensive list of other causes of diabetes:

- Genetic defects of β-cell function

- Maturity onset diabetes of the young

- Mitochondrial DNA mutations

- Genetic defects in insulin processing or insulin action

- Defects in proinsulin conversion

- Insulin gene mutations

- Insulin receptor mutations

- Exocrine pancreatic defects

- Chronic pancreatitis

- Pancreatectomy

- Pancreatic neoplasia

- Cystic fibrosis

- Hemochromatosis

- Fibrocalculous pancreatopathy

- Endocrinopathies

- Growth hormone excess (acromegaly)

- Cushing syndrome

- Hyperthyroidism

- Pheochromocytoma

- Glucagonoma

- Infections

- Cytomegalovirus infection

- Coxsackievirus B

- Drugs

- Glucocorticoids

- Thyroid hormone

- β-adrenergic agonists

- Statins

Among preschoolers, the prognosis for recovery is good. Based on research, about 65% of preschoolers who stutter recover spontaneously in the first two years of stuttering, and about 74% recover by their early teens. In particular, girls seem to recover well. For others, early intervention is effective in helping the child overcome disfluency.

Once stuttering has become established, and the child has developed secondary behaviors, the prognosis is more guarded, and only 18% of children who stutter after five years recover spontaneously. However, with treatment young children may be left with little evidence of stuttering.

With adult people who stutter, there is no known cure, though they may make partial recovery or even complete recovery with intervention. People who stutter often learn to stutter less severely, though others may make no progress with therapy.

Emotional sequelae associated with stuttering primarily relates to state-dependent anxiety related to the speech disorder itself. However, this is typically isolated to social contexts that require speaking, is not a trait anxiety, and this anxiety does not persist if stuttering remits spontaneously. Research attempting to correlate stuttering with generalized or state anxiety, personality profiles, trauma history, or decreased IQ have failed to find adequate empirical support for any of these claims.

In rare cases, stuttering may be acquired in adulthood as the result of a neurological event such as a head injury, tumour, stroke, or drug use. The stuttering has different characteristics from its developmental equivalent: it tends to be limited to part-word or sound repetitions, and is associated with a relative lack of anxiety and secondary stuttering behaviors. Techniques such as altered auditory feedback (see below), which may promote decreasing disfluency in people who stutter with the developmental condition, are not effective with the acquired type.

Psychogenic stuttering may also arise after a traumatic experience such as a grief, the breakup of a relationship or as the psychological reaction to physical trauma. Its symptoms tend to be homogeneous: the stuttering is of sudden onset and associated with a significant event, it is constant and uninfluenced by different speaking situations, and there is little awareness or concern shown by the speaker.

Although the incidence of underage drinking is still significant, government, university and national statistics have confirmed that alcohol use and binge drinking among high school students has declined steadily over the past three decades, and continues to decline annually. According to a United States Substance Abuse and Mental Health Services Administration study involving 30,000 youths aged 12 to 20 years old, between 2002 and 2013 the percentage of underage drinkers declined from 28.8% to 22.7%. Underage binge drinkers decreased 19.3% to 14.2%. A December 2014 study performed by the University of Michigan also found that 75% of senior high school students disapproved of drinking excessively on the weekends. Alcohol still proved to be the favored substance of abuse among American youths however, with tobacco and illicit drugs following in rank.

A survey of over 6000 teenagers revealed (1):

- Teenagers and young adults typically get their alcohol from persons 21 or older. The second most common source for high school students is someone else under age 21, and the third most common source for 18- to 20-year-old adults is buying it from a store, bar or restaurant (despite the fact that such sales are against the law).

- In the 12th grade, boys were more likely than girls to buy alcohol from a store, bar or restaurant.

- The higher a teenager's weekly income, the more likely he/she will buy alcohol from a store, bar or restaurant.

- It is easy to get alcohol at a party and from siblings or others 21 or older.

How easy is it for youth to buy alcohol?

- When young females attempted to buy beer without an ID at liquor, grocery or convenience stores, 47–52% of the attempts, beer was sold (1, 2) and nearly 80% of all the stores sold beer to the buyers at least once in three attempts; nearly 25% sold beer all three times.(1)

- When young females attempted to buy beer without an ID at bars or restaurants, 50% of the attempts resulted in a sale to the buyer.(2)

- When young males and females attempted to buy beer without an ID at community festivals, 50% of the attempts resulted in a sale to the buyer.(3)