Some PanNETs do not cause any symptoms, in which case they may be discovered incidentally on a CT scan performed for a different purpose. Symptoms such as abdominal or back pain or pressure, diarrhea, indigestion, or yellowing of the skin and whites of the eyes can arise from the effects of a larger PanNET tumor, either locally or at a metastasis. About 40% of PanNETS have symptoms related to excessive secretion of hormones or active polypeptides and are accordingly labeled as "functional"; the symptoms reflect the type of hormone secreted, as discussed below. Up to 60% of PanNETs are nonsecretory or nonfunctional, in which there is no secretion, or the quantity or type of products, such as pancreatic polypeptide (PPoma), chromogranin A, and neurotensin, do not cause a clinical syndrome although blood levels may be elevated. In total, 85% of PanNETs have an elevated blood marker.

Functional tumors are often classified by the hormone most strongly secreted, for example:

- gastrinoma: the excessive gastrin causes Zollinger–Ellison syndrome (ZES) with peptic ulcers and diarrhea

- insulinoma: hypoglycemia occurs with concurrent elevations of insulin, proinsulin and C peptide

- glucagonoma: the symptoms are not all due to glucagon elevations, and include a rash, sore mouth, altered bowel habits, venous thrombosis, and high blood glucose levels

- VIPoma, producing excessive vasoactive intestinal peptide, which may cause profound chronic watery diarrhea and resultant dehydration, hypokalemia, and achlorhydria (WDHA or pancreatic cholera syndrome)

- somatostatinoma: these rare tumors are associated with elevated blood glucose levels, achlorhydria, cholelithiasis, and diarrhea

- less common types include ACTHoma, CRHoma, calcitoninoma, GHRHoma, GRFoma, and parathyroid hormone–related peptide tumor

In these various types of functional tumors, the frequency of malignancy and the survival prognosis have been estimated dissimilarly, but a pertinent accessible summary is available.

PanNETs are sometimes abbreviated as PETs or PNETs: such use should not to be confused with the primitive neuroectodermal tumor (PNET).

The majority of PanNETs are benign, while some are malignant. The World Health Organization (WHO) classification scheme places neuroendocrine tumors into three main categories, which emphasize the tumor grade rather than the anatomical origin. In practice, those tumors termed well or intermediately differentiated PanNETs in the WHO scheme are sometimes called "islet cell tumors." The high grade subtype, termed neuroendocrine cancer (NEC) in the WHO scheme, is synonymous with "islet cell carcinoma".

Somatostatinoma is a malignant tumor of the delta cells of the endocrine pancreas that produces somatostatin. Increased levels of somatostatin inhibit pancreatic hormones and gastrointestinal hormones. Thus somatostatinomas are associated with mild diabetes mellitus (due to inhibition of insulin release), steatorrhoea and gallstones (due to inhibition of cholecystokinin release), and achlorhydria (due to inhibition of gastrin release). Somatostatinomas are commonly found in head of pancreas.

In a normal subject actions of somatostatin include:

This explains how abnormally elevated somatostatin can cause diabetes mellitus, by inhibiting insulin secretion, steatorrhoea by inhibiting cholecystokinin and secretin, gall stones by inhibiting cholecystokinin which normally induce gallbladder myocytes to contract, and hypochlorhydria caused by inhibiting gastrin, which normally stimulate acid secretion.

Somatostatinomas are associated with calcium deposits called psammoma bodies.

From early adolescence, patients with this condition gradually (and much of the time 'silently') develop hundreds to thousands of colorectal polyps (and sometimes polyps elsewhere)—small abnormalities at the surface of the intestinal tract, especially in the large intestine including the colon or rectum. These may bleed, leading to blood in the stool. If the blood is not visible, it is still possible for the patient to develop anemia due to gradually developing iron deficiency. If malignancy develops, this may present with weight loss, altered bowel habit, or even metastasis to the liver or elsewhere. FAP can also develop 'silently' in some individuals, giving few or no signs until it has developed into advanced colorectal cancer.

Because familial polyposis develops very gradually over years, and can also manifest in an 'attenuated' form even more gradually, polyps resulting from FAP can lead to cancer developing at any point from adolescence to old age.

Depending on the nature of the defect in the APC gene, and whether it is the full or attenuated form, familial polyposis may manifest as polyps in colon or in the duodenal tract, or in any combination of these. Therefore, an absence of polyps in, for example, the rectum, may not of itself be sufficient to confirm absence of polyps. It may be necessary to consider and visually examine other possible parts of the intestinal tract. Colonoscopy is preferred over sigmoidoscopy for this, as it provides better observation of the common right-side location of polyps.

The genetic determinant in familial polyposis may also predispose carriers to other malignancies, e.g., of the duodenum and stomach (particularly ampullary adenocarcinoma). Other signs that may point to FAP are pigmented lesions of the retina ("CHRPE—congenital hypertrophy of the retinal pigment epithelium"), jaw cysts, sebaceous cysts, and osteomata (benign bone tumors). The combination of polyposis, osteomas, fibromas and sebaceous cysts is termed "Gardner's syndrome" (with or without abnormal scarring).

Periampullary cancer is a cancer that forms near the ampulla of Vater, an enlargement of the ducts from the liver and pancreas where they join and enter the small intestine.It consists of:

1. ampullary tumour from ampulla of Vater,

2. cancer of lower common bile duct, and

3. duodenal cancer adjacent to ampulla.

4. carcinoma head of pancreas

It presents with painless jaundice which may have waxing and waning nature because at times the sloughing of the tumor tissue relieves the obstruction partially.

Familial adenomatous polyposis (FAP) is an autosomal dominant inherited condition in which numerous adenomatous polyps form mainly in the epithelium of the large intestine. While these polyps start out benign, malignant transformation into colon cancer occurs when they are left untreated. Three variants are known to exist, FAP and attenuated FAP (originally called hereditary flat adenoma syndrome) are caused by APC gene defects on chromosome 5 while autosomal recessive FAP (or MYH-associated polyposis) is caused by defects in the "MUTYH" gene on chromosome 1. Of the three, FAP itself is the most severe and most common; although for all three, the resulting colonic polyps and cancers are confined to the colon wall and removal can greatly reduce the spread of cancer.

The root cause of FAP is understood to be a genetic mutation—a flaw in the body's tumour suppressor genes that prevent development of tumours. The flaw allows numerous cells of the intestinal wall to develop into potentially cancerous polyps when they would usually reach the end of their life; inevitably one or more will eventually progress and give rise to cancer (7% risk by age 21, rising to 87% by age 45 and 93% by age 50). The flawed genes do not trigger cancer, but rather, they reduce the body's ability to protect against the risk of aged cells becoming cancerous. Even with the flawed gene, it may still take time before a cell actually does develop that is cancerous as a result, and the gene may in some cases still partially operate to control tumours, therefore cancer from FAP takes many years to develop and is almost always an adult-onset disease.

The second form of FAP, known as attenuated familial adenomatous polyposis has the APC gene functional but slightly impaired. It is therefore somewhat able to operate as usual. Attenuated FAP still presents a high 70% lifetime risk of cancer (as estimated), but typically presents with far fewer polyps (typically 30) rather than the hundreds or thousands usually found in FAP, and arises at an age when FAP is usually no longer considered likely—typically between 40 and 70 years old (average 55) rather than the more usual 30's upward. Because it has far fewer polyps, options for management may be different.

The third variant, autosomal recessive familial adenomatous polyposis or MYH-associated polyposis, is also milder and, as its name suggests, requires both parents to be 'carriers' to manifest the condition.

In some cases FAP can manifest higher in the colon than usual (for example, the ascending colon, or proximal to the splenic flexure, or in the gastric or duodenal tracts) where they show no symptoms until cancer is present and greatly advanced. APC mutations have been linked to certain other cancers such as thyroid cancer. As the mutation causing FAP is genetic, it can be inherited hereditarily from either parent, and passed to children. A genetic blood test of the APC gene exists that can determine whether it is deficient, and therefore can predict the possibility of FAP. Individuals at risk (due to family links or genetic testing) are usually offered routine monitoring of the intestinal tract every 1 – 5 years for life, from early adulthood, to detect the slow-forming polyps and act if found, before they can pose a threat. International polyposis registries exists that track known cases of FAP or APC gene defects, for research and clinical purposes. Mutation of APC also occurs commonly in incident cases of colorectal carcinoma, emphasizing its importance in this form of cancer.

Different concentrations of alcohol in the human body have different effects on the subject.

The following lists the common effects of alcohol on the body, depending on the blood alcohol concentration (BAC). However, tolerance varies considerably between individuals, as does individual response to a given dosage; the effects of alcohol differ widely between people. Hence, BAC percentages are just estimates used for illustrative purposes.

- Euphoria (BAC = 0.03% to 0.12%):

- Overall improvement in mood and possible euphoria

- Increased self-confidence

- Increased sociability

- Decreased anxiety

- Shortened attention span

- Flushed appearance

- Impaired judgment

- Impaired fine muscle coordination

- Lethargy (BAC = 0.09% to 0.25%)

- Sedation

- Impaired memory and comprehension

- Delayed reactions

- Ataxia; balance difficulty; unbalanced walk

- Blurred vision; other senses may be impaired

- Confusion (BAC = 0.18% to 0.30%)

- Profound confusion

- Impaired senses

- Analgesia

- Increased ataxia; impaired speech; staggering

- Dizziness often associated with nausea ("the spins")

- Vomiting (emesis)

- Stupor (BAC = 0.25% to 0.40%)

- Severe ataxia

- Lapses in and out of consciousness

- Unconsciousness

- Anterograde amnesia

- Vomiting (death may occur due to inhalation of vomit (pulmonary aspiration) while unconscious)

- Respiratory depression (potentially life-threatening)

- Decreased heart rate (usually results in coldness and/or numbness of the limbs)

- Urinary incontinence

- Coma (BAC = 0.35% to 0.80%)

- Unconsciousness (coma)

- Depressed reflexes (i.e., pupils do not respond appropriately to changes in light)

- Marked and life-threatening respiratory depression

- Markedly decreased heart rate

- Most deaths from alcohol poisoning are caused by dosage levels in this range.

The short-term effects of alcohol (also known formally as ethanol) consumption–due to drinking beer, wine, distilled spirits or other alcoholic beverages–range from a decrease in anxiety and motor skills and euphoria at lower doses to intoxication (drunkenness), stupor, unconsciousness, anterograde amnesia (memory "blackouts"), and central nervous system depression at higher doses. Cell membranes are highly permeable to alcohol, so once alcohol is in the bloodstream it can diffuse into nearly every cell in the body.

The concentration of alcohol in blood is measured via blood alcohol content (BAC). The amount and circumstances of consumption play a large part in determining the extent of intoxication; for example, eating a heavy meal before alcohol consumption causes alcohol to absorb more slowly. The amount of alcohol consumed largely determines the extent of hangovers, although hydration also plays a role. After excessive drinking, stupor and unconsciousness can occur. Extreme levels of consumption can lead to alcohol poisoning and death (a concentration in the blood stream of 0.40% will kill half of those affected). Alcohol may also cause death indirectly, by asphyxiation from vomit.

Alcohol can greatly exacerbate sleep problems. During abstinence, residual disruptions in sleep regularity and sleep patterns are the greatest predictors of relapse.

Up to 10% of women with ectopic pregnancy have no symptoms, and one-third have no medical signs. In many cases the symptoms have low specificity, and can be similar to those of other genitourinary and gastrointestinal disorders, such as appendicitis, salpingitis, rupture of a corpus luteum cyst, miscarriage, ovarian torsion or urinary tract infection. Clinical presentation of ectopic pregnancy occurs at a mean of 7.2 weeks after the last normal menstrual period, with a range of 4 to 8 weeks. Later presentations are more common in communities deprived of modern diagnostic ability.

Signs and symptoms of ectopic pregnancy include increased hCG, vaginal bleeding (in varying amounts), sudden lower abdominal pain, pelvic pain, a tender cervix, an adnexal mass, or adnexal tenderness. In the absence of ultrasound or hCG assessment, heavy vaginal bleeding may lead to a misdiagnosis of miscarriage. Nausea, vomiting and diarrhea are more rare symptoms of ectopic pregnancy.

Rupture of an ectopic pregnancy can lead to symptoms such as abdominal distension, tenderness, peritonism and hypovolemic shock. A woman with ectopic pregnancy may be excessively mobile with upright posturing, in order to decrease intrapelvic blood flow, which can lead to swelling of the abdominal cavity and cause additional pain.

Ectopic pregnancy, also known as tubal pregnancy, is a complication of pregnancy in which the embryo attaches outside the uterus. Signs and symptoms classically include abdominal pain and vaginal bleeding. Less than 50 percent of affected women have both of these symptoms. The pain may be described as sharp, dull, or crampy. Pain may also spread to the shoulder if bleeding into the abdomen has occurred. Severe bleeding may result in a fast heart rate, fainting, or shock. With very rare exceptions the fetus is unable to survive.

Risk factors for ectopic pregnancy include: pelvic inflammatory disease, often due to Chlamydia infection, tobacco smoking, prior tubal surgery, a history of infertility, and the use of assisted reproductive technology. Those who have previously had an ectopic pregnancy are at much higher risk of having another one. Most ectopic pregnancies (90%) occur in the Fallopian tube which are known as tubal pregnancies. Implantation can also occur on the cervix, ovaries, or within the abdomen. Detection of ectopic pregnancy is typically by blood tests for human chorionic gonadotropin (hCG) and ultrasound. This may require testing on more than one occasion. Ultrasound works best when performed from within the vagina. Other causes of similar symptoms include: miscarriage, ovarian torsion, and acute appendicitis.

Prevention is by decreasing risk factors such as chlamydia infections through screening and treatment. While some ectopic pregnancies will resolve without treatment, this approach has not been well studied as of 2014. The use of the medication methotrexate works as well as surgery in some cases. Specifically it works well when the beta-HCG is low and the size of the ectopic is small. Surgery is still typically recommended if the tube has ruptured, there is a fetal heartbeat, or the person's vital signs are unstable. The surgery may be laparoscopic or through a larger incision, known as a laparotomy. Outcomes are generally good with treatment.

The rate of ectopic pregnancy is about 1 and 2% that of live births in developed countries, though it may be as high as 4% among those using assisted reproductive technology. It is the most common cause of death among women during the first trimester at approximately 10% of the total. In the developed world outcomes have improved while in the developing world they often remain poor. The risk of death among those in the developed world is between 0.1 and 0.3 percent while in the developing world it is between one and three percent. The first known description of an ectopic pregnancy is by Al-Zahrawi in the 11th century. The word "ectopic" means "out of place".

Premature ejaculation (PE) occurs when a man experiences orgasm and expels semen soon after sexual activity and with minimal penile stimulation. It has also been called "early ejaculation," "rapid ejaculation," "rapid climax," "premature climax," and (historically) "ejaculatio praecox." There is no uniform cut-off defining "premature", but a consensus of experts at the International Society for Sexual Medicine endorsed a definition including "ejaculation which always or nearly always occurs prior to or within about one minute". The International Classification of Diseases (ICD-10) applies a cut-off of 15 seconds from the beginning of sexual intercourse. Hong argued that rapid ejaculation is an evolutionary adaptation.

Although men with premature ejaculation describe feeling that they have less control over ejaculating, it is not clear if that is true, and many or most average men also report that they wish they could last longer. Men's typical ejaculatory latency is approximately 4–8 minutes. The opposite condition is delayed ejaculation.

Men with PE often report emotional and relationship distress, and some avoid pursuing sexual relationships because of PE-related embarrassment. Compared with men, women consider PE less of a problem, but several studies show that the condition also causes female partners distress.

The 1948 Kinsey Report suggested that three-quarters of men ejaculate within two minutes of penetration in over half of their sexual encounters.

Current evidence supports an average intravaginal ejaculation latency time (IELT) of six and a half minutes in 18- to 30-year-olds. If the disorder is defined as an IELT percentile below 2.5, then premature ejaculation could be suggested by an IELT of less than about two minutes. Nevertheless, it is possible that men with abnormally low IELTs could be satisfied with their performance and do not report a lack of control. Likewise, those with higher IELTs may consider themselves premature ejaculators, suffer from detrimental side effects normally associated with premature ejaculation, and even benefit from treatment.