While most carcinoids are asymptomatic through the natural lifetime and are discovered only upon surgery for unrelated reasons (so-called "coincidental carcinoids"), all carcinoids are considered to have malignant potential.

About 10% of carcinoids secrete excessive levels of a range of hormones, most notably serotonin (5-HT), causing:

- Flushing (serotonin itself does not cause flushing). Potential causes of flushing in carcinoid syndrome include bradykinins, prostaglandins, tachykinins, substance P, and/or histamine, diarrhea, and heart problems. Because of serotonin's growth-promoting effect on cardiac myocytes,[14] a serotonin-secreting carcinoid tumour may cause a tricuspid valve disease syndrome, due to the proliferation of myocytes onto the valve.

- Diarrhea

- Wheezing

- Abdominal cramping

- Peripheral edema

The outflow of serotonin can cause a depletion of tryptophan leading to niacin deficiency. Niacin deficiency, also known as pellagra, is associated with dermatitis, dementia, and diarrhea.

This constellation of symptoms is called "carcinoid syndrome" or (if acute) "carcinoid crisis". Occasionally, haemorrhage or the effects of tumor bulk are the presenting symptoms. The most common originating sites of carcinoid is the small bowel, particularly the ileum; carcinoid tumors are the most common malignancy of the appendix. Carcinoid tumors may rarely arise from the ovary or thymus.

They are most commonly found in the midgut at the level of the ileum or in the appendix. The next most common affected area is the respiratory tract, with 28% of all cases — per PAN-SEER data (1973 – 1999). The rectum is also a common site.

Metastasis of carcinoid can lead to carcinoid syndrome. This is due to the over-production of many substances, including serotonin, which are released into the systemic circulation, and which can lead to symptoms of cutaneous flushing, diarrhea, bronchoconstriction, and right-sided cardiac valve disease. It is estimated that less than 6% of carcinoid patients will develop carcinoid syndrome, and of these, 50% will have cardiac involvement.

The carcinoid syndrome occurs in approximately 5% of carcinoid tumors and

becomes manifest when vasoactive substances from the tumors enter the systemic circulation escaping hepatic degradation. Interestingly, if the primary tumor is from the GI tract (hence releasing serotonin into the hepatic portal circulation), carcinoid syndrome generally does not occur until the disease is so advanced that it overwhelms the liver's ability to metabolize the released serotonin.

- Flushing: The most important clinical finding is flushing of the skin, usually of the head and the upper part of thorax.

- Diarrhea: When the diarrhea is intense and explosive, it may lead to electrolyte disturbance and dehydration.

- Abdominal pain: Due to desmoplastic reaction of the mesentery or hepatic metastases.

- Bronchoconstriction, which may be histamine-induced, affects a smaller number of patients and often accompanies flushing.

- Secondary restrictive cardiomyopathy: About 50% of patients have cardiac abnormalities classically of the restrictive-type caused by serotonin-induced fibrosis of the valvular endocardium, notably the tricuspid and pulmonary valves, called cardiac fibrosis. This results in a heart with normal rhythm and contractility, but reduced preload and end-diastolic volume. "TIPS" is an acronym for Tricuspid Insufficiency, Pulmonary Stenosis (fibrosis of tricuspid and pulmonary valves).

- Nausea and Vomiting

The strumal carcinoid is a type of monodermal teratoma with histomorphologic features of (1) the thyroid gland and (2) a neuroendocrine tumour (carcinoid).

Atypical pulmonary carcinoid tumour is a subtype of pulmonary carcinoid tumor. It is an uncommon low-grade malignant lung mass that is most often in the central airways of the lung. It is also known as "atypical lung carcinoid tumour", " atypical lung carcinoid" or "moderately differentiated neuroendocrine carcinoma".

It is a more aggressive than typical carcinoid tumors: nodal metastases in 70% vs. 5%. The 5 year survival is 49-69%.

Atypical carcinoid tumors have increased mitotic activity (2-10 per 10 HPF), nuclear pleomorphism or foci of necrosis.

Carcinoids most commonly affect the small bowel, particularly the ileum, and are the most common malignancy of the appendix. Many carcinoids are asymptomatic and are discovered only upon surgery for unrelated causes. These coincidental carcinoids are common; one study found that one person in ten has them. Many tumors do not cause symptoms even when they have metastasized. Other tumors even if very small can produce adverse effects by secreting hormones.

Ten per cent (10%) or less of carcinoids, primarily some midgut carcinoids, secrete excessive levels of a range of hormones, most notably serotonin (5-HT) or substance P, causing a constellation of symptoms called carcinoid syndrome:

- flushing

- diarrhea

- asthma or wheezing

- congestive heart failure (CHF)

- abdominal cramping

- peripheral edema

- heart palpitations

A carcinoid crisis with profound flushing, bronchospasm, tachycardia, and widely and rapidly fluctuating blood pressure can occur if large amounts of hormone are acutely secreted, which is occasionally triggered by factors such as diet, alcohol, surgery chemotherapy, embolization therapy or radiofrequency ablation.

Chronic exposure to high levels of serotonin causes thickening of the heart valves, particularly the tricuspid and the pulmonic valves, and over a long period can lead to congestive heart failure. However, valve replacement is rarely needed. The excessive outflow of serotonin can cause a depletion of tryptophan leading to niacin deficiency, and thus pellagra, which is associated with dermatitis, dementia, and diarrhea. Many other hormones can be secreted by some of these tumors, most commonly growth hormone that can cause acromegaly, or cortisol, that can cause Cushing's syndrome.

Occasionally, haemorrhage or the effects of tumor bulk are the presenting symptoms. Bowel obstruction can occur, sometimes due to fibrosing effects of NET secretory products with an intense desmoplastic reaction at the tumor site, or of the mesentery.

Conceptually, there are two main types of NET within this category: those which arise from the gastrointestinal (GI) system and those that arise from the pancreas. In usage, the term "carcinoid" has often been applied to both, although sometimes it is restrictively applied to NETs of GI origin (as herein), or alternatively to those tumors which secrete functional hormones or polypeptides associated with clinical symptoms, as discussed.

Pulmonary carcinoid tumour is a neuroendocrine tumour of the lung.

There are two types:

- Typical pulmonary carcinoid tumour

- Atypical pulmonary carcinoid tumour

Pulmonary neuroendocrine tumor are classified according to tumoral grade:

- Low grade pulmonary neuroendocrine tumor: Typical pulmonary carcinoid tumour (TC; low-grade);

- Intermediate-grade pulmonary neuroendocrine tumor: Atypical pulmonary carcinoid tumour (AC; intermediate-grade)

- High-grade pulmonary neuroendocrine tumor

- Small cell lung cancer (SCLC)

- Large cell neuroendocrine carcinoma (LCNEC of the lung)

Low-grade nodular neuroendocrine proliferations ≥ 0.5 cm are classified as carcinoid tumors and smaller ones are called pulmonary tumorlets.

When neuroendocrine cell hyperplasia and tumorlets are extensive, they represent the rare preinvasive lesion for carcinoids known as "diffuse idiopathic pulmonary neuroendocrine cell hyperplasia".

Both LCNEC and SCLC can demonstrate histologic heterogeneity with other major histologic types of lung carcinoma, such as pulmonary adenocarcinoma or pulmonary squamous cell carcinoma, but is not characteristic of TC or AC.

Lung carcinoids typically present with a cough or hemoptysis. Findings may closely mimic malignant tumours of the lung, i.e. lung cancer.

The definitive diagnosis is rendered by a microscopic examination, after excision. Typical carcinoids have cells with stippled chromatin and a moderate quantity of cytoplasm. They typically have few mitoses and lack necrosis. By definition, they are greater than 4 mm in largest dimension; smaller lesions are referred to as "pulmonary carcinoid tumourlets".

The differential diagnosis of typical pulmonary carcinoid tumour includes: "atypical pulmonary carcinoid tumour", "pulmonary carcinoid tumourlet" and "lung adenocarcinoma".

Carcinoid syndrome is a paraneoplastic syndrome comprising the signs and symptoms that occur secondary to carcinoid tumors. The syndrome includes flushing and diarrhea, and less frequently, heart failure, emesis and bronchoconstriction. It is caused by endogenous secretion of mainly serotonin and kallikrein.

Pulmonary neuroendocrine tumors are neuroendocrine tumors localized to the lung: bronchus or pulmonary parenchyma.

Pulmonary neuroendocrine tumors include a spectrum of tumors from the low-grade typical pulmonary carcinoid tumor and intermediate-grade atypical pulmonary carcinoid tumor to the high-grade pulmonary large cell neuroendocrine carcinoma (LCNEC) and pulmonary small cell carcinoma (SCLC), with significant clinical, epidemiologic and genetic differences.

The signs and symptoms of a pheochromocytoma are those of sympathetic nervous system hyperactivity, including:

- Skin sensations

- Flank pain

- Elevated heart rate

- Elevated blood pressure, including paroxysmal (sporadic, episodic) high blood pressure, which sometimes can be more difficult to detect; another clue to the presence of pheochromocytoma is orthostatic hypotension (a fall in systolic blood pressure greater than 20 mmHg or a fall in diastolic blood pressure greater than 10 mmHg upon standing)

- Palpitations

- Anxiety often resembling that of a panic attack

- Diaphoresis (excessive sweating)

- Headaches – most common symptom

- Pallor

- Weight loss

- Localized amyloid deposits found microscopically

- Elevated blood glucose level (due primarily to catecholamine stimulation of lipolysis (breakdown of stored fat) leading to high levels of free fatty acids and the subsequent inhibition of glucose uptake by muscle cells. Further, stimulation of beta-adrenergic receptors leads to glycogenolysis and gluconeogenesis and thus elevation of blood glucose levels).

A pheochromocytoma can also cause resistant arterial hypertension. A pheochromocytoma can be fatal if it causes a hypertensive emergency, that is, severely high blood pressure that impairs one or more organ systems (formerly called "malignant hypertension"). This hypertension is not well controlled with standard blood pressure medications.

Not all patients experience all of the signs and symptoms listed. The most common presentation is headache, excessive sweating, and increased heart rate, with the attack subsiding in less than one hour.

Tumors may grow large, but most are smaller than .

The major clinical symptom of metastatic medullary thyroid carcinoma is diarrhea; occasionally a patient will have flushing episodes. Both occur particularly with liver metastasis, and either symptom may be the first manifestation of the disease. The flushing that occurs in medullary thyroid carcinoma is indistinguishable from that associated with carcinoid syndrome. In MTC, the flushing, diarrhea, and itching (pruritis) are all caused by elevated levels of calcitonin gene products (calcitonin or calcitonin gene-related peptide). Alternatively, the flushing and diarrhea observed in carcinoid syndrome is caused by elevated levels of circulating serotonin.

Medullary thyroid carcinoma may also produce a thyroid nodule and enlarged cervical lymph nodes.

Sites of spread of medullary thyroid carcinoma include local lymph nodes in the neck, lymph nodes in the central portion of the chest (mediastinum), liver, lung, and bone. Spread to other sites such as skin or brain occurs but is uncommon.

The differential diagnoses of pheochromocytoma include:

- Anxiety disorders, including Benzodiazepine withdrawal syndrome

- Paragangliomas

- Von Hippel–Lindau Disease

- Essential hypertension

- Hyperthyroidism

- Insulinoma

- Mercury poisoning

- Paroxysmal supraventricular tachycardia

- Renovascular hypertension

- Carcinoid

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.

Second most common primary anterior mediastinal mass in adults. Most are seen in the anterior compartment and rest are seen in middle compartment. Hodgkin's usually present in 40-50's with nodular sclerosing type (7), and non-Hodgkin's in all age groups. Can also be primary mediastinal B-cell lymphoma with exceptionally good prognosis. Common symptoms include fever, weight loss, night sweats, and compressive symptoms such as pain, dyspnea, wheezing, Superior vena cava syndrome, pleural effusions (10,11). Diagnosis usually by CT showing lobulated mass. Confirmation done by tissue biopsy of accompanying nodes if any, mediastinoscopy, mediastinotomy, or thoracotomy. FNA biopsy is usually not adequate. (12,13,14) Treatment of mediastinal Hodgkin's involves chemotherapy and/or radiation. 5 year survival is now around 75%. (15) Large-cell type may have somewhat better prognosis. Surgery is generally not performed because of invasive nature of tumor.

Of all cancers involving the same class of blood cell, 2% of cases are mediastinal large B cell lymphomas.

Most common primary anterior mediastinal tumor (20%) in adults but rarely seen in children. It can be classified as lymphocytic, epithelial, or spindle cell histologies, but the clinical significance of these classifications is controversial. Tonofibrils seen under electron microscopy can differentiate thymoma from other tumors such as carcinoid, Hodgkin's, and seminoma. Patients are usually asymptomatic but can present with myasthenia gravis-related symptoms, substernal pain, dyspnea, or cough. Invasive tumors can produce compression effects such as superior vena cava syndrome. (3,4) Thymomas are diagnosed with CT or MRI revealing a mass in anterior mediastinum. Therapy in stage I tumors consists of surgical resection with good prognosis. Stage II-III requires maximal resection possible followed by radiation. Stage IV disease requires addition of cisplatin-based chemotherapy in addition to those in stage II and III. For those with invasive thymoma, treatment is based on induction chemotherapy, surgical resection, and post-surgical radiation. 5-year survival for invasive thymoma is between 12-54% regardless of any myasthenia gravis symptoms (5,6).

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".

The following diseases manifest by means of mucocutaneous dysfunction: acanthosis nigricans, dermatomyositis, Leser-Trélat sign, necrolytic migratory erythema, Sweet's syndrome, Florid cutaneous papillomatosis, pyoderma gangrenosum, and acquired generalized hypertrichosis. Mucocutaneous dysfunctions of paraneoplastic syndromes can be seen in cases of itching (hypereosinophilia), immune system depression (latent varicella-zoster virus in sensory ganglia), pancreatic tumors (leading to adipose nodular necrosis of subcutaneous tissues, flushes (prostaglandin secretions), and even dermic melanosis (cannot be eliminated via urine and results in grey to black-blueish skin tones).

The following diseases manifest by means of endocrine dysfunction: Cushing syndrome, syndrome of inappropriate antidiuretic hormone, hypercalcemia, hypoglycemia, carcinoid syndrome, and hyperaldosteronism.

An adenoma of a parathyroid gland may secrete inappropriately high amounts of parathyroid hormone and thereby cause primary hyperparathyroidism.

An adenoma (from Greek αδένας, "", "gland" + -ώμα, "", "tumor") (; plural adenomas or adenomata ) is a benign tumor of epithelial tissue with glandular origin, glandular characteristics, or both. Adenomas can grow from many glandular organs, including the adrenal glands, pituitary gland, thyroid, prostate, and others. Some adenomas grow from epithelial tissue in nonglandular areas but express glandular tissue structure (as can happen in familial polyposis coli). Although adenomas are benign, over time they may transform to become malignant, at which point they are called adenocarcinomas. Most adenomas do not transform. But even while benign, they have the potential to cause serious health complications by compressing other structures (mass effect) and by producing large amounts of hormones in an unregulated, non-feedback-dependent manner (causing paraneoplastic syndromes). Some adenomas are too small to be seen macroscopically but can still cause clinical symptoms.

Medullary thyroid cancer (MTC) is a form of thyroid carcinoma which originates from the parafollicular cells (C cells), which produce the hormone calcitonin.

Medullary tumors are the third most common of all thyroid cancers. They make up about 3% of all thyroid cancer cases.

Approximately 25% of medullary thyroid cancer is genetic in nature, caused by a mutation in the RET proto-oncogene. This form is classified as familial MTC. When MTC occurs by itself it is termed sporadic MTC. When it coexists with tumors of the parathyroid gland and medullary component of the adrenal glands (pheochromocytoma) it is called multiple endocrine neoplasia type 2 (MEN2).It was first characterized in 1959.