HGPIN in isolation is asymptomatic. It is typically discovered in prostate biopsies taken to rule-out prostate cancer and very frequently seen in prostates removed for prostate cancer.

On a subsequent biopsy, given a history of a HGPIN diagnosis, the chance of finding prostatic adenocarcinoma is approximately 30%.

Penile cancer arises from precursor lesions, which generally progress from low-grade to high-grade lesions. For HPV related penile cancers this sequence is as follows:

- A. Squamous hyperplasia;

- B. Low-grade penile intraepithelial neoplasia (PIN);

- C. High-grade PIN (carcinoma in situ—Bowen's disease, Erythroplasia of Queyrat and bowenoid papulosis (BP));

- D. Invasive Carcinoma of the Penis.

However, in some cases non-dysplastic or mildly dysplastic lesions may progress directly into cancer. Examples include flat penile lesions (FPL) and condylomata acuminata.

In HPV negative cancers the most common precursor lesion is lichen sclerosus (LS).

Like many malignancies, penile cancer can spread to other parts of the body. It is usually a primary malignancy, the initial place from which a cancer spreads in the body. Much less often it is a secondary malignancy, one in which the cancer has spread to the penis from elsewhere. The staging of penile cancer is determined by the extent of tumor invasion, nodal metastasis, and distant metastasis.

The T portion of the AJCC TNM staging guidelines are for the primary tumor as follows:

- TX: Primary tumor cannot be assessed.

- T0: No evidence of primary tumor.

- Tis: Carcinoma "in situ".

- Ta: Noninvasive verrucous carcinoma.

- T1a: Tumor invades subepithelial connective tissue without lymph vascular invasion and is not poorly differentiated (i.e., grade 3–4).

- T1b: Tumor invades subepithelial connective tissue with lymph vascular invasion or is poorly differentiated.

- T2: Tumor invades the corpus spongiosum or cavernosum.

- T3: Tumor invades the urethra or prostate.

- T4: Tumor invades other adjacent structures.

Anatomic Stage or Prognostic Groups of penile cancer are as follows:

- Stage 0—Carcinoma "in situ".

- Stage I—The cancer is moderately or well differentiated and only affects the subepithelial connective tissue.

- Stage II—The cancer is poorly differentiated, affects lymphatics, or invades the corpora or urethra.

- Stage IIIa—There is deep invasion into the penis and metastasis in one lymph node.

- Stage IIIb—There is deep invasion into the penis and metastasis into multiple inguinal lymph nodes.

- Stage IV—The cancer has invaded into structures adjacent to the penis, metastasized to pelvic nodes, or distant metastasis is present.

Early prostate cancer usually has no clear symptoms. Sometimes, however, prostate cancer does cause symptoms, often similar to those of diseases such as benign prostatic hyperplasia. These include frequent urination, nocturia (increased urination at night), difficulty starting and maintaining a steady stream of urine, hematuria (blood in the urine), and dysuria (painful urination). A study based on the 1998 Patient Care Evaluation in the US found that about a third of patients diagnosed with prostate cancer had one or more such symptoms, while two-thirds had no symptoms.

Prostate cancer is associated with urinary dysfunction as the prostate gland surrounds the prostatic urethra. Changes within the gland, therefore, directly affect urinary function. Because the "vas deferens" deposits seminal fluid into the prostatic urethra, and secretions from the prostate gland itself are included in semen content, prostate cancer may also cause problems with sexual function and performance, such as difficulty achieving erection or painful ejaculation.

Metastatic prostate cancer that has spread to other parts of the body can cause additional symptoms. The most common symptom is bone pain, often in the vertebrae (bones of the spine), pelvis, or ribs. Spread of cancer into other bones such as the femur is usually to the proximal or nearby part of the bone. Prostate cancer in the spine can also compress the spinal cord, causing tingling, leg weakness and urinary and fecal incontinence.

Prostate cancer is the development of cancer in the prostate, a gland in the male reproductive system. Most prostate cancers are slow growing; however, some grow relatively quickly. The cancer cells may spread from the prostate to other parts of the body, particularly the bones and lymph nodes. It may initially cause no symptoms. In later stages it can lead to difficulty urinating, blood in the urine, or pain in the pelvis, back or when urinating. A disease known as benign prostatic hyperplasia may produce similar symptoms. Other late symptoms may include feeling tired due to low levels of red blood cells.

Factors that increase the risk of prostate cancer include: older age, a family history of the disease, and race. About 99% of cases occur in those over the age of 50. Having a first-degree relative with the disease increases the risk two to threefold. In the United States, it is more common in the African American population than the white American population. Other factors that may be involved include a diet high in processed meat, red meat, or milk products or low in certain vegetables. An association with gonorrhea has been found, but a reason for this relationship has not been identified. Prostate cancer is diagnosed by biopsy. Medical imaging may then be done to determine if the cancer has spread to other parts of the body.

Prostate cancer screening is controversial. Prostate-specific antigen (PSA) testing increases cancer detection but does not decrease mortality. The United States Preventive Services Task Force recommends against screening using the PSA test, due to the risk of overdiagnosis and overtreatment, as most cancer diagnosed would remain asymptomatic. The USPSTF concludes that the potential benefits of testing do not outweigh the expected harms. While 5α-reductase inhibitors appear to decrease low-grade cancer risk they do not affect high-grade cancer risk and thus are not recommended for prevention. Supplementation with vitamins or minerals does not appear to affect the risk.

Many cases can be safely followed with active surveillance or watchful waiting. Other treatments may include a combination of surgery, radiation therapy, hormone therapy or chemotherapy. When it only occurs inside the prostate it may be curable. In those in whom the disease has spread to the bones, pain medications, bisphosphonates and targeted therapy, among others, may be useful. Outcomes depend on a person's age and other health problems as well as how aggressive and extensive the cancer is. Most people with prostate cancer do not end up dying from the disease. The 5-year survival rate in the United States is 99%. Globally it is the second most common type of cancer and the fifth leading cause of cancer-related death in men. In 2012 it occurred in 1.1 million men and caused 307,000 deaths. It was the most common cancer in males in 84 countries, occurring more commonly in the developed world. Rates have been increasing in the developing world. Detection increased significantly in the 1980s and 1990s in many areas due to increased PSA testing. Studies of males who died from unrelated causes have found prostate cancer in 30% to 70% of those over age 60.

Bowenoid papulosis is a cutaneous condition characterized by the presence of pigmented verrucous papules on the body of the penis. They are associated with human papillomavirus, the causative agent of genital warts. The lesions have a typical dysplastic histology and are generally considered benign, although a small percentage will develop malignant characteristics.

It is considered as a pre-malignant condition. Other terms used to describe the condition are: Erythroplasia of Queyrat, Squamous cell carcinoma in situ and Bowen’s disease. The term "Bowenoid papulosis" was coined in 1977 by Kopf and Bart and is named after dermatologist John Templeton Bowen.

The term “intraepithelial neoplasia” defines a premalignant intraepithelial change.

On the vulva it is termed VIN (vulvar or vulval intraepithelial neoplasia); on the penis, PIN (penile intraepithelial neoplasia); and on or around the anus, AIN (anal intraepithelial neoplasia). The terminology has been very confusing and it is now recommended that the terms Bowen’s disease, erythroplasia of Queyrat, and bowenoid papulosis should not be used for lesions in the anogenital area. However, dermatologists still recognize a distinct clinical variant, bowenoid papulosis, characterized by discrete papules in a younger age group and a tendency for spontaneous regression. Additionally, some authorities believe that erythroplasia of Queyrat and Bowen’s disease remain useful terms in men.

The symptoms can be mild or severe and may include:

- Not able to chew or swallow

- Sores on the inside of the cheeks or gums

- Fever

- General discomfort, uneasiness, or ill feeling

- Very sore mouth with no desire to eat

- Halitosis (bad breath)

Gingivostomatitis symptoms in infants may wrongly be dismissed as teething. "Coincidentally, primary tooth eruption begins at about the time that infants are losing maternal antibody protection against the herpes virus. Also, reports on teething difficulties have recorded symptoms which are remarkably consistent with primary oral herpetic infection such as fever, irritability, sleeplessness, and difficulty with eating." "Younger infants with higher residual levels of antibodies would experience milder infections and these would be more likely to go unrecognized or be dismissed as teething difficulty."

Gingivostomatitis must also be differentiated from herpangina, another disease that also commonly causes ulcers in the oral cavity of children, but is caused by the Coxsackie A virus rather than a herpes virus. In herpangina, ulcers are usually isolated to the soft palate and anterior pillar of the mouth. In herpetic gingivostomatitis, lesions can be found in these locations, but they are almost always accompanied by ulcerations on the gums, lips, tongue or buccal mucosa and/or by hyperemia, hypertrophy or hemorrhage of the gums.

Bing–Neel syndrome (BNS) is an extremely rare neurologic complication of Waldenström macroglobulinemia (WM), which is a chronic lymphoproliferative disorder.

There's no clear definition of BNS but what is known so far is that unlike WM, It involves the central nervous system (CNS), infiltrated by differentiated malignant B cells and by having hyperglobulinemia. This infiltration increases blood viscosity, which impairs blood circulation through small blood vessels of the brain and the eye. Some scientists proposed that a person diagnosed with BNS is typically classified into Group A and Group B depending on whether or not plasma cells are present within the brain parenchyma, leptomeninges, dura, and/or the cerebral spinal fluid (CSF). Symptoms are diverse and nonspecific, and they can vary depending on which aspect of the CNS is being affected. Symptoms can include a range of severity of nausea and seizures. Since the symptoms vary, there are multiple treatment options to treat the symptoms for this non-curable disease. Although there is no specific set of diagnosis for BNS, different combinations of diagnostic tools are used to narrow down and conclude the presence of BNS.

Centronuclear myopathies (CNM) are a group of congenital myopathies where cell nuclei are abnormally located in skeletal muscle cells. In CNM the nuclei are located at a position in the center of the cell, instead of their normal location at the periphery.

Symptoms of CNM include severe hypotonia, hypoxia-requiring breathing assistance, and scaphocephaly. Among centronuclear myopathies, the X-linked myotubular myopathy form typically presents at birth, and is thus considered a congenital myopathy. However, some centronuclear myopathies may present later in life.

Symptoms of BNS gradually progress over the span of a week or even a month, and there is typically a delay in diagnosis after the initial symptoms arise. Although BNS arises due to complications from WM, some individuals may experience symptoms of BNS without having a past history of WM.

Given that BNS is so rare, the symptoms are diverse and nonspecific. Symptoms range in severity from nausea to seizures and are characterized by how they interfere with the function of the CNS. Where certain symptoms are present depends on which branch of the CNS is being affected by plasma B-cells. People diagnosed with BNS experience some sensory symptoms as well. Some sensory symptoms include a pin and needles sensation experienced in the lower limbs, the hands, and in the arms, along with pain and extreme numbness.

The Newton classification divides denture-related stomatitis into three types based on severity. Type one may represent an early stage of the condition, whilst type two is the most common and type three is uncommon.

- Type 1 - Localized inflammation or pinpoint hyperemia

- Type 2 - More diffuse erythema (redness) involving part or all of the mucosa which is covered by the denture

- Type 3 - Inflammatory nodular/papillary hyperplasia usually on the central hard palate and the alveolar ridge

Despite the alternative name for this condition, "denture sore mouth", it is usually painless and asymptomatic. The appearance of the involved mucosa is erythematous (red) and edematous (swollen), sometimes

with petechial hemorrhage (pin-points of bleeding). This usually occurs beneath an upper denture. Sometimes angular cheilitis can coexist, which is inflammation of the corners of the mouth, also often associated with "Candida albicans". Stomatitis rarely develops under a lower denture. The affected mucosa is often sharply defined, in the shape of the covering denture.

As with other myopathies, the clinical manifestations of MTM/CNM are most notably muscle weakness and associated disabilities. Congenital forms often present with neonatal low muscle tone, severe weakness, delayed developmental milestones (particularly gross motor milestones such as head control, crawling, and walking) and pulmonary complications (presumably due to weakness of the muscles responsible for respiration). While some patients with centronuclear myopathies remain ambulatory throughout their adult life, others may never crawl or walk and may require wheelchair use for mobility. There is substantial variability in the degree of functional impairment among the various centronuclear myopathies. Although this condition only affects the voluntary muscles, several children have suffered from cardiac arrest, possibly due to the additional stress placed on the heart.

Other observed features have been high arched palate, long digits, bell shaped chest and long face.

Myotubular myopathy only affects muscles and does not impact intelligence in any shape or form.

X-linked myotubular myopathy was traditionally a fatal condition of infancy, with life expectancy of usually less than two years. There appears to be substantial variability in the clinical severity for different genetic abnormalities at that same MTM1 gene. Further, published cases show significant differences in clinical severity among relatives with the same genetic abnormality at the MTM1 gene. Most truncating mutations of MTM1 cause a severe and early lethal phenotype, while some missense mutations are associated with milder forms and prolonged survival (up to 54 years).

Centronuclear myopathies typically have a milder presentation and a better prognosis. Recently, researchers discovered mutations at the gene dynamin 2 (DNM2 on chromosome 19, at site 19p13.2), responsible for the autosomal dominant form of centronuclear myopathy. This condition is now known as dynamin 2 centronuclear myopathy (abbreviated DNM2-CNM). Research has indicated that patients with DNM2-CNM have a slowly progressive muscular weakness usually beginning in adolescence or early adulthood, with an age range of 12 to 74 years.

Most signs and symptoms of AML are caused by the replacement of normal blood cells with leukemic cells. A lack of normal white blood cell production makes people more susceptible to infections; while the leukemic cells themselves are derived from white blood cell precursors, they have no infection-fighting capacity. A drop in red blood cell count (anemia) can cause fatigue, paleness, and shortness of breath. A lack of platelets can lead to easy bruising or bleeding with minor trauma.

The early signs of AML are often vague and nonspecific, and may be similar to those of influenza or other common illnesses. Some generalized symptoms include fever, fatigue, weight loss or loss of appetite, shortness of breath, anemia, easy bruising or bleeding, petechiae (flat, pin-head sized spots under the skin caused by bleeding), bone and joint pain, and persistent or frequent infections.

Enlargement of the spleen may occur in AML, but it is typically mild and asymptomatic. Lymph node swelling is rare in AML, in contrast to acute lymphoblastic leukemia. The skin is involved about 10% of the time in the form of leukemia cutis. Rarely, Sweet's syndrome, a paraneoplastic inflammation of the skin, can occur with AML.

Some people with AML may experience swelling of the gums because of infiltration of leukemic cells into the gum tissue. Rarely, the first sign of leukemia may be the development of a solid leukemic mass or tumor outside of the bone marrow, called a chloroma. Occasionally, a person may show no symptoms, and the leukemia may be discovered incidentally during a routine blood test.

Acute myeloid leukemia (AML) is a cancer of the myeloid line of blood cells, characterized by the rapid growth of abnormal cells that build up in the bone marrow and blood and interfere with normal blood cells. Symptoms may include feeling tired, shortness of breath, easy bruising and bleeding, and increased risk of infection. Occasionally spread may occur to the brain, skin, or gums. As an acute leukemia, AML progresses rapidly and is typically fatal within weeks or months if left untreated.

Risk factors include smoking, previous chemotherapy or radiation therapy, myelodysplastic syndrome, and exposure to the chemical benzene. The underlying mechanism involves replacement of normal bone marrow with leukemia cells, which results in a drop in red blood cells, platelets, and normal white blood cells. Diagnosis is generally based on bone marrow aspiration and specific blood tests. AML has several subtypes; for which treatments and outcomes may vary.

AML is typically initially treated with chemotherapy aimed at inducing remission. People may than go on to receive additional chemotherapy, radiation therapy, or a stem cell transplant. The specific genetic mutations present within the cancer cells may guide therapy, as well as determine how long that person is likely to survive. Arsenic trioxide may be tried in cases that have recurred following usual treatments.

AML affected about one million people globally in 2015 and resulted in 147,000 deaths. It most commonly occurs in older adults. Males are affected more often than females. AML is curable in about 35% of people under 60 years old and 10% over 60 years old. Older people who are not healthy enough to receive intensive chemotherapy have a typical survival of 5–10 months. It accounts for roughly 1.8% of cancer deaths in the United States.

Secondary organic delusional parasitosis occurs when the state of the patient is caused by a medical illness or substance (medical or recreational) use. In the DSM-IV this corresponds with "psychotic disorder due to general medical condition". Physical illnesses that can underlie secondary organic delusional parasitosis include: hypothyroidism, cancer, cerebrovascular disease, tuberculosis, neurological disorders, vitamin B12 deficiency, and diabetes mellitus. Any illness or medication for which formication is a symptom or side effect can become a trigger or underlying cause of delusional parasitosis.

Other physiological factors which can cause formication and thus can sometimes lead to this condition include: menopause (i.e. hormone withdrawal); allergies, and drug abuse, including but not limited to cocaine and methamphetamine (as in amphetamine psychosis). It appears that many of these physiological factors, as well as environmental factors such as airborne irritants, are capable of inducing a "crawling" sensation in otherwise healthy individuals; however, some people become fixated on the sensation and its possible meaning, and this fixation may then develop into delusional parasitosis.

Secondary functional delusional parasitosis occurs when the delusions are associated with a psychiatric condition such as schizophrenia or clinical depression.

Cutaneous disorders in musicians include frictional injury ("fiddler's neck"), hyperhidrosis, acne mechanica and vascular compromise. Other agents of irritant and allergic contact dermatitis may be rosewood, Makassar ebony, cocobolo wood, African blackwood, nickel, reed, propolis (bee glue), chromium and paraphenylenediamine. Patch testing can be performed for identification of the cause.

Unlike ataxias of cerebellar origin, Bruns apraxia exhibits many frontal lobe ataxia characteristics, with some or all present.

- Difficulty in initiating movement

- Poor truncal mobility

- Falls due to minor balance disturbances

- Greatly hindered postural responses

- Characteristic magnetic gait, the inability to raise one's foot off of the floor.

- Wide base, poor balance control when in stance

- Short stride

- En bloc turns

Often patients with frontal lobe ataxia may experience minute cognitive changes that accompany the gait disturbances, such as frontal dementia and presentation of frontal release signs (Plantar reflex). Urinary incontinence may also be present.

Bruns apraxia can be distinguished from Parkinsonian ataxia and cerebellar ataxia in a number of ways. Patients typically afflicted with Parkinsonian ataxia typically have irregular arm swing, a symptom not typically present in frontal ataxia. Walking stride in cerebellar ataxia varies dramatically, accompanied by erratic foot placement and sudden, uncontrolled lurching, not generally characteristic of Bruns apraxia.

Abietic acid dermatitis is a contact dermatitis often seen in association with musical instruments.

Acute dystonia nearly always develops a few weeks after a dopamine blocking agent/medication has begun or a substantial increase in antipsychotic dosage. An acute dystonic reaction consists of sustained, painful muscular spasms, producing twisting of the trunk/body and abnormal posture. The most frequent occurrences of these spasms have been reported in the neck, tongue, and jaw. Oculogyric crisis and opisthotonus are also very common. Acute effects of dopamine antagonists also include Parkinsons-like symptoms, manifested by bradykinesia, pin rolling tremor, and rigidity of the body. These movements may fluctuate over hours and temporarily dissipate in response to reassurance, and the individual episodes may last minutes to hours. Acute reactions are more common in older patients and females. The pathophysiology underlying these reactions is unknown, but the movements usually occur during the period when blood medication level is dropping. The acute syndromes which occur due to prolonged exposure to a dopamine antagonist are collectively termed extrapyramidal symptoms, EPS.

The predominant symptom of Pisa syndrome is dystonia. Dystonia is a neurological movement disorder characterized by sustained muscle contraction leading to abnormal posture, twisting, and repetitive movement. In Pisa Syndrome specifically there is commonly a tonic flexion of the trunk of the body to one side, leading to a slight lean (reminiscent of the Leaning Tower of Pisa, hence the name "Pisa syndrome"). This is usually associated with a backward axial rotation of the spine and indifferent to markedly abnormal posture. Patients diagnosed with Pisa Syndrome usually experience either acute dystonia or tardive dystonia, also known as tardive dyskinesia. Differential diagnosis between the two may be hard to accomplish without a complete patient history, since both types of dystonia may occur simultaneously in a patient. These symptoms generally disappear after discontinuation of the antipsychotic drug. The time of onset of symptoms may vary depending on drug being administered and the neurological characteristics of the patient in question.

Symptoms include pain during sports movements, particularly hip extension, and twisting and turning. This pain usually radiates to the adductor muscle region and even the testicles, although it is often difficult for the patient to pin-point the exact location.

Following sporting activity the person with athletic pubalgia will be stiff and sore. The day after a match, getting out of bed or a car will be difficult. Any exertion that increases intra-abdominal pressure, such as coughing, sneezing, or sporting activity can cause pain. In the early stages, the person may be able to continue playing their sport, but the problem usually gets progressively worse.

As pain in the groin and pelvis can be referred from a number of problems, including injuries to the lumbar spine, the hip joint, the sacro-iliac joint, the abdomen, and the genito-urinary system, diagnosis of athletic pubalgia requires skillful differentiation and pubic examination in certain cases where there is intense groin pain.

The diagnosis is based on the patient's history, clinical signs, and, increasingly, an MRI exam. Symptoms can often be reproduced by maneuvers such as performing sit-ups or crunches. Pain can also be elicited with the patient in a "frog position," in which the patient is supine with knees bent and heels together.

The exact lesion may differ, but common pathologic findings at operation are:

- torn external oblique aponeurosis

- tear in the conjoint tendon

- conjoint tendon torn from pubic tubercle

- dehiscence between conjoined tendon and inguinal ligament

- tear in the fascia transversalis

- abnormal insertion of the rectus abdominis muscle

- tear of the abdominal internal oblique muscle from the pubic tubercle

- entrapment of the ilioinguinal nerve or genitofemoral nerve

Several of these lesions may occur simultaneously. Also, many athletes have concomitant weakness or tearing of the adductor muscles or labral tears of the hip.

When the adductor muscles are tight post injury, that can be enough to trigger symptoms. The first conservative treatment option should be to restore normal motion after the adductor has begun to heal (usually 6–8 weeks post injury). Sleeping in a prone position with the hip on the affected side flexed and externally rotated can be a cure in some individuals.

The exact incidence of these entities is unknown: some believe it is the most common cause of chronic groin pain in athletes, while others argue that it is only rare. Conservative therapies (gentle stretching and a short period of rest) may temporarily alleviate the pain, but definitive treatment consists of surgical repair followed by a structured rehabilitation.