How does Erection happens?

The penis is shaped like a banana or sausage. It has a duct or tube called the urethra running right through it. Semen and urine pass along the urethra to get out of the body. Around the whole urethra is tissue called the corpus spongiosum penis (which is Latin for "body of the penis that is like a sponge"). It is near the lower surface of the penis. Also inside the penis near its upper surface are two cylindrical tissues called the corpora cavernosa penis (Latin for "bodies of the penis that are like caves"). (One of these tissues by itself is called a corpus cavernosum.) The corpus spongiosum penis and corpora cavernosa penis are filled with many blood vessels called arteries which carry blood.
When a man is sexually aroused or stimulated (made sexually excited) by touch – for example, if he masturbates or another person touches him in a sexual way – the touching is picked up by nerves in the arteries of the corpus spongiosum penis and corpora cavernosa penis. The nerves then cause a chemical called nitric oxide to be released into the arteries. This makes the arteries dilate (become wider), and they fill up with blood. Thus, the corpus spongiosum penis and corpora cavernosa penis all fill with blood and become larger and harder. This makes the penis grow longer, thicker and harder. The corpora cavernosa penis press against blood vessels called veins that let blood flow out of the penis. Since less blood can flow out of the penis through the veins, more of it stays in the penis, which remains hard. During an erection, a valve stops urine from entering the urethra so that only semen flows along it. This is why it is very difficult for a man to urinate when he is having an erection.
A man can also become sexually aroused without being touched, for example, if he sees a naked person or thinks about having sex with someone. In this case, his brain sends messages through his spinal cord (which is inside his vertebral column or backbone) to his penis and makes an erection happen. The brain can also stop an erection from happening, even if the man is being touched sexually.
An erection of the penis can also happen by itself when a man is asleep, often when he is dreaming. The scientific term for this is nocturnal penile tumescence (which means "swelling of the penis at night"). It is also common for a man to wake up after a night's sleep to find that he has an erection. This is often caused by his bladder being full of urine, which presses on the tissues in the penis. Such an erection is sometimes informally called a morning glory or morning wood.
After a man has had an orgasm and has ejaculated, his erection usually ends. How long this takes depends on the length and thickness of his penis. A man can also stop having an erection without having an orgasm and ejaculating, if he is no longer sexually aroused. Nerves in his body cause the arteries in the penis to constrict (become narrower). This forces blood out of the corpus spongiosum penis and corpora cavernosa penis. As they go back to their normal size, they do not press so much on the veins leading out of the penis. This lets blood flow faster out of the corpus spongiosum penis and corpora cavernosa penis. The scientific term for this process is detumescence.

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Prvention of Esophageal varices

Ideally, patients with known varices should receive treatment to reduce their risk of bleeding.

The non-selective β-blockers (e.g., propranolol 10 mg PO TID, timolol or nadolol 20 mg PO OD) and nitrates (e.g. isosorbide mononitrate (IMN) 20 mg BD to TID) have been evaluated for secondary prophylaxis. Non-selective β-blockers (but not cardioselective β-blockers like atenolol) are preferred because they decrease both cardiac output by β1 blockade and splanchnic blood flow by blocking vasodilating β2 receptors at splanchnic vasculature. The effectiveness of this treatment has been shown by a number of different studies.

Unfortunately, non-selective β-blockers do not prevent the formation of esophageal varices.

Ultimately the treatment of portal hypertension can prevent development of esophageal varices.

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Treatment of Esophageal varices

In emergency situations, the care is directed at stopping blood loss, maintaining plasma volume, correcting disorders in coagulation induced by cirrhosis, and appropriate use of antibiotics (usually a quinolone or ceftriaxone, as infection by gram-negative strains is either concomitant, or a precipitant).

Blood volume resuscitation should be done promptly and with caution. Goal should be hemodynamic stability and hemoglobin of over 8. Resuscitation of all lost blood leads to increase in portal pressure leading to more bleeding. Volume resuscitation can also worsen ascites and increase portal pressure. (AASLD guildlines)

Therapeutic endoscopy is considered the mainstay of urgent treatment. Two main therapeutic approaches exist:

1. Variceal ligation, or banding
2. Sclerotherapy

In cases of refractory bleeding, balloon tamponade with Sengstaken-Blakemore tube may be necessary, usually as a bridge to further endoscopy or treatment of the underlying cause of bleeding (usually portal hypertension). Methods of treating the portal hypertension include: transjugular intrahepatic portosystemic shunt (TIPS), or a distal splenorenal shunt procedure or a liver transplantation.
Nutritional supplementation is not necessary if the patient is not eating for four days or less.
Terlipressin and octreotide (50mcg bolus IV followed by 25-50mcg/h IVF for 1 to 5 days) have also been used.

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Esophageal varices

In medicine (gastroenterology), esophageal varices are extremely dilated sub-mucosal veins in the lower esophagus. They are most often a consequence of portal hypertension, commonly due to cirrhosis; patients with esophageal varices have a strong tendency to develop bleeding.

Esophageal varices are diagnosed with endoscopy.

The majority of blood from the esophagus is drained via the esophageal veins, which carry deoxygenated blood from the esophagus to the azygos vein, which in turn drains directly into the superior vena cava. These veins have no part in the development of esophageal varices. The remaining blood from the esophagus is drained into the superficial veins lining the esophageal mucosa, which drain into the coronary vein (left gastric vein), which in turn drains directly into the portal vein. These superficial veins (normally only approximately 1mm in diameter) become distended up to 1–2 cm in diameter in association with portal hypertension.

Normal portal pressure is approximately 9 mmHg compared to an inferior vena cava pressure of 2-6 mmHg. This creates a normal pressure gradient of 3-7 mmHg. If the portal pressure rises above 12mmHg, this gradient rises to 7-10 mmHg.[2] A gradient greater than 5 mmHg is considered portal hypertension. At gradients greater than 10 mmHg, blood flow though the hepatic portal system is redirected from the liver into areas with lower venous pressures. This means that collateral circulation develops in the lower esophagus, abdominal wall, stomach, and rectum. The small blood vessels in these areas become distended, becoming more thin-walled, and appear as varicosities. In addition, these vessels are poorly supported by other structures, as they are not designed for high pressures.

In situations where portal pressures increase, such as with cirrhosis, there is dilation of veins in the anastomosis, leading to esophageal varices. Splenic vein thrombosis is a rare condition which causes esophageal varices without a raised portal pressure. Splenectomy can cure the variceal bleeding due to splenic vein thrombosis. The most common cause of esophageal varices is from aging changes in the vessels.

Varices can also form in other areas of the body, including the stomach (gastric varices), duodenum (duodenal varices), and rectum (rectal varices). Treatment of these types of varices may differ.

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Focal nodular hyperplasia

Focal nodular hyperplasia (FNH) is a benign tumour of the liver (hepatic tumour), which is the second most prevalent tumour of the liver (the first is hepatic hemangioma). It is usually asymptomatic, rarely grows or bleeds, and has no malignant potential. This tumour is often resected because it is difficult to distinguish from hepatic adenoma.

Presentation

Focal nodular hyperplasia's most recognizable gross feature is a central stellate scar seen in 60-70% of cases. Microscopically, a lobular proliferation of bland-appearing hepatocytes with a bile ductular proliferation and malformed vessels within the fibrous scar is the most common pattern. Other patterns include telangiectatic, hyperplastic-adenomatous, and lesions with focal large-cell dysplasia.[ Rarely, these lesions may be multiple or can occur as part of a syndrome with hemangiomas, epithelioid hemangioendothelioma, hepatic adenomas, fibrolamellar hepatocellular carcinoma, vascular malformations of the brain, meningiomas, and/or astrocytomas.

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Asbestosis

Asbestosis is a chronic inflammatory and fibrotic medical condition affecting the parenchymal tissue of the lungs caused by the inhalation and retention of asbestos fibers. It usually occurs after high intensity and/or long-term exposure to asbestos (particularly in those individuals working on the production or end-use of products containing asbestos) and is therefore regarded as an occupational lung disease. People with extensive occupational exposure to the mining, manufacturing, handling or removal of asbestos are at risk of developing asbestosis. Sufferers may experience severe dyspnea (shortness of breath) and are at an increased risk for certain malignancies, including lung cancer but especially mesothelioma. Asbestosis specifically refers to interstitial (parenchymal) fibrosis from asbestos, and not pleural fibrosis or plaquing.

Signs and symptoms

The signs and symptoms of asbestosis do not manifest until after an appreciable latency (time since first exposure), often several decades under current conditions in the US. The primary symptom of asbestosis is generally the slow onset of dyspnea, especially on exertion.Clinically advanced cases of asbestosis may lead to respiratory failure. On auscultation of the lungs, the physician may hear inspiratory rales.

The characteristic pulmonary function finding in asbestosis is a restrictive ventilatory defect. This manifests as a reduction in lung volumes, particularly the Vital Capacity (VC) and Total Lung Capacity (TLC). The TLC may be reduced through alveolar wall thickening; however this is not always the case. Large airway function, as reflected by FEV1/FVC, is generally well preserved. In the more severe cases, the drastic reduction in lung function due to the stiffening of the lungs and reduced TLC may induce right-sided heart failure (cor pulmonale).[ In addition to a restrictive defect, asbestosis may produce reduction in Diffusion Capacity and arterial hypoxemia.

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What is Mesothelioma?

Mesothelioma, more precisely malignant mesothelioma, is a rare form of cancer that develops from the protective lining that covers many of the body's internal organs, themesothelium. It is usually caused by exposure to asbestos.
Its most common site is the pleura (outer lining of the lungs and internal chest wall), but it may also occur in the peritoneum (the lining of the abdominal cavity), the pericardium (a sac that surrounds the heart), or the tunica vaginalis (a sac that surrounds the testis).

Most people who develop mesothelioma have worked on jobs where they inhaled asbestos and glass particles, or they have been exposed to asbestos dust and fiber in other ways. It has also been suggested that washing the clothes of a family member who worked with asbestos or glass can put a person at risk for developing mesothelioma.Unlike lung cancer, there is no association between mesothelioma and smoking, but smoking greatly increases the risk of other asbestos-induced cancers. Those who have been exposed to asbestos have collected damages for asbestos-related disease, including mesothelioma. Compensation via asbestos funds or lawsuits is an important issue in law practices regarding mesothelioma (see asbestos and the law).

The symptoms of mesothelioma include shortness of breath due to pleural effusion (fluid between the lung and the chest wall) or chest wall pain, and general symptoms such as weight loss. The diagnosis may be suspected with chest X-ray and CT scan, and is confirmed with abiopsy (tissue sample) and microscopic examination. A thoracoscopy (inserting a tube with a camera into the chest) can be used to take biopsies. It allows the introduction of substances such as talc to obliterate the pleural space (called pleurodesis), which prevents more fluid from accumulating and pressing on the lung. Despite treatment with chemotherapy, radiation therapy or sometimes surgery, the disease carries a poor prognosis. Research aboutscreening tests for the early detection of mesothelioma is ongoing.

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