Signs and symptoms of portal hypertension include:

In addition, a widened portal vein as seen on a CT scan or MRI may raise the suspicion about portal hypertension. A cutoff of 13 mm is widely used in this regard, but the diameter is often larger than this is in normal individuals as well.

Portal hypertension is hypertension (high blood pressure) in the hepatic portal system – made up of the portal vein and its branches, that drain from most of the intestines to the liver. Portal hypertension is defined as a hepatic venous pressure gradient. Cirrhosis (a form of chronic liver failure) is the most common cause of portal hypertension; other, less frequent causes are therefore grouped as non-cirrhotic portal hypertension. When it becomes severe enough to cause symptoms or complications, treatment may be given to decrease portal hypertension itself or to manage its complications.

Smoking does not directly cause high blood pressure. However it is a known risk factor for other serious cardiovascular disease.

It has been suggested that vitamin D deficiency is associated with cardiovascular risk factors. It has been observed that individuals with a vitamin D deficiency have higher systolic and diastolic blood pressures than average. Vitamin D inhibits renin secretion and its activity, it therefore acts as a "negative endocrine regulator of the renin-angiotensin system". Hence, a deficiency in vitamin D leads to an increase in renin secretion. This is one possible mechanism of explaining the observed link between hypertension and vitamin D levels in the blood plasma.

Also, some authorities claim that potassium might both prevent and treat hypertension.

Hypertension results from a complex interaction of genes and environmental factors. Numerous common genetic variants with small effects on blood pressure have been identified as well as some rare genetic variants with large effects on blood pressure. Also, genome-wide association studies (GWAS) have identified 35 genetic loci related to blood pressure; 12 of these genetic loci influencing blood pressure were newly found. Sentinel SNP for each new genetic loci identified has shown an association with DNA methylation at multiple nearby Cpg sites. These sentinel SNP are located within genes related to vascular smooth muscle and renal function. DNA methylation might affect in some way linking common genetic variation to multiple phenotypes even though mechanisms underlying these associations are not understood. Single variant test performed in this study for the 35 sentinel SNP (known and new) showed that genetic variants singly or in aggregate contribute to risk of clinical phenotypes related to high blood pressure.

Blood pressure rises with aging and the risk of becoming hypertensive in later life is considerable. Several environmental factors influence blood pressure. High salt intake raises the blood pressure in salt sensitive individuals; lack of exercise, obesity, and depression can play a role in individual cases. The possible role of other factors such as caffeine consumption, and vitamin D deficiency are less clear. Insulin resistance, which is common in obesity and is a component of syndrome X (or the metabolic syndrome), is also thought to contribute to hypertension. One review suggests that sugar may play an important role in hypertension and salt is just an innocent bystander.

Events in early life, such as low birth weight, maternal smoking, and lack of breastfeeding may be risk factors for adult essential hypertension, although the mechanisms linking these exposures to adult hypertension remain unclear. An increased rate of high blood urea has been found in untreated people with hypertensive in comparison with people with normal blood pressure, although it is uncertain whether the former plays a causal role or is subsidiary to poor kidney function. Average blood pressure may be higher in the winter than in the summer.

Secondary hypertension results from an identifiable cause. Kidney disease is the most common secondary cause of hypertension. Hypertension can also be caused by endocrine conditions, such as Cushing's syndrome, hyperthyroidism, hypothyroidism, acromegaly, Conn's syndrome or hyperaldosteronism, renal artery stenosis (from atherosclerosis or fibromuscular dysplasia), hyperparathyroidism, and pheochromocytoma. Other causes of secondary hypertension include obesity, sleep apnea, pregnancy, coarctation of the aorta, excessive eating of liquorice, excessive drinking of alcohol, and certain prescription medicines, herbal remedies, and illegal drugs such as cocaine and methamphetamine. Arsenic exposure through drinking water has been shown to correlate with elevated blood pressure.

Several studies have found that patients with portal hypertension develop increased blood flow to the stomach. The physiological findings that correlate with worsening portal hypertensive gastropathy include an increased portal venous pressure gradient and decreased hepatic blood flow. Biopsies of the stomach in patients with portal hypertensive gastropathy show ectatic (or dilated) blood vessels, evidence of bleeding by means of red blood cells in the lamina propria, and edema in the stomach wall.

Prognosis of individuals with renovascular hypertension is not easy to determine. Those with atherosclerotic renal artery disease have a high risk of mortality, furthermore those who also have renal dysfunction have a higher mortality risk.

However, the majority of renovascular diseases can be improved with surgery.

Portal hypertensive gastropathy refers to changes in the mucosa of the stomach in patients with portal hypertension; by far the most common cause of this is cirrhosis of the liver. These changes in the mucosa include friability of the mucosa and the presence of ectatic blood vessels at the surface. Patients with portal hypertensive gastropathy may experience bleeding from the stomach, which may uncommonly manifest itself in vomiting blood or melena; however, portal hypertension may cause several other more common sources of upper gastrointestinal bleeding, such as esophageal varices and gastric varices. On endoscopic evaluation of the stomach, this condition shows a characteristic mosaic or "snake-skin" appearance to the mucosa of the stomach.

It is the goal of evolutionary medicine to find treatments for diseases that are informed by the evolutionary history of a disease. It has been suggested that gestational hypertension is linked to insulin resistance during pregnancy. Both the increase in blood sugar that can lead to gestational diabetes and the increase in blood pressure that can lead to gestational hypertension are mechanisms that mean to optimize the amount of nutrients that can be passed from maternal tissue to fetal tissue. It has been suggested that techniques used to combat insulin insensitivity might also prove beneficial to those suffering from gestational hypertension. Measures to avoid insulin resistance include avoiding obesity before pregnancy, minimizing weight gain during pregnancy, eating foods with low glycemic indexes, and exercising.

Based on these studies, treating to a systolic blood pressure of 140, as long as the diastolic blood pressure is 68 or more, seems safe. Corroborating this, a reanalysis of the SHEP data suggests allowing the diastolic to go below 70 may increase adverse effects.

A meta-analysis of individual patient data from randomized controlled trials found the lowest diastolic blood pressure for which cardiovascular outcomes improve is 85 mm Hg for untreated hypertensives and 80 mm Hg for treated hypertensives. The authors concluded "poor health conditions leading to low blood pressure and an increased risk for death probably explain the J-shaped curve". Interpreting the meta-analysis is difficult, but avoiding a diastolic blood pressure below 68–70 mm Hg seems reasonable because:

- The low value of 85 mm Hg for treated hypertensives in the meta-analysis is higher than the value of 68–70 mm Hg that is suggested by the two major randomized controlled trials of isolated systolic hypertension

- The two largest trials in the meta-analysis, Hypertension Detection and Follow-up Program (HDFP) and Medical Research Council trial in mild hypertension (MRC1) were predominantly middle-aged subjects, all of whom had diastolic hypertension before treatment.

- The independent contributions of diseases and factors other than hypertension versus effects of treatment are not clear in the meta-analysis.

A more contemporary meta-analysis by the Cochrane Hypertension group found no benefits in terms of reduced mortality or morbidity from treating patients to lower diastolic targets than 90–100 mmHg.

The goal of treating systolic hypertension is to delay and reduce the extent of damage to the heart, the cerebrovascular system, and the kidneys. Lifestyle interventions are a crucial element of successful treatment, including a diet low in sodium (salt) and rich in whole grains, fruits, and vegetables. Clinical trials have also documented the beneficial effects of weight loss, increased physical activity, and limiting alcohol consumption.

In addition to lifestyle changes, medication can also be used to reduce systolic hypertension to safe levels, although medications frequently have side effects, often serious.

Causes can include pancreatitis, cirrhosis, diverticulitis, and cholangiocarcinoma. It is also a known complication of splenectomy.

Gestational hypertension is one of the most common disorders seen in human pregnancies. Though relatively benign on its own, in roughly half of the cases of gestational hypertension the disorder progresses into preeclampsia, a dangerous condition that can prove fatal to expectant mothers. However, gestational hypertension is a condition that is fairly rare to see in other animals. For years, it has been the belief of the scientific community that gestational hypertension and preeclampsia were relatively unique to humans, although there has been some recent evidence that other primates can also suffer from similar conditions, albeit due to different underlying mechanisms. The underlying cause of gestational hypertension in humans is commonly believed to be an improperly implanted placenta. Humans have evolved to have a very invasive placenta to facilitate better oxygen transfer from the mother to the fetus, to support the growth of its large brain.

Portal vein thrombosis, previously known as Cauchois–Eppinger–Frugoni syndrome, is a form of venous thrombosis affecting the hepatic portal vein, which can lead to portal hypertension and reduction in the blood supply to the liver.

In ideal circumstances, patients with known varices should receive treatment to reduce their risk of bleeding. The non-selective β-blockers (e.g., propranolol, timolol or nadolol) and nitrates (e.g., isosorbide mononitrate (IMN) 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 β blockade and splanchnic blood flow by blocking vasodilating β receptors at splanchnic vasculature. The effectiveness of this treatment has been shown by a number of different studies.

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

When medical contraindications to beta-blockers exist, such as significant reactive airway disease, then treatment with prophylactic endoscopic variceal ligation is often performed.

In general, individuals with white coat hypertension have lower morbidity than patients with sustained hypertension, but higher morbidity than the clinically normotensive.

However, it should be remembered that all the established published trials on the consequences of high blood pressure and the benefits of treating are based on one-time measurement in clinical settings rather than the generally slightly lower readings obtained from ambulatory recordings.

The debate and conflicting ideas revolve around whether or not it would be feasible to treat white coat hypertension, as there still is no conclusive evidence that a temporary rise in blood pressure during office visits has an adverse effect on health.

In fact, many cross sectional studies have shown that "target-organ damage (as exemplified by left ventricular hypertrophy) is less in white-coat hypertensive patients than in sustained hypertensive patients even after the allowance has been made for differences in clinic pressure". Many believe that patients with "white coat" hypertension do not require even very small doses of antihypertensive therapy as it may result in hypotension, but must still be careful as patients may show signs of vascular changes and may eventually develop hypertension. Even patients with established hypertension that is well-controlled based on home blood pressure monitoring may experience elevated readings during office visits.

It is characterized by 'obliterative portovenopathy', which leads to various problems such as portal hypertension, massive splenomegaly, and variceal bleeding. It is estimated that about 85% of people with NCPF have repeated episodes of variceal bleeding.

Hallmark of the disease is thrombosis/sclerosis of branches of portal vein. Vessels formed are often termed as mesangiosinusoids or periportal cavernoma.

Dilated submucosal veins are the most prominent histologic feature of esophageal varices. The expansion of the submucosa leads to elevation of the mucosa above the surrounding tissue, which is apparent during endoscopy and is a key diagnostic feature. Evidence of recent variceal hemorrhage includes necrosis and ulceration of the mucosa. Evidence of past variceal hemorrhage includes inflammation and venous thrombosis.

The cause of renovascular hypertension is consistent with any narrowing/blockage of blood supply to the renal organ (renal artery stenosis). As a consequence of this action the renal organs release hormones that indicate to the body to maintain a higher amount of sodium and water, which in turn causes blood pressure to rise. Factors that may contribute are: diabetes, high cholesterol and advanced age, also of importance is that a unilateral

condition is sufficient to cause renovascular hypertension.

Anorectal varices are the dilation of collateral submucosal vessels due to backflow in the veins of the rectum. Typically this occurs due to portal hypertension which shunts venous blood from the portal system through the portosystemic anastomosis present at this site into the systemic venous system. This can also occur in the oesophagus, causing oesophageal varices, and at the level of the umbilicus, causing caput medusae. Between 44% and 78% of patients with portal hypertension get anorectal varices.

The intrahepatic shunts found in large dog breeds are passed on in a simple autosomal recessive way, while the extrahepatic shunts of the small breeds are inherited on a polygenic basis.

Treatment is directed largely to removing the cause, or, where that is impossible, to modifying its effects. Thus, therapy aimed at improving right heart function will also improve congestive hepatopathy. True nutmeg liver is usually secondary to left-sided heart failure causing congestive right heart failure, so treatment options are limited.

Few women of childbearing age have high blood pressure, up to 11% develop hypertension of pregnancy. While generally benign, it may herald three complications of pregnancy: pre-eclampsia, HELLP syndrome and eclampsia. Follow-up and control with medication is therefore often necessary.