Hepatic hypertension symptoms. Causes of the onset and development of portal hypertension

Portal hypertension- increased pressure in the portal vein - a vessel that collects venous blood (read what kind of blood this is) from many abdominal organs and carries it to the liver.

Complications of pathology are:

• Hepatosplenomegaly;
• Accumulation of ascitic fluid in the free abdominal cavity;
• Decreased mental function due to intoxication;
• Bleeding of the esophageal vessels.

ICD-10 code

Portal hypertension is a syndrome established on the basis of clinical symptoms, physical examination and data endoscopic examination. ICD 10 code – K 76.6.

A little anatomy

The portal vein is one of the most large vessels body, normal pressure in the vein – 5-10 mm Hg. Art. With portal hypertension it increases to 12 mmHg. Art. and higher, which causes dilation of the vessels flowing into the portal vein and increases the risk of bleeding from them.

The portal vessel collects blood from most of the intestine and other unpaired organs of the abdominal cavity. These include the pancreas and spleen.

Subsequently, the portal vein divides into smaller branches, blood bearers into the hepatic sinuses. Purified blood is collected in the hepatic veins, then into the superior vena cava.

Therapeutic measures for this disease consist of the prevention of bleeding from the esophagus and stomach, and completely getting rid of portal hypertension is only possible through surgery; shunting is performed between the portal vein and others with the creation of anastomoses.

Bleeding from esophageal varices can be fatal.

Causes of the disease

An increase in pressure in the vessel causes the vein to expand.

Such anomalies include:

• Pylephlebitis – purulent inflammation the walls of the portal vein, leading to its thrombosis;
• Phlebosclerosis - growth in a vessel connective tissue, which can cause its obliteration;
• Sometimes congenital stenosis of the mouth and even atresia occurs - complete absence vein or its fusion.

The disease is accompanied by fever, rash, an increase in the number of white blood cells and a decrease in performance.

Schistosomiasis can easily be contracted through contaminated water.

Pathogenesis of the disease

Emergence pathological symptoms with portal hypertension occurs due to increased pressure in the portal vein.

This is facilitated by a number of mechanisms:

• Increased resistance of hepatic vessels: usually associated with the synthesis of substances that narrow the vein and increase its tone;
• Presence of obstruction to blood flow: tumors, stenoses, fibrous bridges;
• The appearance of collaterals (connecting vessels);
• Increased volumetric blood flow in the system.

These factors trigger a vicious circle and aggravate each other. An increase in blood volume provokes the opening of shunts in lung tissue, the oxygen supply to the blood is disrupted. This, in turn, provokes the formation of fibrous tissue.

Vasoactive components that increase vascular tone negatively affect cardiac function. And increasing heart failure worsens liver function.

Portal hypertension in liver cirrhosis

Most often in clinical practice Portal hypertension is observed in liver cirrhosis, which is among the top ten causes of death in the world.

Every year, about 40 million people, mostly men, die from cirrhosis of the liver. Cirrhosis with hypertension causes the liver to first become enlarged, then shrink and harden.

The replacement of normal liver tissue with fibrous connective tissue is irreversible and leads to a rapid deterioration of liver function.

The etiology of cirrhotic liver is diverse:

In 10-20% of patients, the cause of the disease remains unclear, then they speak of primary biliary cirrhosis.

The following stages are distinguished:

• Effect of infection or toxins;
• Excessive growth of connective tissue;
• Development of fibrosis;
• Impaired blood supply to liver cells with necrosis;
• Activation of immune mechanisms.

To diagnose cirrhosis, a detailed biochemical analysis blood, assessment of enzyme activity, decrease in the level of blood cells. Instrumental methods include angiography, ultrasound, and computed tomography.

Complications of cirrhosis:

• Bleeding from dilated veins of the upper gastrointestinal tract;
• Thrombotic masses of the portal vein;
• Encephalopathy and coma of hepatic etiology;
• Hepatocellular carcinoma – dangerous cancer liver;
• General complications: sepsis, pneumonia, inflammation of the peritoneum with ascites.

Organ function in cirrhosis international standards assessed according to the Child-Pugh classification:

Interpretation of results:

1. A score of 5-6 corresponds to first class, life expectancy is 20 years;
2. 7-9 points are classified as class B, which is an indication for liver transplantation;
3. The third class, gaining 10-15 points, corresponds to survival of up to 3 years and postoperative mortality of up to 80%.

Classification

There are several classifications of portal hypertension: based on the localization of the block, by the level of pressure, by the degree of development various complications and endoscopic picture.

According to the level of development of the portal block, the following types are distinguished:

1. Suprahepatic is caused by thrombosis, compression by a tumor, obstructive processes in the inferior vena cava, accumulation of fluid in the cardiac sac, or severe regurgitation in the tricuspid valve;
2. Intrahepatic - the most extensive group, combines pre-sinusoidal and sinusoidal causes;
3. Subhepatic is caused by thrombosis of the portal vein itself, its cavernous transformation, idiopathic tropical splenomegaly;
4. Mixed.

Hepatic hypertension is the most common. This type is justified by the pathology of the liver itself, for example, with cirrhosis of the liver, alcoholic hepatitis, and vitamin A intoxication. Similar symptoms can occur with an overdose of cytotoxic drugs.

Causes of presinusoidal intrahepatic hypertension include liver fibrosis, bile duct inflammation, sarcoidosis, amyloid accumulation, hemochromatosis, copper and arsenic exposure.

According to the level of pressure in the portal vein system, the classification is as follows:

• I degree corresponds to a pressure of 250-400 mm water column;
• II degree– up to 600 mm;
• III degree- at a pressure of more than 600 mm of water column.

A classification is proposed according to the endoscopic picture, which reveals varicose nodules in the walls of the esophagus, and according to the size of the varicose veins:

• Single veins;
• Columns of veins that do not respond to pressure with the device;
• At the last degree - confluent veins.

Development of extrahepatic hypertension

Often, extrahepatic causes contribute to the occurrence of venous congestion in the vessels of the liver. These include congenital stenosis and tumor-like growths in the wall of the inferior vena cava, which aggravate the increase in pressure in the portal system. A more rare cause is membranous fusion of the vessel, which occurs in utero.

Hypertension is often preceded by diseases of the heart muscle, for example, cardiomyopathy, extensive necrosis. Stagnation also causes reduced cardiac output, for example, due to valve defects or pericarditis.

Stages of the disease

The staging of symptoms is explained gradual decline functions of hepatic cells.

The following stages are distinguished:

Clinical manifestations

Signs of portal hypertension vary in severity depending on the time of development and severity of the disease.

The first symptoms of the disease can be general and nonspecific, but without timely diagnosis and proper treatment, more serious symptoms will arise.

There are 4 stages of the disease:

1. The initial stage is characterized by rare mild complaints and general weakness;
2. The second stage appears more pronounced manifestations from the digestive tract;
3. At the third stage, there is an accumulation of fluid in the abdominal cavity - ascites;
4. The final stage is characterized by complications and bleeding.

Early symptoms of hypertension in the system may include slight bloating, dry skin, and nausea. There may be heaviness in the right hypochondrium after consumption fatty foods, which usually goes away on its own. There is often a feeling of fullness in the stomach when eating a small amount of food.

As the pressure in the portal vein increases, the symptoms also worsen. An enlargement of the abdomen appears, an increase in the venous pattern on the skin of the abdominal wall.

Timely consultation with a doctor similar symptoms allows you to start treatment before the formation irreversible changes in the liver.

Upon examination, the patient is diagnosed with liver enlargement:

• Palpated several centimeters below the right costal arch;
• Its edge is pointed;
• The surface is compacted and deformed.

In a third of cases, it is possible to palpate nodules on the surface of the organ. A moderately enlarged spleen is often observed. Often there is an increase in temperature, resistant to the use of antibiotics.

Due to the deterioration of liver function, including the synthesis of coagulation factors, hemorrhages and petechiae occur. Sometimes hair loss armpits and pubic area.

The terminal stage is characterized by:

• Tense ascites;
• Expressed peripheral edema, especially lower limbs;
• Bleeding from the veins of the esophagus, which can end in death.

Portal liver failure leads to the development of encephalopathy - a decrease in cognitive and intellectual functions, brain damage.

Portal encephalopathy is characterized by:

Ascites was previously called abdominal hydrops. In the terminal stages of the disease, the abdominal cavity may accumulate huge quantities transudate.

Increased pressure in the portal vein leads to its expansion and increased permeability of the vascular wall, which leads to fluid leakage into the free cavity.

The symptom is manifested by the fact that the abdomen evenly increases, the skin stretches, on the front abdominal wall a “jellyfish head” is formed - convoluted dilated veins. When combined with stretching umbilical ring protrusion of the navel occurs.

Often with ascites, infection of the fluid occurs and bacterial peritonitis develops.

One of the causes of subhepatic hypertension is portal vein thrombosis.

Complications

The decompensated stage of the disease without proper treatment is transformed into a complicated one.

Common complications include:

Features of the disease in children

Symptoms of portal hypertension in childhood does not differ from that in adult patients.

The most common causes of the disease are congenital pathologies:

• Suprahepatic hypertension in Budd-Chiari syndrome, there is a violation of the outflow of blood and the development of necrotic changes in the liver;
• Intrahepatic is caused by congenital hepatitis and fibrosis;
• Extrahepatic is caused by an anomaly of the vessels: the formation of blood clots, inflammation of the vascular wall.

A harbinger of increased pressure in the portal vein system in children can be cavernomatosis - rare disease, manifested by thrombosis with a decrease in the lumen of the vessel. The portal vein is transformed into an angioma, replaced small vessels. Syndromes lead to severe complications.

The prognosis of the disease is unfavorable, the maximum life expectancy is 8-9 years.

Diagnostics

The provisional diagnosis is based on characteristic complaints and physical examination data. Portal hypertension is suspected in individuals with frequent bleeding from the veins of the esophagus and stomach, suffering from alcoholism and chronic hepatitis B and C.

Conduct laboratory tests:

Instrumental diagnostics is actively carried out.

Ultrasound allows you to evaluate:

• Liver size;
• Structure;
• Presence of nodules on the surface.

Dopplerography indicates collaterals, the state of blood flow in different areas vascular bed. Tomography demonstrates a more detailed structure of the organ, possible tumors and anastomoses between the vascular beds.

Complications of the disease - dilated veins of the esophagus - are examined by performing esophagogastroscopy, in which the size and nature of the veins are visible, as well as “red markers” - dilated venules, vascular nodules.

There are three types of “red markers”:

Treatment and modern recommendations

In the early stages of the disease, treatment can be conservative and include the use of nitroglycerin, ACE inhibitors.

If complications develop, the main therapy should be aimed at preventing and eliminating bleeding and ligating bleeding vessels. Whether portal hypertension can be cured depends on its stage.

Sometimes surgeons are able to create anastomoses between the portal vein and the vena cava, which reduces the pressure in the vessel and relieves symptoms.

The diet for this disease and the cirrhosis that causes it should include a sufficient protein content (up to 1.5 g per kg of body weight). A proper drinking regime is necessary to prevent edema. Excluded canned food, additives.

Limit the consumption of salt, which retains fluid in the body and provokes increased blood pressure and edema syndrome.

Conservative treatment includes protection of liver cells and stimulation of the bile ducts. Bile acid deficiency is corrected by the administration of ursodeoxycholic acid.

This drug normalizes digestion and improves the function of liver tissue. Take it at night at a dose of 10-15 mg per kg.

The effect of the drug is in the following moments:

Indications for surgical treatment are intense bleeding, intense ascites, and significant enlargement of the spleen. An anastomosis is created between the portal vein and other vessels.

The problem of preventing a complicated course

Diseases that contribute to the occurrence of portal hypertension often develop rapidly and have an irreversible course. If the pathology is suspected in time, it can be treated, and careful adherence to the doctor’s instructions will help control severe symptoms for as long as possible.

Complications are prevented by strict diet, regular examination by a specialist, timely surgical treatment.

Preventive measures for developing portal hypertension:

• Prevention of hepatitis infection;
• Complete cessation of alcohol consumption;
• Caution in prescribing hepatotoxic drugs.

Forecast

The prognosis of the disease depends on the type of portal hypertension and the stage at which it is started. specialized treatment. In extrahepatic hypertension with treatable causes, the outcome may be good.

However, with intrahepatic causes, especially with the addition of liver failure, the prognosis is in most cases unfavorable.

Portal hypertension is an increase in pressure in the portal vein system (normal pressure is 7 mm Hg), which develops as a result of obstruction of blood flow in any part of this vein.

Increase over 12-20 mm Hg. leads to expansion of the portal vein. Varicose veins rupture easily, leading to bleeding.

Causes

Intrahepatic causes of portal hypertension

• Nodular proliferation (with rheumatoid arthritis, Felty's syndrome)
• Spicy alcoholic hepatitis
• Taking cytostatics (methotrexate, azathioprine, mercaptopurine)
• Vitamin A toxicity
• Schistosomiasis
• Caroli disease
• Wilson's disease
• Congenital liver fibrosis (hepatoportal sclerosis)
• Gaucher disease
• Polycystic liver disease
• Tumors of the liver
• Myeloproliferative diseases
• Impact toxic substances(vinyl chloride, arsenic, copper)

Prehepatic causes

• Compression of the trunk of the portal or splenic vein
• Surgical interventions on the liver, biliary tract; removal of the selenium
• Damage to the portal vein due to trauma or injury
• Enlarged spleen with polycythemia, osteomyelofibrosis, hemorrhagic thrombocythemia
• Congenital portal vein anomalies

Posthepatic causes of portal hypertension

• Budd-Chiari syndrome
• Constrictive pericarditis (eg, pericardial calcification) causes increased pressure in the inferior vena cava, increasing resistance venous blood flow in the liver
• Thrombosis or compression of the inferior vena cava.

The main importance is the expansion of veins lower third esophagus and fundus of the stomach, because Varicose veins rupture easily, leading to bleeding.

Manifestations of portal hypertension

• Dilation of the saphenous veins of the anterior abdominal wall ("Medusa's head"), veins of the lower 2/3 of the esophagus, stomach, hemorrhoidal veins
• Bleeding from varicose veins - esophagogastric bleeding (vomiting "coffee grounds", black feces), hemorrhoidal bleeding
• Pain in the epigastric region, a feeling of heaviness in the hypochondrium, nausea, constipation, etc.
• Edema
• May be jaundice

Survey

• In the general blood test - a decrease in platelets, leukocytes, erythrocytes
• IN functional tests liver - changes characteristic of hepatitis and cirrhosis of the liver
• Determination of markers of viral hepatitis
• Detection of autoantibodies
• Determination of iron concentration in blood serum and liver
• Determination of alpha-1-antitrypsin activity in blood serum
• Determination of cerulloplasmin content and daily urinary copper excretion and quantification of copper content in liver tissue.
• Esophagography
• Fibrogastroduodenoscopy allows to identify varicose veins of the esophagus and stomach
• Sigmoidoscopy: under the mucous membrane of the rectum and sigmoid colon Varicose veins are clearly visible
• Ultrasound allows you to assess the diameter of the portal and splenic veins and diagnose portal vein thrombosis.
• Dopplerography
• Venography
• Angiography

Treatment of portal hypertension

When treating portal hypertension, it is important to eliminate the causes of the underlying disease. Also applies:

• Propranolol 20-180 mg 2 times a day in combination with sclerotherapy or ligation of varicose vessels
• Stopping bleeding: terlipressin 1 mg IV bolus, then 1 mg every 4 hours for 24 hours - acts more stable and longer than vasopressin. Somatostatin for portal hypertension 250 mg intravenously as a bolus, then 250 mg intravenously as a drip over an hour (infusions can be continued for up to 5 days) reduces the frequency of recurrent bleeding by 2 times. Somatostatin impairs blood circulation in the kidneys and water-salt metabolism, therefore, in case of ascites it should be prescribed with caution.
• Endoscopic sclerotherapy (“gold standard” of treatment): tamponade is preliminarily performed and somatostatin is administered. A sclerosing drug injected into varicose veins leads to their blockage. The manipulation is effective in 80% of cases.
• Esophageal tamponade using a Sengstaken-Blakemore probe. After inserting the probe into the stomach, air is pumped into the cuffs, pressing against the veins of the stomach and the lower third of the esophagus. The esophageal balloon should not be kept inflated for more than 24 hours.
• Endoscopic ligation of varicose veins of the esophagus and stomach with elastic rings. The effectiveness is the same as with sclerotherapy, but the procedure is difficult in the presence of ongoing bleeding. Prevents rebleeding but does not affect survival.
• Planned surgery varicose veins of the esophagus and stomach are performed to prevent recurrent bleeding in the event of failure to prevent bleeding with propranolol or sclerotherapy. Survival is determined functional state liver. After surgery, the likelihood of ascites, peritonitis, and hepatorenal syndrome decreases
• Liver transplantation is indicated for patients with cirrhosis who have suffered at least 2 episodes of bleeding requiring blood transfusion

Forecast

The prognosis for portal hypertension depends on the underlying disease. In cirrhosis, it is determined by the severity of liver failure. The mortality rate for each bleeding is 40%.

Characterized by a number of specific clinical characteristics. manifestations and occurs when

some internal diseases. At the same time, the basis of what occurs in the body

changes is an increase in pressure in the portal vein system. In accordance with

the level of obstruction to the outflow of blood through the portal vein system and the nature

pathological process that caused this obstacle, there are four main

forms of portal hypertension syndrome - prehepatic (prehepatic),

intrahepatic, suprahepatic and mixed.

The prehepatic form of the syndrome is caused by congenital developmental anomalies

portal vein and its thrombosis. Congenital anomalies of the portal vein -

congenital absence (aplasia, hypoplasia, atresia, fusion of the vein lumen at

for everyone

zheniya or on any segment). Portal vein atresia is associated with

extension of the normal process of obliteration to the portal vein,

occurring in the umbilical vein and the duct of Arancia Portal vein thrombosis

observed in septic processes (purulent processes in the abdominal organs

cavity, sepsis, septicopyemia, umbilical sepsis) as a result of its compression

inflammatory, tumor-like infiltrate, cysts, etc.

Intrahepatic form of portal hypertension syndrome in overwhelming

in most patients is associated with liver cirrhosis. Less commonly, the cause of the block may be

focal sclerotic and cicatricial processes in liver tissue. About 80% of patients with

portal hypertension syndrome have an intrahepatic block form.

The suprahepatic form is caused by difficulty in the outflow of blood from the hepatic veins.

The cause of difficulty in the outflow of blood from the liver may be endophlebitis of the hepatic veins

with their partial or complete obstruction (Chiari disease). Also distinguished

Budd-Chiari syndrome, in which the suprahepatic form of portal hypertension

associated with thrombotic occlusion of the vena cava at the level of the hepatic veins or

slightly more proximal. One of the reasons is anomalies in the development of the inferior vena cava

Difficulty in the outflow of blood from the liver may also be associated with constriction

pericarditis, tricuspid valve insufficiency, with compression of the lower

vena cava from the outside (s. (ulcers, cysts, etc.).

The mixed, or combined, form of portal hypertension syndrome is associated with

development of portal vein thrombosis in patients with liver cirrhosis.

With portal hypertension due to a sharp increase in hydrostatic pressure

pressure in the portal vein system up to 350-- 450 mm H2O and above (at a norm of 200 mm

water art) blood outflow occurs through natural portocaval anastomoses

Collateral pathways of blood outflow from the portal vein.

There are three groups of portocaval anastomoses.

1. Anastomoses in the area of ​​the cardial part of the stomach and the abdominal part

esophagus Blood from the portal vein enters through the venous plexuses of the indicated

organs along the azygos vein into the inferior vena cava For varicose veins

Bleeding may occur from the esophagus. Bleeding may occur.

promote wall ulcerations associated with reflux esophagitis

2. Anastomoses between the upper, middle and lower rectus-intestinal (rectal)

veins. In this case, blood from the upper rectal veins belonging to the portal

system, through the anastomotic system it enters the internal iliac veins and further

into the inferior vena cava When the veins of the submucosal plexus of the rectum dilate to

Against the background of portal hypertension, quite abundant rectal

bleeding

3. Anastomoses between the peri-umbilical veins and the umbilical vein (if it is not closed),

draining blood from the portal vein through the umbilical vein and further into the anterior veins

abdominal wall, from where blood flows into both the inferior and superior vena cava.

expressed

A significant expansion of this group of portocaval anastomoses can be noted

a peculiar pattern of convoluted dilated saphenous veins of the anterior abdominal wall,

denoted by the term "jellyfish head".

Basics syndromes of portal hypertension and special research methods.

portal vein.

(hypoalbuminemia).

Prognosis: unfavorable. D: X-ray is used first for portal hypertension

examination of the esophagus and stomach to identify varicose veins in

distal part of the esophagus in the form of multiple oval and round defects

filling. However, the effectiveness of this research method does not exceed 50%.

Fibroesophagoscopy is more informative. Importance in diagnosing the syndrome

portal hypertension - determining the level of obstruction to the outflow of blood from

portal vein, have instrumental research methods (celiacography -

arterial and venous phases, cavagraphy, splenoportography, etc.). At

intrahepatic form of the syndrome, valuable information can be obtained from

laboratory research methods reflecting the functional state of the liver.

Splenoportography and splenomanometry. Manipulations are performed under X-ray

office, preferably under the control of an X-ray television screen. Under local

the spleen is punctured with anesthesia (focusing on its percussion boundaries and shadow

on the X-ray screen). A needle inserted into the spleen tissue is attached to

Waldmann apparatus and measure blood pressure. For portal hypertension

pressure usually exceeds 250 mm water. Art., sometimes reaches 500-600 mm of water. Art.

and more. After measuring the pressure, a contrast agent is injected through the needle.

(Verografin, Cardiotrast, etc.) and take a series of radiographs. Characteristic

symptoms of portal hypertension during splenoportography: significant expansion

portal vein and its tributaries, poor intrahepatic vascular pattern with

intrahepatic form of the syndrome; site of thrombotic occlusion of the portal or

splenic vein in the prehepatic form of the syndrome. For diagnostics

cavagraphy is used for the suprahepatic form of portal hypertension syndrome

(injection of contrast into the inferior vena cava through the femoral veins according to Seldinger). At

cavagraphy can determine the level of obstruction of blood outflow from the hepatic veins,

site of narrowing or occlusion of the inferior vena cava. Possible+ selective

catheterization of the hepatic veins with a series of x-rays. At

Celiacography can differentiate intra- and prehepatic forms

syndrome. Usually there is dilatation and tortuosity of the splenic artery,

narrowing of the hepatic artery, depletion of the intrahepatic vascular pattern. IN

In the venous phase, the dilated splenic and portal veins are clearly visible.

K-ka and d-ka liver block.

K: Clinical manifestations of various forms of portal hypertension are related

primarily with the primary disease that caused the increase

pressure in the portal vein. This must be taken into account when questioning the patient and

analysis clinical picture diseases when serious complications have already arisen

portal hypertension - blood pressure, portal vein thrombosis, etc.

The following symptoms and syndromes are characteristic of portal hypertension:

splenomegaly, varicose veins veins of the esophagus and stomach, from

them, + from hemorrhoidal veins, ascites, dyspepsia (pain in

epigastric region, lack of appetite, nausea, constipation), liver signs

(“spider veins”, “liver palms”, etc.), hypersplenism

(thrombocytopenia, leukopenia, less often anemia), coagulation system disorders

blood towards hypocoagulation

For the intrahepatic form of portal hypertension, the clinical leaders are:

symptoms of liver cirrhosis. The nature of the disease depends on the nature of cirrhosis

liver (postnecrotic, alcoholic, etc.), activity of the process, degree

compensation for impaired liver functions. Portal hypertension occurs in

these patients with hemorrhagic complications, splenomegaly, varicose veins

anterior abdominal wall, ascites. A terrible complication is c/t from

veins of the esophagus and stomach. In this case, regurgitation or vomiting occurs unchanged

blood without any previous pain sensations in epigastric region

When blood flows into the stomach, with massive bleeding, vomiting can be observed

changed blood the color of coffee grounds, melena. Symptoms occur quickly

posthemorrhagic anemia. Mortality during the first bleeding from the esophageal veins

with cirrhosis it is high - 30% or more. Repeated bleeding, ascites, jaundice (for

due to damage to the liver parenchyma) - signs of an advanced stage of liver cirrhosis,

which leaves little chance of success with drug or surgical treatment

portal hypertension syndrome in this disease.

K-ka and d-ka subhepatic block.

K: Clinical manifestations of various forms of portal hypertension are related

primarily with the primary disease that caused the increase

pressure in the portal vein. This must be taken into account when questioning the patient and

analysis of the clinical picture of the disease, when serious complications have already arisen

portal hypertension - blood pressure, portal vein thrombosis, etc.

The following symptoms and syndromes are characteristic of portal hypertension:

splenomegaly, varicose veins of the esophagus and stomach, c/t from

them, + from hemorrhoidal veins, ascites, dyspepsia (pain in

epigastric region, lack of appetite, nausea, constipation), liver signs

(“spider veins”, “liver palms”, etc.), hypersplenism

(thrombocytopenia, leukopenia, less often anemia), coagulation system disorders

blood towards hypocoagulation

In the prehepatic form of the syndrome, the disease occurs more often in childhood,

proceeds relatively favorably. Macroscopically in some patients

the portal vein is replaced by many small dilated veins (cavernoma). Most

Frequent manifestations of the disease are bleeding from the veins of the esophagus (which sometimes

are the first symptom of the disease), splenomegaly, hypersplenism, thrombosis

portal vein

K-ka and d-ka mixed block shape.

K: Clinical manifestations of various forms of portal hypertension are related

primarily with the primary disease that caused the increase

pressure in the portal vein. This must be taken into account when questioning the patient and

analysis of the clinical picture of the disease, when serious complications have already arisen

portal hypertension - blood pressure, portal vein thrombosis, etc.

The following symptoms and syndromes are characteristic of portal hypertension:

splenomegaly, varicose veins of the esophagus and stomach, c/t from

them, + from hemorrhoidal veins, ascites, dyspepsia (pain in

epigastric region, lack of appetite, nausea, constipation), liver signs

(“spider veins”, “liver palms”, etc.), hypersplenism

(thrombocytopenia, leukopenia, less often anemia), coagulation system disorders

blood towards hypocoagulation

In the prehepatic form of the syndrome, the disease occurs more often in childhood,

proceeds relatively favorably. Macroscopically in some patients

the portal vein is replaced by many small dilated veins (cavernoma). Most

Frequent manifestations of the disease are bleeding from the veins of the esophagus (which sometimes

are the first symptom of the disease), splenomegaly, hypersplenism, thrombosis

portal vein.

For the intrahepatic form of portal hypertension, the clinical leaders are:

symptoms of liver cirrhosis. The nature of the disease depends on the nature of cirrhosis

liver (postnecrotic, alcoholic, etc.), activity of the process, degree

compensation for impaired liver functions. Portal hypertension occurs in

these patients with hemorrhagic complications, splenomegaly, varicose veins

anterior abdominal wall, ascites. A terrible complication is c/t from

veins of the esophagus and stomach. In this case, regurgitation or vomiting occurs unchanged

blood without any previous pain in the epigastric region

When blood flows into the stomach, with massive bleeding, vomiting can be observed

changed blood the color of coffee grounds, melena. Symptoms occur quickly

posthemorrhagic anemia. Mortality during the first bleeding from the esophageal veins

with cirrhosis it is high - 30% or more. Repeated bleeding, ascites, jaundice (for

due to damage to the liver parenchyma) - signs of an advanced stage of liver cirrhosis,

which leaves little chance of success with drug or surgical treatment

portal hypertension syndrome in this disease.

The suprahepatic form of portal hypertension syndrome is often caused by the disease

Chiari or Budd-Chiari syndrome. In the acute form of the disease, the development of the disease suddenly

Quite severe pain occurs in the epigastric region, right hypochondrium,

hepatomegaly, hyperthermia, and ascites increase rapidly. Death of patients

occurs as a result of profuse bleeding from the veins of the esophagus or from

hepatic-renal failure.

In the chronic form, hepatomegaly and isplenomegaly gradually increases, a collateral venous network develops on the anterior abdominal wall, ascites increases, exhaustion increases, and protein metabolism is impaired (hypoalbuminemia). Prognosis: unfavorable.

D/d portal hypertension from other diseases.

K: Clinical manifestations of various forms of portal hypertension are related

primarily with the primary disease that caused the increase

pressure in the portal vein. This must be taken into account when questioning the patient and

analysis of the clinical picture of the disease, when serious complications have already arisen

portal hypertension - blood pressure, portal vein thrombosis, etc.

The following symptoms and syndromes are characteristic of portal hypertension:

splenomegaly, varicose veins of the esophagus and stomach, c/t from

them, + from hemorrhoidal veins, ascites, dyspepsia (pain in

epigastric region, lack of appetite, nausea, constipation), liver signs

(“spider veins”, “liver palms”, etc.), hypersplenism

(thrombocytopenia, leukopenia, less often anemia), coagulation system disorders

blood towards hypocoagulation

In the prehepatic form of the syndrome, the disease occurs more often in childhood,

proceeds relatively favorably. Macroscopically in some patients

the portal vein is replaced by many small dilated veins (cavernoma). Most

Frequent manifestations of the disease are bleeding from the veins of the esophagus (which sometimes

are the first symptom of the disease), splenomegaly, hypersplenism, thrombosis

portal vein.

For the intrahepatic form of portal hypertension, the clinical leaders are:

symptoms of liver cirrhosis. The nature of the disease depends on the nature of cirrhosis

liver (postnecrotic, alcoholic, etc.), activity of the process, degree

compensation for impaired liver functions. Portal hypertension occurs in

these patients with hemorrhagic complications, splenomegaly, varicose veins

anterior abdominal wall, ascites. A terrible complication is c/t from

veins of the esophagus and stomach. In this case, regurgitation or vomiting occurs unchanged

blood without any previous pain in the epigastric region

When blood flows into the stomach, with massive bleeding, vomiting can be observed

changed blood the color of coffee grounds, melena. Symptoms occur quickly

posthemorrhagic anemia. Mortality during the first bleeding from the esophageal veins

with cirrhosis it is high - 30% or more. Repeated bleeding, ascites, jaundice (for

due to damage to the liver parenchyma) - signs of an advanced stage of liver cirrhosis,

which leaves little chance of success with drug or surgical treatment

portal hypertension syndrome in this disease.

The suprahepatic form of portal hypertension syndrome is often caused by the disease

Chiari or Budd-Chiari syndrome. In the acute form of the disease, the development of the disease suddenly

Quite severe pain occurs in the epigastric region, right hypochondrium,

hepatomegaly, hyperthermia, and ascites increase rapidly. Death of patients

occurs as a result of profuse bleeding from the veins of the esophagus or from

hepatic-renal failure.

In the chronic form of the disease, hepatomegaly and

splenomegaly, collateral venous vascular network develops in the anterior

abdominal wall, ascites increases, exhaustion occurs, protein metabolism disorders occur

(hypoalbuminemia).

Prognosis: unfavorable.

K-ka and d-ka suprahepatic block.

K: Clinical manifestations of various forms of portal hypertension are related

primarily with the primary disease that caused the increase

pressure in the portal vein. This must be taken into account when questioning the patient and

analysis of the clinical picture of the disease, when serious complications have already arisen

portal hypertension - blood pressure, portal vein thrombosis, etc.

The following symptoms and syndromes are characteristic of portal hypertension:

splenomegaly, varicose veins of the esophagus and stomach, c/t from

them, + from hemorrhoidal veins, ascites, dyspepsia (pain in

epigastric region, lack of appetite, nausea, constipation), liver signs

(“spider veins”, “liver palms”, etc.), hypersplenism

(thrombocytopenia, leukopenia, less often anemia), coagulation system disorders

blood towards hypocoagulation

The suprahepatic form of portal hypertension syndrome is often caused by the disease

Chiari or Budd-Chiari syndrome. In the acute form of the disease, the development of the disease suddenly

Quite severe pain occurs in the epigastric region, right hypochondrium,

hepatomegaly, hyperthermia, and ascites increase rapidly. Death of patients

occurs as a result of profuse bleeding from the veins of the esophagus or from

hepatic-renal failure.

In the chronic form of the disease, hepatomegaly and

splenomegaly, collateral venous vascular network develops in the anterior

abdominal wall, ascites increases, exhaustion occurs, protein metabolism disorders occur

(hypoalbuminemia).

Prognosis: unfavorable.

L uncomplicated form of portal hypertension.

portocaval anastomosis.

mortality

strict indications.

anastomosis.

L portal hypertension complicated by k/tm.

L bleeding from varicose veins of the esophagus begins with

conservative measures: perform tamponade of the esophagus with a Blackmore probe,

hemostatic therapy, blood transfusion, pituitrin are used (to reduce

portal pressure). The Blackmore probe consists of a three-lumen rubber tube

with two cylinders of round and cylindrical shape

Two channels of the probe are used to inflate the balloons, the third one (opening in

distal part of the probe) for aspiration of gastric contents (monitoring

efficiency of hemostasis). The Blackmore probe is inserted through the nose into the stomach, inflated

distal (gastric) balloon, forcing 60--70 ml of air. Then the probe

tighten until resistance is felt when the balloon is localized in

cardia areas. After that, 100-150 ml of air is injected into the esophageal balloon. IN

In this state, the walls of the elastic balloon exert uniform pressure across

the entire circumference of the esophagus, squeezing the bleeding veins of the distal

esophagus and cardia of the stomach. Relax after a few hours

pressure in the balloons, controlling the effect of hemostasis on the probe. Duration

the presence of the probe in the esophagus should not exceed 2 days due to the risk of developing

bedsores. The use of phlebosclerosing drugs (varicocid, thrombovar and

etc.) in the treatment of bleeding from varicose veins of the esophagus is carried out

through an esophagoscope. Through the endoscope with a special needle into the lumen of the vein or

a drug is injected paravenously, causing damage to the intima of the vein, its adhesion into

obliteration of the lumen. In order to create favorable conditions for adhesion

walls of varicose veins for 1 day, a Blackmore probe is inserted.

If drug treatment fails, bleeding from varices

veins of the esophagus as a necessary measure is used Various types surgical

interventions aimed at stopping bleeding and uncoupling

portocaval anastomoses of the gastroesophageal zone. Due to severe

For the patient's condition, transgastric ligation is the most commonly used procedure.

dilated veins of the esophagus and cardia or suturing of the subcardial region

stitching machines. Proximal gastrectomy is performed much less frequently

and abdominal esophagus, application of vascular direct lortocaval

anastomosis.

Prognosis: unfavorable, mortality after these types of operations reaches 75%.

Main types of surgery for portal hypertension, indications.

Indicated: 1.bleeding.from varicose veins of the food and stomach, if unsuccessful. conservative therapy;

2. varic.dilat.veins food. and stomach, often complicated. bleeding;

3. with splenomegaly with hypersplenism;

4. with ascites;

5. for correction of portal blood flow, if there are rough morpho-functional conditions. changed. there is no liver or spleen in the condition.

Contraindication: 1. means. morpho-functional changed. in the liver and spleen; 2.severe concomitant pathology.

Operations: 1. Disconnection of the veins of the stomach and esophagus from the portal system:

a).Tanner – transverse. crossed. stomach in cardiac department with subsequent stitched walls

b).Patients – gastrotomy with an oblique incision from the fundus to the lesser cyrus. with stitching expanded. veins and the esophagus from the mucous side.

2.Creation of new pathways for blood outflow from the portal. Systems:

a).portocaval shunting (splenorenal - Whipple-Blakemore procedure, cavomesenteric - Bogoraz procedure);

b).organoanastomoses (fusion of the omentum and the organ enveloping it - omentopexy or between organs due to a pressure gradient on opposite sides of the block - organopexy (omentohepatopexy, omentospleno-, hepatopneumopexy, cologhepatopexy);

3.Discharge of ascitic fluid from the abdominal area. cavities:

a).laparocentesis;

b).oper.Kalb - constant. drainage; abdominal Cavities (excised parietal abdomen, abdominal muscles to the pancreas in the region of the lumbar triangles outward from the ascending and descending colon.

c).peritoneovenous. bypass (the GSV of the thigh is isolated over a length of 10-12 cm, crossed and sutured above the Pupart ligament into the hole in the peritoneum);

4.Reducing blood flow into the portal system:

a).splenectomy;

b).ligation of arteries and veins (left stomach and right gastric-epiploic, inferior mesenteric vein, hepatic artery);

5.To enhance liver regeneration:

a).liver resection;

b).arterioportal anastomoses

Combined operations are used more often.

If the process in the liver is ideal, a liver transplant with histocompatibility.

Prognosis and results of treatment of portal hypertension and bleeding from varicose veins of the esophagus.

L: complex therapeutic measures as in relation to the disease that caused

portal hypertension, and in relation to the portal syndrome itself

hypertension. In the prehepatic form of the syndrome, patients undergo surgical

treatment. The most commonly used operation is splenectomy with omentoropexy.

After removal of the spleen, there is a significant decrease in portal pressure,

the phenomena of hypersplenism are eliminated. Suturing the greater omentum to the kidney

(after preliminary decapsulation) provides for subsequent development

organ porto-caval anastomoses, which also leads to a further decrease

pressure in the portal vein. In the presence of prehepatic block in patients with

recurrent bleeding from esophageal varices

splenectomy is combined with the application of direct portocaval vascular

anastomoses: splenorenal, mesenteric-caval or direct

portocaval anastomosis.

In the treatment of patients with liver cirrhosis complicated by portal hypertension,

surgical L is possible only in the absence of an active process in the liver and

symptoms of liver failure The choice of the method of operation is determined taking into account

age, general condition of the patient, presence of concomitant diseases, degree

compensation of impaired liver functions, height of portal pressure, severity

hypersplenism, etc. It was noted that the best results when applying

portocaval anastomoses are observed in patients with bilirubin levels in the blood

below 0.02 g/l (2 mg%), blood albumin level above 0.35 g/l (3.5 g%), with

absence of ascites and neurological disorders. In the group of patients at the level

bilirubin in the blood over 0.03 g/l (3 mg%), albumin concentration in the blood is lower

0.03 g/l (3 g%), in the presence of ascites, nutritional disorders and neurological

disorders, the results of the operation are poor. Very high postoperative

mortality

The use of direct vascular porto-caval anastomoses is aimed at rapid

decrease in portal pressure due to the massive discharge of blood into the system of the lower

vena cava Direct porto-caval anastomoses often produce severe encephalopathy for

due to hyperammonemia, so they are now used less frequently due to

strict indications.

Splenectomy has no independent value in the treatment of portal

hypertension, it is used for severe hypersplenism (see section

"Spleen"), and, as a rule, supplement with the imposition of a vascular splenorenal

anastomosis The latter is quite often thrombosed and does not provide the desired

decompression in the portal system

combination of splenectomy with omentorenopexy (after decapsulation of the kidney), ligation

left gastric artery and veins in the cardia and abdominal esophagus

in order to stop the outflow of blood from the veins of the stomach into the dilated veins of the esophagus.

L bleeding from varicose veins of the esophagus begins with

conservative measures: perform tamponade of the esophagus with a Blackmore probe,

hemostatic therapy, blood transfusion, pituitrin are used (to reduce

portal pressure). The Blackmore probe consists of a three-lumen rubber tube

with two cylinders of round and cylindrical shape

If drug treatment fails, bleeding from varices

veins of the esophagus as a necessary measure, various types of surgical

interventions aimed at stopping bleeding and uncoupling

portocaval anastomoses of the gastroesophageal zone. Due to severe

For the patient's condition, transgastric ligation is the most commonly used procedure.

dilated veins of the esophagus and cardia or suturing of the subcardial region

stitching machines. Proximal gastrectomy is performed much less frequently

and abdominal esophagus, application of vascular direct lortocaval

anastomosis.

Prognosis: unfavorable, mortality after these types of operations reaches 75%.

Portal hypertension is a condition of the portal vein in which excess pressure arises in it for one reason or another. This primarily has a most destructive effect on the liver, due to which the person is at serious risk, up to and including fatal outcome. Treatment of portal hypertension is always very complex and requires complex urgent measures. To understand what portal hypertension is, and not to confuse it with arterial hypertension(another name is hypertension), you need to understand the essence of its occurrence.

Classification of portal hypertension

First of all, doctors distinguish between the types of portal hypertension according to the location of the formation of barriers to the outflow of blood:

• prehepatic occurs directly in the portal vein itself or in its main branches;
• intrahepatic, according to its name, is formed directly in the liver, and taking into account the relationship with the sinusoids located there, it is divided into three types: presinusoidal, sinusoidal and postsinusoidal;
• suprahepatic is characterized by an obstruction to the movement of blood in the area of ​​the hepatic vessels lying outside the liver, or in the inferior vena cava;
• mixed type of hypertension.

It should also be added that there are additional principles for dividing portal hypertension based on measuring the level of pressure increase, as well as according to the volume of varicose thickenings in the esophageal veins.

Characteristics of the disease

The portal vein is one of the key venous trunks in the entire human circulatory system, which receives blood from a number of organs (contained in the abdomen) such as the stomach, intestines and spleen. It is formed by the confluence of two mesenteric and one splenic vein, while a number of other key vessels flow into it. The pressure that occurs with the described syndrome can be localized in different places– portal vessels, vein cava inferior or vessels inside the liver, and it causes a decrease in the volume of blood flowing into this organ. This further leads to a significant reduction in the liver and degradation of its regenerative function, which is not last turn caused by a lack of insulin and glucagon from the pancreas.

The consequences of this process are very difficult for the patient, as they include, among other things, varicose veins of the esophagus and encephalopathy of the portal veins. At healthy person the pressure in the portal vein ranges from five to ten mm Hg. Art., while portal hypertension increases these values ​​to 12 mmHg. Art., which leads to varicose veins.

Causes of the syndrome

Each type of portal hypertension, except mixed, is provoked by its own group of diseases. Thus, the prehepatic form is provoked, firstly, by thrombosis or complete closure of the portal veins or splenic vessels. In addition, this may be a consequence of an increase in portal blood flow in the veins, which, in turn, is a consequence of an arteriovenous fistula, splenomegaly of other organs, or pathological cavernomatosis of the portal vein itself.

In turn, the most common intrahepatic portal hypertension may be a consequence of both acute diseases, and chronic. The first is usually referred to as alcoholic hepatitis or fatty liver caused by alcoholism, as well as acute viral hepatitis. As for chronic diseases, the list is as follows:

• alcoholic liver damage;
• viral or primary biliary cirrhosis;
• hemochromatosis;
• chronic types of hepatitis;
• idiopathic portal hypertension;
• Wilson's disease;
• congenital liver fibrosis;
• schistomatosis;
• carcinoma;
• sarcoidosis;
• use of cytostatic drugs;
• nodular or focal hyperplasia;
• liver damage from toxic substances.

Finally, suprahepatic portal hypertension is usually associated with either heart disease such as cardiomyopathy, pericarditis, and valvular disease, or with hepatic vein pathology. The latter include the following factors:

• compression of the inferior vena cava and hepatic veins by tumor formation;
• thrombosis of the inferior vena cava or hepatic veins;
• pathology of the development of the inferior vena cava;
• veno-occlusive disease.

There are other diseases that can, under one or another set of events, lead to portal hypertension. For example, the suprahepatic form in infants is sometimes triggered by omphalitis - inflammation of the peri-umbilical wound. Doctors can cause the same disease through poorly performed catheter insertion into the umbilical vein. Portal vein obstruction may occur due to appendicitis, peritonitis, Crohn's disease, nonspecific ulcerative colitis, infections of the biliary tract.

In turn, there are a number surgical operations, which can lead to the formation of portal hypertension, and these include splenectomy, removal of a narrowing of the vessel, removal of a cyst in the bile ducts. Sometimes the cause of damage to the portal vein is various kinds of mechanical injuries such as accidents or injuries to the peritoneum. Risk factors also include people suffering from increased blood clotting (polycythemia, myelofibrosis, thrombocythemia, myeloid leukemia). Portal hypertension is significantly less likely to be provoked by congenital anomalies portal and adjacent veins, compression of the portal veins by tumor formations, hepatic cirrhosis, hepatocellular carcinoma, thrombophlebitis, and some complications during pregnancy and the use of oral contraceptives.

Symptoms of portal hypertension

Symptoms of portal hypertension can be divided into two groups: common features and individual, characteristic of each of the three types of this disease. Speaking about the first group, doctors note the following approximately sequential symptoms of portal hypertension:

• pain in the digestive system, nausea, flatulence;
• dry skin, decrease in subcutaneous fat and muscle mass;
• varicose veins located close to the anterior abdominal wall, due to which they begin to appear through the skin;
), swelling of the lower extremities, bleeding from upper sections Gastrointestinal tract and rectum;
• enlargement of the spleen with simultaneous accumulation of platelets, leukocytes and red blood cells in it (hypersplenism);
• enlargement, hardening and tenderness of the liver (portal hypertension in liver cirrhosis);
• prolonged course of portal hypertension can lead to encephalopathy, causing disturbances sleep, dizziness, headaches, central nervous system damage.

Clinical manifestations of portal hypertension of the suprahepatic type cause, for example, early ascites that cannot be treated, a significant increase in liver size (with weak severe splenomegaly) and spicy painful attacks in the area of ​​the liver itself. The subhepatic type of portal hypertension is distinguished by the opposite picture - with a minimally enlarged liver and obvious splenomegaly. In addition, it is characterized by constant bleeding in the gastrointestinal tract with a relatively slow development of the disease itself.

Finally, intrahepatic hypertension, being the most common, causes next row symptoms:

• stomach pain, nausea, diarrhea, weight loss;
• in the later stages, splenomegaly, abdominal varicose veins, ascites, enlarged spleen, and liver failure appear;
• Depending on the subtype of intrahepatic portal hypertension, pain can be localized both in the anterior abdominal wall on the left, and around the navel and near the liver.

Diagnosis of the disease

Differential diagnosis of portal hypertension includes about one and a half dozen research methods, each of which is focused on a particular clinical manifestation of the disease.

The simplest, most effective and non-invasive diagnostic methods are the use of different types of ultrasound (ultrasound).

It can be conventional or Doppler, as well as duplex - combining both types. Its purpose is to study the condition of the portal vein, hepatic veins and liver arteries for their patency, possible blood flow disorders and anatomical anomalies. In addition, ultrasound can detect Budd-Chiari syndrome (a rare disease that causes partial or complete blockage of the hepatic veins) in a patient.

As for other methods for diagnosing portal hypertension, the most effective today are the following:

• splenomanometry - insertion of a needle into the spleen followed by connection to a pressure gauge to determine the pressure;
• hepatomanometry – similar action in relation to the liver;
• portomanometry is the same operation aimed at measuring pressure in the portal vein (the catheter is inserted through the umbilical vein);
• splenoportography – injection of contrast into the splenic veins;
• hepatic venography – also using contrast agent(especially effective in the case of Budd-Chiari syndrome);
• gastroscopy - allows you to detect varicose veins of the gastric veins;
• esophagography – detection of varicose veins in the esophagus using x-rays;
• sigmoidoscopy - visual examination of the rectum using a special device to differentiate the type of disease;
• angiography, in which a contrast agent is injected into the lumen of the vessel;
• CT of the portal and other veins;
• MRI to assess the state of the shunt lumen and portal blood flow;
• , allowing to detect enlargement of the liver and spleen, as well as ascites and calcifications in the portal vein, hepatic and splenic arteries;
• venography, most often used before liver transplantation or portal vein surgery;
• assessment of hepatic blood flow using a green dye (indocyanine) continuously injected into the hepatic vein.

Treatment of the presented syndrome

Treatment of portal hypertension, in general, consists of a complex of medicinal and endoscopic actions, the purpose of which is to eliminate bleeding from varicose veins of the abdominal cavity and gastrointestinal tract. In addition, it is necessary to eliminate the disease that caused portal hypertension syndrome, since the original disease can sometimes pose an even greater threat to the patient’s health (for example, carcinoma that has grown into the portal vein). There are a number of other measures to help a person suffering from acute portal hypertension: blood transfusions, injections of the hormone somatostatin, sclerotherapy, splenectomy and vein bypass surgery. Unfortunately, last method, although considered the most effective, is possible only in rare cases, because due to thrombosis the veins are unsuitable for bypass surgery.

In the future, liver failure is relieved by the use of various drugs as therapy, including the use of beta blockers (propranol, nadolol). As a measure to combat blood loss, which is most common in liver cirrhosis, the attending physician prescribed the patient a complete abstinence from alcohol, adherence special diet and drug use. Unfortunately, in most cases of treatment of portal hypertension (with accompanying massive internal bleeding from varicose veins) the prognosis is disappointing, since even blood transfusions do not always allow one to cope with the deterioration of the patient’s condition. It is noted that the mortality rate in such situations reaches 50%, and survivors will almost certainly experience bleeding again in the next one to two years. Even a combination of drug and endoscopic therapy for such a diagnosis only slightly prolongs the life of such patients. It should be added that portal hypertension in children is especially difficult due to the weakness of their bodies.

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1.Can cancer be prevented?
The occurrence of a disease such as cancer depends on many factors. No person can ensure complete safety for himself. But significantly reduce the chances of occurrence malignant tumor everyone can.

2.How does smoking affect the development of cancer?
Absolutely, categorically forbid yourself from smoking. Everyone is already tired of this truth. But quitting smoking reduces the risk of developing all types of cancer. Smoking is associated with 30% of deaths from oncological diseases. In Russia, lung tumors kill more people than tumors of all other organs.
Eliminating tobacco from your life - best prevention. Even if you smoke not a pack a day, but only half a day, the risk of lung cancer is already reduced by 27%, as the American Medical Association found.

3. Does it affect excess weight on the development of cancer?
Keep your eyes on the scales! Overweight will affect not only the waist. The American Institute for Cancer Research has found that obesity promotes the development of tumors of the esophagus, kidneys and gallbladder. The fact is that adipose tissue serves not only to preserve energy reserves, it also has a secretory function: fat produces proteins that affect the development of a chronic inflammatory process in the body. And oncological diseases appear against the background of inflammation. In Russia, WHO associates 26% of all cancer cases with obesity.

4.Do exercise help reduce the risk of cancer?
Spend at least half an hour a week training. Sport is on the same level as proper nutrition when it comes to cancer prevention. In the United States, a third of all deaths are attributed to the fact that patients did not follow any diet or pay attention to physical exercise. American Cancer Society recommends training 150 minutes a week at a moderate pace or half as much, but more actively. However, a study published in the journal Nutrition and Cancer in 2010 shows that even 30 minutes can reduce the risk of breast cancer (which affects one in eight women worldwide) by 35%.

5.How does alcohol affect cancer cells?
Less alcohol! Alcohol has been blamed for causing tumors of the mouth, larynx, liver, rectum and mammary glands. Ethyl alcohol breaks down in the body to acetaldehyde, which then, under the action of enzymes, turns into acetic acid. Acetaldehyde is a strong carcinogen. Alcohol is especially harmful for women, as it stimulates the production of estrogens - hormones that affect the growth of breast tissue. Excess estrogen leads to the formation of breast tumors, which means that every extra sip of alcohol increases the risk of getting sick.

6.Which cabbage helps fight cancer?
Love broccoli. Vegetables are not only included in healthy diet, they also help fight cancer. This is also why recommendations for healthy eating contain the rule: half of the daily diet should be vegetables and fruits. Particularly useful are cruciferous vegetables, which contain glucosinolates - substances that, when processed, acquire anti-cancer properties. These vegetables include cabbage: regular cabbage, Brussels sprouts and broccoli.

7. Red meat affects which organ cancer?
The more vegetables you eat, the less red meat you put on your plate. Research has confirmed that people who eat more than 500g of red meat per week have a higher risk of developing colorectal cancer.

8.Which of the proposed remedies protect against skin cancer?
Stock up on sunscreen! Women aged 18–36 are especially susceptible to melanoma, the most dangerous form of skin cancer. In Russia, in just 10 years, the incidence of melanoma has increased by 26%, world statistics show an even greater increase. Both tanning equipment and Sun rays. The danger can be minimized with a simple tube of sunscreen. A 2010 study in the Journal of Clinical Oncology confirmed that people who regularly apply a special cream have half the incidence of melanoma than those who neglect such cosmetics.
You need to choose a cream with a protection factor of SPF 15, apply it even in winter and even in cloudy weather (the procedure should turn into the same habit as brushing your teeth), and also not expose it to the sun's rays from 10 a.m. to 4 p.m.

9. Do you think stress affects the development of cancer?
Stress itself does not cause cancer, but it weakens the entire body and creates conditions for the development of this disease. Research has shown that constant worry alters activity immune cells, responsible for turning on the “hit and run” mechanism. As a result, a large amount of cortisol, monocytes and neutrophils, which are responsible for inflammatory processes, constantly circulate in the blood. And as already mentioned, chronic inflammatory processes can lead to the formation of cancer cells.

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Can cancer be prevented?

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   Portal hypertension is a complex symptom complex that is characterized by a noticeable increase in pressure in the portal vein as a result of obstructed blood circulation. Normally, the pressure in this vein does not exceed 7 mmHg. If the blood pressure in the portal vein rises to 12–20 mmHg, it begins to expand. Varicose veins are susceptible to rupture, which in turn leads to bleeding. This pathological condition has a large number of prerequisites for development, which will be discussed below.

   Portal hypertension syndrome

   Portal hypertension is a disease that is not an independent nosology. This syndrome is associated a large number somatic diseases. The basis of all changes occurring in the human body is high blood pressure in the portal vein. The forms and severity of portal hypertension directly depend on the degree of obstruction to blood flow through the vein system. There are such forms of portal hypertension syndrome as prehepatic or prehepatic, intrahepatic, suprahepatic, and mixed.

   The prehepatic form of portal hypertension develops due to the congenital abnormal structure of the portal vein, as well as due to the formation of blood clots in it. TO birth defects veins include: hypo- and aplasia, narrowing of the lumen of the vein in any area or total narrowing. The cause of fusion of the portal vein is associated with the spread of normal obliteration occurring in the Arancia duct and umbilical vein. Thrombosis and, as a consequence, blockage of a vein occurs during various septic processes in the body (suppuration in the abdominal cavity, umbilical sepsis, septicopyemia), when it is compressed by an infiltrate or cyst.

   The cause of the intrahepatic form of portal hypertension in most reported cases is cirrhotic changes in the liver. Sometimes the cause for the development of portal hypertension can be local foci of sclerosis in the liver tissue. According to statistics, out of five patients with portal hypertension, four suffer from intrahepatic blockage.

   With suprahepatic portal hypertension, the outflow of blood from the liver veins is significantly affected. The cause of problems with normal blood flow is often endophlebitis with partial or total obstruction of the vessel. This condition is called Chiari syndrome. Separately called Budd-Chiari disease. In this case, suprahepatic portal hypertension is directly related to blockage of the vena cava by thrombotic masses at the level of the hepatic veins. Among the reasons, not the least important is the anomaly of the inferior vena cava. Compressive, tumor-like and cystic neoplasms, as well as tricuspid valve insufficiency can impede blood flow through the vessels and cause suprahepatic portal hypertension.

   The combined form of portal hypertension occurs when the portal vein is blocked by a blood clot in people suffering from cirrhosis of the liver.

   At sharp increase pressure in the portal vein is up to 450 mm Hg (the norm is 200) in people with portal hypertension, blood flow is carried out through portocaval anastomoses. These anastomoses are divided into three groups. Normal anastomoses are present in the lower third of the esophagus and the cardiac part of the stomach. From the portal vein system, blood flows through the venous plexuses of the above organs into the azygos vein, which in turn flows into the inferior vena cava. So, if a patient with portal hypertension has varices in the esophagus, this can lead to massive bleeding from this organ. Reflux esophagitis or esophageal ulcers can contribute to the development of bleeding. There are also anastomoses between the rectal veins (upper, middle and lower). In this case, the blood flows from the upper rectal veins, which are related to the portal system, continues to move through the anastomotic system, passes through the internal iliac veins and flows directly into the inferior vena cava.

   If a person suffering from portal hypertension syndrome experiences stable dilatation venous plexus rectum, this may end heavy bleeding from anal passage. There is also an anastomosis between the paraumbilical and umbilical veins (if the umbilical vein has not undergone involution). This anastomosis drains blood from the portal vein system into the umbilical vein. Then it enters the veins of the outer abdominal wall, the inferior and superior vena cava. If this particular group of anastomoses is affected by portal hypertension syndrome, a so-called pattern of enlarged veins of the abdominal wall will be visible on the patient’s abdomen. This design is called “jellyfish head”.

   Causes of portal hypertension

   Portal hypertension can begin with chronic pathological changes, caused by intra- and extrahepatic stagnation of bile, with biliary cirrhosis (primary and secondary), neoplasms of the bile duct, as well as the common bile duct itself. The reason may be calculous cholecystitis, cancer tumor head of the pancreas, medical error during ligation of the bile ducts during surgery. The influence of various toxins that are tropic to the liver parenchyma (certain types of fungi, drugs) also plays a major role in the pathogenesis of portal hypertension.

   Portal hypertension can also be caused by abnormal congenital atresia, thrombosis, stenosis or tumor of the portal vein, venous thrombosis in Budd-Chiari disease, restrictive hypertension, namely increased pressure in the right atrium and ventricle, as well as compressive pericarditis. In certain cases, portal hypertension syndrome is associated with crises during surgical interventions, with massive burns with a large percentage of soft tissue damage, disseminated intravascular coagulation syndrome, sepsis, and trauma.

   Direct predisposing factors that can give impetus to the development of a detailed clinical picture of portal hypertension with all the ensuing consequences are various infections, bleeding of the stomach and intestines, alcoholism, the predominance of animal fats over vegetable fats in food, long-term treatment tranquilizers, diuretics, heavy operations With long period recovery.

   Symptoms of portal hypertension

   The clinical picture of any form of portal hypertension directly depends on the disease that caused a persistent increase in pressure in the portal vein system. This is important to remember and use when interviewing the patient and in analyzing the clinical picture, especially in cases where there are already serious complications of portal hypertension (vein thrombosis, massive bleeding from dilated veins of the esophagus or rectum).

   Portal hypertension can be characterized the following symptoms: a sharp enlargement of the spleen, the presence of varicose veins in the esophagus or stomach, bleeding from these vessels, an increase in the abdomen in size due to the accumulation of fluid (ascites), signs (pain in the epigastric region, absence of stool for several days, nausea, lack of appetite up to and including complete refusal to eat). People with portal hypertension have characteristic spider veins on the skin, a blood test shows a decrease in the number of platelets and leukocytes, anemia develops much less frequently, and changes in the coagulation system are noted (there is a tendency to hypocoagulation).

   The prehepatic form of portal hypertension usually manifests itself in childhood and has a favorable course. On macroscopic examination, in some patients it may be noted that the portal vein has been replaced by small dilated veins. This formation is called a “cavernoma”. Most often, the disease manifests itself as esophageal bleeding, which is the first sign of the development of the disease in childhood; there is an increase in the size of the spleen, hypersplenism, and thrombus formation in the vein system.

   The intrahepatic form also has its own characteristics, since such portal hypertension develops in liver cirrhosis. The nature and rate of development of the symptom complex depends on the type of cirrhotic changes (post-necrotic cirrhosis, alcoholic cirrhosis, etc.), the level of compensation for the impaired function. Portal hypertension in such patients is manifested by hemorrhages, the appearance of a “jellyfish head”, and an enlarged spleen and abdomen.

   A serious complication that threatens human life is bleeding from the veins of the esophagus and stomach. It usually occurs unexpectedly and is not preceded by any painful sensations in the epigastrium and even discomfort. A patient with this form of portal hypertension suddenly vomits blood without impurities. Vomiting of altered blood can occur if blood from the esophagus flows into the stomach. This type of vomit will be the color of coffee grounds, and the patient will have bloody stools. In this condition, the phenomena of posthemorrhagic anemia increase very quickly. Fatal outcome already the first bleeding with portal hypertension is equal to thirty percent. If there has already been bleeding in the anamnesis, jaundice and an enlarged abdomen are visible, then in this case there is an advanced stage of cirrhosis, which is practically not amenable to effective drug or surgical treatment.

   The suprahepatic form of portal hypertension is a consequence of Chiari disease or Budd-Chiari syndrome. If the disease is acute, the patient suddenly experiences intense pain in the epigastrium, under the ribs on the right, the liver rapidly increases in size, persistent febrility is noted, and ascites appears. The main causes of death in this form of portal hypertension are massive blood loss during bleeding from the esophagus and acute renal and hepatic failure.

   When chronic course diseases of hepato- and splenomegaly progress slowly, a collateral from small veins develops on the anterior abdominal wall, symptoms of ascites increase, disturbances occur in the protein metabolism of the body, the person looks emaciated.

   Signs of portal hypertension

   Diagnosis of portal hypertension is based on the study of the anamnesis of life and disease, on clinical manifestations and their severity, as well as on the mass instrumental studies, capable of detecting and indicating the signs of this syndrome.

   The first thing to do if you suspect portal hypertension in a patient is to conduct a thorough examination. During the examination, attention should be paid to the presence or absence of venous collaterals: varicose veins on the abdomen, near the navel, hemorrhoids, hernia, ascites. It is necessary to carefully examine the color of the skin, sclera, visible mucous membranes, to determine the presence of characteristic spider veins. Then it is necessary to palpate the liver and spleen. Normally, in a healthy person, the liver does not protrude from under the edge of the left costal arch, and the spleen is not palpated.

   Laboratory testing for suspected portal hypertension general analysis capillary blood and urine, coagulogram, biochemistry venous blood, tests for hepatitis pathogens, determination of antibodies to immunoglobulins A, M, G.

   For the purpose of correct and accurate diagnosis diseases, X-ray methods are used: porto- and cavography, angiography of mesenteric blood vessels, celiacography and splenoportography. The totality of data obtained from the above studies will determine the degree of blockage of blood flow in the portal vein system and assess the chances of anastomoses. If it is necessary to determine the quality of the blood flow to the liver, it is necessary to do a liver scintigraphy to the patient.

   Ultrasound examination will help to accurately determine the enlargement of the spleen, liver, the presence of free liquid in the abdominal cavity. Doppler measurements of the hepatic vessels will show the size of the portal, superior mesenteric and splenic veins, and an increase in the lumen of these vessels is a direct sign of portal hypertension.

   Transcutaneous splenomanometry is done to record the pressure in the portal venous system. In the splenic vein, normal pressure does not exceed one hundred twenty millimeters of mercury, and with portal hypertension it reaches five hundred millimeters of mercury.

   Patients with portal hypertension are required to undergo esophagoscopy. Esophagoscopy can reveal such a sign of portal hypertension as varicose veins in the esophagus. Fibrogastroduodenoscopy is also a fairly informative way to detect signs of portal hypertension in the esophagus and cardia.

   Sigmoidoscopy – instrumental method, which will allow you to detect altered veins in the patient’s rectum. In some cases, due to contraindications or the patient’s refusal to undergo instrumental studies, these methods are replaced with radiography of the esophagus and stomach.

   Liver biopsy and laparoscopic diagnostic surgery are performed only in cases where, for some reason, it was not possible to confirm the diagnosis using the above methods or if there is a suspicion of a malignant neoplasm.

   Portal hypertension in children

   In children, it is the extrahepatic form of portal hypertension that most often occurs. This is almost always caused by anomalies in the formation of the portal vein system, expressed in cavernous transformation. Some role among the etiological factors is played by incorrect catheterization in the early neonatal period, leading to the development of thrombophlebitis umbilical vein. This entails consequences such as thrombosis of the portal vein system.

   Portal hypertension in a child can begin due to various congenital or acquired liver diseases. These diseases include fetal and viral hepatitis, various cholangiopathies, expressed in at different levels damage to the bile ducts (from slight hypoplasia to complete loss of function). Periductular fibrosis significantly stimulates the development of symptoms of portal hypertension in children ( adhesive process between the ducts), accompanying all of the above processes.

   Extrahepatic portal hypertension in a child can be recognized by pronounced splenomegaly. The spleen is large on palpation, practically motionless, and does not hurt. Manifestations of hypersplenism are also present. Often, with this form of portal hypertension, there is a rapid expansion of the venous vessels of the esophagus and the cardiac part of the stomach, which leads to spontaneous massive hemorrhages.

   In the vast majority of patients with extrahepatic portal hypertension, hemorrhage is the first manifestation of this disease. From one bleeding to the next the patient feels quite well, the disease does not bother him. An increase in liver size with this pathology is not characteristic feature, which can only develop as a consequence of thrombus formation in the portal vein due to umbilical sepsis. Ascites is also extremely rare. Functional tests do not undergo any changes.

   The decompensated stage of portal hypertension is observed in cirrhosis and is observed mainly in adolescents. Bleeding from the veins of the esophagus is also rare.

   Treatment of portal hypertension

   Conservative treatment of a disease such as portal hypertension is only possible if changes occur only at the level of intrahepatic hemodynamics. To treat portal hypertension, drugs such as beta-blockers, nitrates, glycosaminoglycans and angiotensin-converting enzyme inhibitors are used.

   The dosage and duration of treatment with a drug such as Nitrosorbide is selected by the attending physician individually. In most cases, a single dose ranges from ten to twenty milligrams, and the number of doses per day ranges from two to five times. Thus, the daily amount of the drug is a purely individual indicator, but it should not exceed one hundred eighty milligrams in twenty-four hours. Often, the course of treatment with this drug is not long, since the body gradually gets used to Nitrosorbide and the effect is reduced to zero over time.

   Among beta blockers, Anaprilin and Atenolol have proven themselves to be excellent in the treatment of portal hypertension. Atenolol in patients with portal hypertension should be used under the supervision of a physician. Usually, taking this medication begins with fifty milligrams once a day, after several weeks the result is assessed and, if it is insufficient, the dose is doubled. Long-term therapy this drug is possible. Anaprilin is taken half an hour before meals once, washed down big amount water. They usually start with ten milligrams, gradually increase the dose every week by twenty milligrams and bring it up to a daily dose of eighty to one hundred and twenty milligrams. This dose is already divided into several doses. The course of treatment is individual and usually lasts from fourteen days to two months, then a break is required.

   Among ACE inhibitors good results Ramipril (Hartil, Cardipril) has been shown to treat portal hypertension. It effectively reduces increased pressure in dilated vessels, which is an integral symptom of portal hypertension. At the beginning of treatment with this drug, you need to take 2.5 milligrams before meals in one dose. If any unwanted effects the dose can be divided into two times. If the effect of therapy is insufficient, after two to three weeks the amount of the drug is doubled. In order to improve the hypotensive effect of this medicine, a diuretic can be prescribed at the same time. It is recommended to take the first dose of the drug in the presence of the attending physician and to be under his supervision for the next eight hours, since there is a risk of an uncontrollable hypotensive reaction. During the course of treatment with Ramipril for portal hypertension, you should limit the consumption of salty foods and not take non-steroidal anti-inflammatory drugs unless absolutely necessary, as all this significantly reduces the effectiveness of the drug.

   If a patient with portal hypertension has already had bleeding or has hypersplenism or fluid accumulation in the abdominal cavity, the only treatment method can be surgical.

   As the first medical care in case of hemorrhage from the RVS, a Sengstaken-Blackmore probe is installed. It is as effective as applying a pressure bandage to a limb. This obturator probe will not be effective only if bleeding from the veins has developed in lower section stomach, which happens, but is extremely rare. The time the probe remains in patients varies from twelve hours to three days. At correct use The probe stops bleeding successfully in almost 99% of all cases, but only every second person suffering from portal hypertension can avoid relapse. After using an obturator probe, a patient may develop a complication such as aspiration pneumonia; in rare cases, a rupture of the stomach wall with the probe may occur. Due to the presence of the device in the patient’s body for more than three days, bedsores of the mucous membrane may appear in the stomach.

   After bleeding due to portal hypertension, drug treatment plays an important role. From the first day, Vikasol (1%) is prescribed in intravenous infusions of six milliliters. The duration of treatment is five days. Ten percent calcium chloride is also injected into a vein, ten cubes per day. The course of treatment should also not exceed five days. Every five to six hours the patient needs to receive infusions of Dicynon. The first injection is with a dosage of 4.0, and subsequent ones - 2.0. Injections are given for three to five days.

   To reduce the severity of fibrinolysis and anticoagulant activity, the patient is injected with five percent aminocaproic acid, one hundred milliliters, four times a day. Also, for bleeding due to portal hypertension, Contrikal injections are required every eight hours.

   In addition to all of the above, it is necessary to neutralize the effect of histamine on capillaries and their permeability. For this purpose, Diphenhydramine is prescribed at a dosage of 1.0 every eight hours. Diphenhydramine can be replaced with Suprastin. The dose and frequency of administration of this drug are the same.

   Very important point successful treatment bleeding in portal hypertension is an improvement in the rheological properties of blood. For this purpose, the patient is administered a drip of 400 milliliters of Reopoliglucin. It is necessary to give a dropper of a 0.025% solution of Strophanthin (1.0 per 100 milliliters of saline and five percent glucose). You should also combat blood acidification. A sodium bicarbonate solution will help normalize the pH. For this purpose, the patient is given a drip containing 200 milliliters of a four percent solution.

   In parallel with hemostatic treatment, it is necessary effective reduction blood pressure and maintaining it at a level not exceeding 110 millimeters of mercury (meaning systole). Nitroglycerin copes well with this task. For hemorrhage caused by portal hypertension, it is prescribed in intravenous injections. Use a four percent solution (1.0 Nitroglycerin per 400 milliliters of saline or Ringer's solution). The drip infusion is carried out slowly, no faster than twelve drops per minute.

   From medicines that have a hepatoprotective effect, it is most advisable to prescribe Heptral. For the first few days, it is administered four hundred milliliters by drop, and by the end of the first week the patient is switched to tablets. In order to prevent multiple organ failure, glucose solution, albumin preparations, glucocorticoids, etc. should be added to the treatment regimen for portal hypertension. saline solutions and vitamins.

   Patients with portal hypertension have elevated ammonia levels. In order to reduce the amount of this substance, Hepa-Merz is prescribed. At the first intravenous infusion, the concentration active substance in 400 milliliters should be 60.0. All subsequent times the concentration of the drug is 30.0. Instead of Hepa-Merz, you can use Hepasol A. It is produced in half-liter bottles in standard dilution. Droppers with Gepasol A should be done twice a day for the first few days after bleeding.

   Inhibitors are also used in the treatment of portal hypertension. proton pump(Losek, Kvamatel). Losek is administered at a dose of forty milligrams intravenously every twelve hours. Kvamatel is administered in twenty milligram doses. The frequency of administration of the drug is the same.

   After effective treatment of bleeding caused by portal hypertension, they proceed to surgical elimination of the cause of the disease. The single most effective treatment for portal hypertension is anastomosis between the vessels. Such operations in adults almost always go without problems, but when operating on children using this method, there are some difficulties. The difficulties are due to the fact that the diameter of a child’s blood vessels is much narrower than that of an adult. In addition to this, small child There are no complete anatomical structures that may be suitable for forming an anastomosis. That is why operations to form anastomoses for portal hypertension are performed in children who are seven to eight years old. Until this age, treatment is almost always exclusively medicinal.