Hepatitis

Symptoms

The vast majority of cases of viral hepatitis are asymptomatic or oligosymptomatic 
•    Lethargy, weakness.
•    Nausea
•    Appetite loss and abdominal heaviness.
•    Yellowing of the sclera and skin
•    Urine darkening and faeces lightening.
•    Urticaria rashes on the body are conceivable at times (urticaria is a red itchy rash in the shape of tiny blisters). Perhaps there will be an increase in liver size.
In more severe cases (severe acute course and decompensation of the cirrhotic stage of hepatitis) 
•    Increased bleeding, 
•    Itching of the skin, 
•    Weight loss, and hepatic breath are observed. 
•    Hepatic encephalopathy occurs, characterised by disorganisation of higher nerve activity (limb tremor, lethargy, loss of focus, stupor, and, in severe instances, coma). A dense accumulation of fluid in the abdominal cavity is known as ascites. 
Extremely heavy    Impaired consciousness, hemorrhagic syndrome, temperature of 38 ° C and above, ascites, decrease in liver size, hepatic dullness percussion (when tapping) is not determined
heavy    Sharply expressed yellowness of the skin and sclera, muscle weakness, drowsiness, aversion to food, nausea, repeated vomiting, a decrease in the size of the liver
Medium    Severe yellowness of the skin and sclera, weakness, lethargy, lack of appetite, nausea, vomiting, enlarged liver
Easy    Slight yellowness of the skin and sclera, slight weakness and loss of appetite, liver enlargement

Treatment

In acute hepatitis of mild severity, treatment can be carried out at home (if conditions are available), moderate and severe forms are treated in a hospital.
In chronic pathology (without significant exacerbation), treatment is carried out on an outpatient basis. In cases of severe exacerbation or decompensation, hospitalization in an infectious diseases hospital is indicated.
Diet. It entails drinking enough water (more than 1.5 litres per day for acute hepatitis; restricting fluid intake in cases of decompensated liver function); avoiding alcoholic and carbonated beverages; avoiding fried, smoky, salted, tinned, and spicy foods; and taking multivitamins.
You can take sorbents, hepatoprotectors, antioxidants, diuretics, probiotics, hormones, and vitamins as necessary.
Etiotropic therapy (aimed at the pathogen) in the acute course of hepatitis is not prescribed, with the exception of severe forms of hepatitis B. In the chronic course of the disease (hepatitis B, C, D, rarely E), it is possible, and in many cases necessary, to prescribe direct antiviral drugs, leading to the complete disappearance of the virus (hepatitis C) or persistent suppression of viral reproduction (hepatitis B, D). 

Tests Required for Diagnosis

Clinical blood test: the amount of leukocytes is normal or slightly decreased, there is a rise in lymphocytes and monocytes and a drop in neutrophils in peripheral blood, a decrease in platelets, and a lowered or normal erythrocyte sedimentation rate (ESR).
Biochemical blood test: Increase in prothrombin index (PTI), decrease in albumin and increase in gamma globulins, increase in thymol test (decrease in albumin and increase in gamma globulins), increase in gamma-glutamine transpeptidase (GGTP), alkaline phosphatase, and alphafetoprotein are all examples of increases in total bilirubin caused by direct and indirect fractions.
Urinalysis: the appearance of hematuria (blood in the urine), proteinuria (protein) and cylindruria (cylinders).
Biochemical analysis of urine: the presence of bile pigments and urobilin as a result of direct bilirubin.
Some clinical and laboratory parameters for viral hepatitis
Criteria    Easy degree    Moderate severity    Severe degree
Blood bilirubin (µmol/l)    Up to 100    100-200    More than 200
Prothrombin index (%)    60    50-60    Less than 50
Duration of jaundice (weeks)    Until 3    3-4    Over 4
Average duration of illness (months)    Up to 1    Up to 1.5    Over 1.5
The prothrombin index is an indicator used in the diagnosis of blood clotting disorders at the stage of conversion of prothrombin to thrombin. The ratio of the standard prothrombin time to the patient's prothrombin time is expressed as a percentage (%)

Serological tests - detection in blood serum (if necessary in leukocyte suspension) of markers of viral hepatitis:
•    Specific antibodies using enzyme immunoassay (ELISA)
•    DNA / RNA viruses using polymerase chain reaction (PCR)
Ultrasound of the abdominal organs: an increase (or decrease) in the size of the liver with a change in the structure of its tissue, an increase in the lymph nodes in the gates of the liver, an increase in the spleen.
Fibroscan - measurement of liver tissue density, specification of the degree of fibrosis on the Metavir scale. 
Fibrogastroduodenoscopy - clarification of the nature of the pathology of the esophagus, stomach and the initial part of the duodenum.
 

Useful info

The pathogenesis of viral hepatitis
Separate articles should be dedicated to the detailed pathophysiology of each kind of viral hepatitis. It is sufficient to grasp the choices for regular liver function and the main processes of its dysfunction.
Stages of formation and excretion of bilirubin:
•    The first phase: The generation of free (indirect) bilirubin in the spleen and hepatocytes (liver tissue cells)

•    The second phase: its entry into the blood and transfer by albumins (simple water-soluble proteins) to hepatocytes.

•    Third phase: binding of free bilirubin to glucuronic acid in hepatocytes (formation of conjugated or direct bilirubin).

•    The fourth phase: the release of direct bilirubin by hepatocytes in the composition of bile into the bile capillary.

•    Fifth phase: entry of bilirubin-diglucoronide (direct bilirubin) into the duodenum in the form of bile.

Pathology of bilirubin metabolism in viral hepatitis:
The depletion of hepatocytes weakens the collection of free bilirubin and disrupts the process of adding glucuronic acid to it (phase 3). As a result, the blood's free bilirubin level rises. When the transit of conjugated bilirubin to the bile capillary is disrupted (phase 4), there is a rise in conjugated bilirubin in the blood. At the same time, intrahepatic cholestasis is noticed, which means that the levels of both free and bound bilirubin in the blood increase, with the latter being greater (the skin turns yellow).
Bound bilirubin enters the urine from the blood and reacts with bile acids, lowering the surface tension of the urine and allowing it to froth readily. Little bound bilirubin penetrates the gut, causing the faeces to become discoloured. Little bile reaches the gut as a result of intrahepatic cholestasis and decreased bile secretion. Because bile is required for the digestion of fatty meals and the absorption of fat-soluble vitamins, its absence in faeces results in a lot of fat remaining (steatorrhea), and vitamin K absorption is reduced. Because of a lack of vitamin K, prothrombin production in the liver declines, causing blood clotting to deteriorate.
Complications of viral hepatitis:
Acute liver failure (acute hepatic encephalopathy syndrome) in acute hepatitis:
•    The first stage (OPE-1). There is weakness, unstable mood, the patient does not want to move, there may be prostration, poor sleep, tremor, hepatic odor from the mouth, sometimes nausea, vomiting, increased yellowness of the skin, a decrease in the size of the liver, agitation and aggression may occur.
•    The second stage (OPE-2, precoma). Sopor increases (severe lethargy), convulsions appear, disorientation in time and space, pronounced tremor of the hands, tachycardia , bleeding and hemorrhage, coffee grounds vomiting, tarry stools, and a decrease in diuresis (urine volume).
•    The third stage (OPE-3, coma I). Loss of an adequate verbal response and response to standard stimuli, the appearance of pathological reflexes. Involuntary urination and defecation. Swallowing is preserved, reaction to bright light is weak, increased levels of bilirubin in the blood, hemorrhages (hemorrhages), sweet and sour liver smell from the mouth, minimal or no urine.
•    The fourth stage (OPE-4, coma II). Complete loss of response to stimuli, lack of reflexes, a symptom of floating eyeballs, pupils are dilated, do not respond to light, tremor ends, swallowing is difficult, abnormal breathing is observed, the pulse is thready, a sharp increase in the level of bilirubin in the blood.
Cholecystocholangitis is an inflammation of the biliary system. Severe pains appear in the right hypochondrium, symptoms of jaundice and itching of the skin increase.
Autoimmune hepatitis (with hepatitis A and C) - various forms of liver damage resulting from the aggression of one's own immune cells against hepatocytes against the background of viral hepatitis.
Hemolytic-uremic syndrome in children with hepatitis A - hemolytic anemia, thrombocytopenia (drop in platelet levels), acute renal failure (decreased diuresis, weakness, abdominal pain, intoxication, increased blood creatinine).
Cirrhosis of the liver is the death of liver cells and their replacement with connective tissue. It occurs mainly in chronic hepatitis B, C and D. As a result of cirrhosis, the functioning of the liver is disrupted:
•    Increased pressure in the portal system;
•    The veins of the esophagus, stomach and spleen expand;
•    The amount of proteins, blood coagulation factors decreases;
•    Detoxification function worsens;
•    Edema, ascites, bleeding, weight loss appear;
•    The general condition worsens, the activity of the central nervous system.
Hepatocellular carcinoma is a tumor of the liver tissue. May occur mainly in chronic hepatitis B.
Cryoglobulinemia is an autoimmune lesion of vessel walls caused by the accumulation of pathological proteins in the walls of small and medium calibers. This can lead to ulceration, necrosis and loss of limbs, fibrosis of the kidneys and lungs.
Premature birth and fetal death. characteristic of hepatitis E.
Neuropathies are autoimmune lesions of the nerves, accompanied by pain, sensory disturbances, and muscle weakness. More common in hepatitis E.
Reactive lesions of internal organs (pancreatitis, glomerulonephritis). Characterized by the appearance of pain in the projection of the affected organ, a violation of its functional activity, a change in specific laboratory parameters.
Residual phenomena (post-hepatitis syndrome) - discomfort in the right hypochondrium, asthenia, enlargement of the liver, bitterness in the mouth.