Urolithiasis

The reasons

Symptoms of urolithiasis

Diagnostics

Treatment of urolithiasis

Complications

Urolithiasis develops due to a metabolic disorder and is manifested by the formation of stones in the organs of the urinary system.

The condition when stones are formed in the kidneys is called nephrolithiasis; ureterolithiasis in the ureters; in the bladder – cistolithiasis.

The reasons

All causes leading to the formation of stones in the urinary system are divided into exogenous (external) and endogenous (internal).

To exogenous include the following:

  • long drinking hard water;
  • living in climatic zones where there is a lack of ultraviolet rays;
  • large use of sour, salty, spicy foods;
  • insufficient water intake during the day;
  • sedentary lifestyle.

To endogenous include the following:

  • renal dysfunction due to chronic diseases;
  • genetic predisposition to stone formation;
  • infectious diseases accompanied by dehydration;
  • severe diseases in which the patient requires prolonged immobilization;
  • pathology of the gastrointestinal tract (due to a violation of the processes of digestion and absorption);
  • metabolic disorders (hyperparathyroidism, gout);
  • congenital anomalies of the structure of the kidneys and urinary tract.

The most common in urolithiasis are inflammatory diseases of the kidneys (pyelonephritis, glomerulonephritis), gout, hyperparathyroidism, gallstone disease, cystitis, prostatitis, pancreatitis, colitis.

There are 5 types of stones:

  • urate, appear in disorders of uric acid metabolism (with gout);
  • oxalate, appear with an increased content of oxalate salts;
  • phosphate, appear when phosphorus metabolism is impaired;
  • cystine, they appear in hereditary pathology;
  • mixed, a combination of several types of exchange disorders.

Symptoms of urolithiasis

In men, this pathology is detected three times more often than in women. The clinical manifestations of urolithiasis in men and women are the same.

The severity of symptoms depends on the size of the stones and where they are located.

In the presence of small stones, the disease is asymptomatic, or after severe physical exertion discomfort may appear in the lumbar region. At this stage, concrements are most often diagnosed by chance during examinations.

Localization of pain in urolithiasis

The most inherent symptom is – pain.

The pain may be permanent or paroxysmal; whining or sharp character; the severity of pain depends on the size of the stone and its location.

Pain with kidney stones

When finding kidney stones or upper ureter, pain occurs in the lumbar region and is aching in nature.

However, if the stone causes obstruction (blockage) of the ureter, the flow of urine is disturbed and the pain is significantly increased. The patient develops   renal colic . It is characterized by severe pain, does not go away with a change in body position. Pain can last from a few minutes to several days. Patients rush about, there are frequent urge to urinate.

The pain is most often unilateral, rarely can be bilateral.

As the stone moves along the urinary tract, the pain subsides.

Pain in the lower abdomen in men can spread to the external genital organs, the scrotum. The pains resemble prostatitis, testicular torsion.

In women, pain in the lower abdomen is given to the labia, vulva.

Difficult urination, it becomes frequent and painful.

Pain in bladder stones

When finding stones in the bladder, pain is localized in the suprapubic area, with small stones, the pain is aching. Irradiation of pain is also in the region of the external genital organs.

Blood in the urine and sand

The second most common symptom is   hematuria   (appearance of blood in the urine).

Hematuria occurs when the stone moves along the urinary tract, due to damage to the mucous membranes. With the passage of small stones, blood can be detected only in the study of urine. And with the passage of large stones, the patient himself may note pink urine staining.

Also, the patient can see small stones (sand) in the urine sediment.

Diagnostics

If there are signs of urolithiasis, it is necessary to consult a urologist or a nephrologist and undergo the necessary examination.

General urine analysis:

  • Allows to detect hematuria – appearance in urine   red blood cells . In the presence of inflammation in the urinary system is detected   increased number of leukocytes,   increase urine density . In the urine sediment detected salts (oxalates, phosphates, urates).
  • If there are stones in the urine sediment, their research is carried out. Sets the character of the stone.

Biochemical blood test:

  • Aimed at identifying abnormalities in metabolism. The level of uric acid, phosphate, oxalate, and kidney function (creatinine, urea, glomerular filtration rate) are evaluated.

General blood analysis.

  • You can detect anemia ( decrease in hemoglobin ) with prolonged blood loss; boost   white blood cell counts and erythrocyte sedimentation rate   ESR with the inflammatory process.

Ultrasound examination of the kidneys, bladder.

  • Allows you to identify the presence of stones, signs of inflammation.

To detect stones in the ureter, clarify their location and the degree of obstruction of the urinary tract – conduct excretory   urography. The study is conducted by introducing a radiopaque substance and then evaluating its elimination rate.

In case of obstruction in the lower parts of the urinary tract, retrograde ureteropyelography is performed. Contrast is not injected into the kidneys, but from the bottom up – along the ureters.

Also to clarify the diagnosis can be assigned   computed tomography . It allows you to specify the size of the stone, its position.

Treatment of urolithiasis

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In the presence of small stones, the treatment is carried out on an outpatient basis. Appointed therapy by a nephrologist or urologist.

If the stones are large or the patient develops renal colic, the treatment is inpatient. The duration of hospitalization depends on the treatment carried out, an average of 10-14 days.

Treatment of urolithiasis is aimed at removing stones and correcting metabolic processes to prevent their re-formation.

Methods for removing stones depend on the size of the stone and its location.

Small stones can independently go through the urinary tract.

To relieve the condition, reduce pain to the patient (in the event of renal colic), antispasmodics and painkillers are prescribed.

  • Drotaverine;
  • Papaverine;
  • Duspatalin;
  • Analgin.

Dissolving stones with drugs

In the presence of urats apply:

  • Allopurinol;
  • Etamide;
  • Ugly.

In the presence of phosphate stones are assigned:

  • Cyston;
  • Marelin;

When oxalate stones are used:

  • Blamaren;
  • Spilled;
  • Pyridoxine.

When cystine stones are used:

  • Penicillamine;
  • Potassium citrate;
  • Uralit.

Crushing stones with their subsequent removal

Shock wave lithotripsy.

  • With the help of a shock wave, the stone is crushed and then discharged along the urinary tract. The method is not suitable in the presence of large concretions.

Also, stones destroy and with the help of ultrasonic waves, a laser.

Percutaneous nephrolithotomy.

  • Endoscopic intervention using tools that destroy the stone, with the subsequent removal of parts of the stone from the kidney.

Litolapaxia.

  • This is an endoscopic removal of stones from the bladder.

Also, when urolithiasis is used physiotherapy treatment:

  • diadynamic amplipulse therapy – used to relieve pain;
  • inductothermy – used as an antispasmodic therapy and pain relief;
  • exposure to sinusoidal currents – used to relieve swelling of the mucous membranes of the ureter and spasms. Used in remission.
  • Magnetic Therapy – used to relieve pain.

Diet

Read more about the diet for kidney stones in our   separate article .

For patients with urolithiasis, it is recommended to follow the following dietary recommendations:

Be sure to drink during the day about two liters of liquid;

When uratnyh stones must be limited to:

  • meat; fish;
  • mushrooms;
  • legumes;
  • beer.

With oxalate stones:

  • chocolate, cocoa;
  • beets, lettuce, spinach;
  • foods rich in oxalic acid;

With phosphate stones:

  • salt;
  • carbonated drinks;
  • alcohol;
  • currant, cranberry;
  • milk products.

Prevention of stones

The main focus in the prevention of urolithiasis is the normalization of metabolism.

If you do not normalize the metabolic processes, the recurrence of the disease is inevitable.

The following preventive measures are recommended:

  • daily exercise;
  • alcohol rejection;
  • maintain a normal weight;
  • drink about 2 liters of fluid per day;
  • reduce salt intake;
  • when establishing the type of stones to comply with dietary recommendations.
  • timely treat inflammatory diseases of the urinary organs.
  • regularly examined by a urologist or nephrologist.

Complications

With incorrect treatment of urolithiasis, the following are the most common complications:

The development of the inflammatory process in the kidney, ureter or bladder. This is the most common complication. Caused by the stagnation of urine and damage to the mucous membranes.

The inflammatory process can spread to the renal cellulose (perinephritis). It develops without treatment.   pyelonephritis   or illiterate treatment of jade.

Due to the prolonged inflammatory process (chronic pyelonephritis) develops  chronic renal failure.

With complete blockage of the urinary tract on both sides, which is extremely rare, may develop  acute renal failure.

With timely diagnosis, proper treatment and compliance with further recommendations for the prevention of the disease, the prognosis is favorable. Compliance with preventive measures will avoid the recurrence of stone formation.

Dysmetabolic nephropathy

Manifestations of dysmetabolic nephropathy

Diagnostics

Treatment of dysmetabolic nephropathy

Forecast

Dysmetabolic nephropathy – a group of diseases that are characterized by kidney damage due to metabolic disorders.

Depending on the cause of development, primary and secondary dysmetabolic nephropathies are distinguished.

Primary diseases are hereditary, characterized by a progressive course, early development urolithiasis chronic renal failure.

Secondary dysmetabolic nephropathies can be associated with an increased intake of certain substances in the body, impaired metabolism due to damage to other organs and systems ( for example , the gastrointestinal tract), drug therapy, etc.

The overwhelming majority of dysmetabolic nephropathies are associated with impaired calcium metabolism (from 70 to 90%), about 85–90% of them with an excess of salts of oxalic acid, oxalates (in the form of calcium oxalate), the rest with an excess of phosphates (calcium phosphates – 3–10 %) or are mixed – oxalate / phosphate- urate.

Primary dismetabolic nephropathy is rare.

Manifestations of dysmetabolic nephropathy

Calcium Nephropathy

It is most common in children. Its occurrence may be associated with a violation of both calcium and oxalate metabolism (oxalate salts).

Oxalates enter the body with food or are synthesized by the body itself.

Reasons for the formation of oxalates:

  • Increased oxalate intake with food
  • Bowel disease –  Crohn’s disease, ulcerative colitis , intestinal anastomoses
  • Increased production of oxalates by the body.

Oxalate nephropathy

This is a multifactorial disease. According to various authors, the proportion of heredity in the development of oxalate nephropathy is up to 70–75%. In addition to genetic, external factors play a major role: nutrition, stress, environmental stress, etc.

The first manifestations of the disease can develop at any age, even in the neonatal period.

Most often they are detected at 5–7 years of age in the form of the detection of oxalate crystals, with a low content of protein, leukocytes and erythrocytes in the general urine analysis. Characteristic   increase urine specific gravity .

The overall development of children with oxalate nephropathy, as a rule, does not suffer; but they are characteristic   allergies,   obesity , vegetative-vascular dystonia with a tendency to lower blood pressure ( hypotension ), headaches.

The disease is exacerbated during puberty at the age of 10–14 years, which, apparently, is connected with hormonal changes.

The progression of oxalate nephropathy can lead to the formation of urolithiasis, the development of inflammation of the kidneys during the layering of a bacterial infection.

Phosphate nephropathy

Phosphate nephropathy occurs in diseases involving a violation of phosphorus and calcium metabolism. The main cause of phosphaturia is chronic urinary tract infection.

Often phosphate-calcium nephropathy accompanies oxalate -calcium , but it is less pronounced.

Uric acid metabolism disorders ( urate nephropathy)

During the day, 570–1000 mg of uric acid is formed in the body, one third of the amount of which is secreted into the intestine and destroyed there by bacteria.

The remaining two thirds are filtered in the kidneys, most are sucked back, and only 6–12% of the filtered amount is excreted in the urine.

Primary urate nephropathy due to hereditary disorders of uric acid metabolism.

Secondary occur as complications of other diseases (erythremia,   multiple myeloma, chronic hemolytic anemia and al.), it is a consequence of the use of certain drugs (thiazides, cytostatic agents, salicylates, cyclosporin A et al.) or dysfunction of kidney tubules and physico-chemical properties of the urine (in kidney inflammation, for example).

Urate crystals are deposited in the kidney tissue – this leads to the development of inflammation and a decrease in renal functions.

The first signs of the disease can be detected at an early age, although in most cases there is a long latent course of the process.

And in the general analysis of urine urates are detected, small amount of protein and red blood cells. In the presence of a large number of urates, urine acquires brick color.

Violations of cystine metabolism

Cystine is a metabolic product of the methionine amino acid. Two main reasons for an increase in the concentration of cystine in the urine can be identified :

  • excessive accumulation of cystine in the kidney cells
  • impaired cystine reabsorption in the renal tubules.

Cystine accumulation in cells is the result of a genetic defect tsistinreduktazy enzyme. This metabolic disorder is systemic and is called cystinosis.

Intracellular and extracellular accumulation of cystine crystals is detected not only in the tubules and interstitium of the kidney, but also in the liver, spleen, lymph nodes, bone marrow, peripheral blood cells, nervous and muscle tissue, and other organs.

Violation of cystine reabsorption in the tubules of the kidney is observed due to a genetically determined defect of transport through the cell wall for amino acids – cystine , arginine, lysine and ornithine.

As the disease progresses, signs of urolithiasis are determined, and when the infection is added, kidney inflammation occurs.

Diagnostics

Laboratory and instrumental diagnosis of dysmetabolic nephropathy is based on

  • identifying salt crystals in   urinalysis,
  • increasing the concentration of certain salts in the biochemical study of urine,
  • study of the crystal- forming ability of urine (АКОСМ),
  • conducting tests for calciphylaxis and peroxides in the urine,
  • Ultrasound of the kidneys.

Detection of salt crystals only in general urine tests is not a basis for making a diagnosis of dysmetabolic nephropathy. It should be borne in mind that the release of crystals with urine in children is often transient and is not associated with metabolic disorders.

To confirm the diagnosis of dysmetabolic nephropathy in the detection of salt crystals in the general analysis of urine biochemical analysis of urine is carried out.

The calciphylaxis test allows you to identify violations of cellular calcium metabolism. The urine peroxide test reflects the activity of cell membrane peroxidation.

Changes detected by ultrasound of the kidneys, as a rule, are not very specific. Detection of micromixes or inclusions in the kidney is possible .

Treatment of dysmetabolic nephropathy

Treatment of any dysmetabolic nephropathy can be reduced to four basic principles:

  • normalization of lifestyle;
  • correct drinking regime;
  • diet;
  • specific methods of therapy.

Receiving a large amount of liquid is a universal way to treat any dysmetabolic nephropathy, as it helps to reduce the concentration of soluble substances in the urine.

One of the goals of treatment is to increase the nightly volume of urination, which is achieved by taking fluids before bedtime. Preference should be given to plain or mineral water.

Diet can significantly reduce the salt load on the kidneys.

Specific therapy should be aimed at preventing crystal formation, excretion of salts, and normalization of metabolic processes.

Treatment of oxalate nephropathy

Nutrition Tips

  • When treating patients with oxalate nephropathy, a potato-cabbage diet is prescribed, which reduces the supply of oxalates from food and the load on the kidneys.
  • It is necessary to exclude jelly, strong meat broth, sorrel, spinach, cranberries, beets, carrots, cocoa, chocolate.
  • It is recommended to enter into the diet dried apricots, prunes, pears.
  • From mineral waters such as Slavyanovskaya and Smirnovskaya are used , 3-5 ml / kg / day . in 3 doses 1 month, 2–3 times a year.

Drug therapy

Drug therapy includes membranotropic drugs and antioxidants. Treatment should be long.

  • Pyridoxine (vitamin B6) is prescribed at a dose of 1-3 mg / kg / day . within 1 month quarterly.
  • Vitamin B6 has a membrane stabilizing effect due to participation in the metabolism of fats as an antioxidant and the metabolism of amino acids. It is also advisable the appointment of the drug Magne B6 at the rate of 5-10 mg / kg / day . course for 2 months 3 times a year.
  • Membrane stabilizing action renders vitamin A, which normalizes the interaction of proteins and lipids of the cell membrane. The daily dose of vitamin A 1000 IU per year of life of the child, the course – 1 month quarterly.
  • Tocopherol acetate (vitamin E) is a powerful antioxidant that enters the body from the outside and is produced by the body itself. It must be remembered that the excessive introduction of vitamin E with food can inhibit its internal production by the mechanism of negative feedback. Vitamin E strengthens the protein-lipid bonds of the cell membranes. It is prescribed with vitamin A in a dose of 1-1.5 mg / kg of body weight per day.

As membrane stabilizers , dimephosphone and xyphon are used .

Dimephosphone is used in a dose of 1 ml of a 15% solution for every 5 kg of weight, 3 doses per day. The course is 1 month, 3 times a year.

Ksidifon prevents the deposition of insoluble calcium salts. It is prescribed in a dose of 10 mg / kg / day . 2% solution in 3 doses. Course – 1 month, 2 times a year.

Ciston has a high efficiency , especially during crystalluria . Cystone is prescribed in a dose of 1-2 tablets 2-3 times a day, a course of 3 to 6 months.

In addition, magnesium oxide is prescribed, especially with a high oxalate content, at a dose of 0.15–0.2 g / day .

Treatment of urate nephropathy

Diet

  • When treating urate nephropathy, the diet provides for the exclusion of foods rich in purine bases (liver, kidney, meat broth, peas, beans, nuts, cocoa, etc.).
  • The advantage should be given to products of dairy and vegetable origin.
  • An important condition for successful therapy is adequate fluid intake – from 1 to 2 liters per day. Preference should be given to slightly alkaline and low-mineralized waters, grass decoctions (horsetail, dill, birch leaf, lingonberry leaf, clover, knotweed, etc.), oats broth.

To maintain the optimum acidity of urine, citrate mixtures can be used (uralite-U, blamaren , magurite , solimok , etc.).

In urate nephropathy, it is important to reduce the concentration of uric acid. To do this, use tools that reduce the synthesis of uric acid – allopurinol , nicotinamide .

The use of allopurinol in pediatrics is limited due to possible complications of the skin, liver, and blood.

Under the strict control of allopurinol prescribed in a dose of 0.2–0.3 g / day . in 2-3 doses within 2-3 weeks, then the dose is reduced. The duration of the general course is up to 6 months.

Nicotinamide is a weaker drug than allopurinol , but is better tolerated; appointed in a dose of 0.005-0.025 g 2-3 times a day for 1-2 months with repeated courses.

Uric acid is output as orotic acid, tsiston, etamid, Cystenalum, Phytolysinum et al.

Treatment of phosphate nephropathy

Treatment in phosphate nephropathy should be directed to the acidification of urine (mineral water – narzan, arzni , dzau- suar , etc .; drugs – cystenal , ascorbic acid, methionine).

A diet with the restriction of foods rich in phosphorus (cheese, liver, caviar, chicken, legumes, chocolate, etc.) is prescribed.

Cystinosis treatment

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Treatment of cystinosis and cystinuria includes diet, high – liquid regimen and drug therapy aimed at alkalinization of the urine and increase the solubility of cystine .

The goal of diet therapy is to prevent excessive intake of the child’s precursor of cystine , methionine and other sulfur-containing acids.

To this end, foods that are rich in methionine and sulfur-containing amino acids — cottage cheese, fish, eggs, meat, etc., are also excluded (or severely limited) from the child’s diet.

Since methionine is necessary for the child’s body to grow, prolonged use of a strict diet is impossible, therefore, after 4 weeks from the start of dietary therapy, the child’s diet expands and approaches the usual one, but is characterized by strict exclusion of fish, cottage cheese and eggs.

The amount of liquid should be at least 2 l / day . It is especially important to take the liquid before going to bed.

For alkalinization of the urine is used citrate mixture, sodium bicarbonate solutions, blemen , alkaline mineral water.

To increase the solubility of cystine and prevent crystallization, penicillamine is prescribed . It has some toxicity, therefore at the beginning of therapy low doses of the drug are prescribed – 10 mg / kg / day . in 4–5 doses, then the dose increases during the week to 30 mg / kg / day , and for cystinosis , to 50 mg / kg / day.

Penicillamine treatment should be carried out under the control of cystine in leukocytes and / or cyanide nitroprusside test (test for cystine in the urine, where the concentration of cystine should be up to 150-200 mg / l). When these indicators are achieved, thepenicillamine dose is reduced to 10–12 mg / kg / day.

Penicillamine treatment is carried out for a long time, for years. Since penicillamine inactivates pyridoxine, vitamin B6 (pyridoxine) is prescribed in parallel at a dose of 1-3 mg / kg / day. within 2-3 months with repeated courses.

To stabilize the membranes of the renal tubules, vitamin A (6,600 IU / day ) and vitamin E (tocopherol, 1 drop for 1 year of life of a 5% solution per day) are prescribed for 4–5 weeks with repeated courses.

There is evidence of a positive effect of using a less toxic analogue of it, cuprenil, in a reduced dose in combination with xidiphon and other membrane stabilizers instead of penicillamine.

Antibacterial therapy is indicated for the addition of infection.

When cystinosis successfully used kidney transplantation, which is carried out before the end-stage development of chronic renal failure. Transplantation of the kidney can significantly increase the life of patients – up to 15-19 years, but the deposition of crystals ofcystine is observed in the graft, which ultimately leads to the defeat of the transplanted kidney.

Forecast

The prognosis for dysmetabolic nephropathy is generally favorable.

In most cases, with the appropriate regimen, diet and drug therapy, it is possible to achieve a stable normalization of the corresponding indicators in the urine.

In the absence of treatment or if it is ineffective, the most natural outcome of dysmetabolic nephropathy is urolithiasis and inflammation of the kidneys.

The most frequent complication of dysmetabolic nephropathy is the development of an infection of the urinary system, primarily pyelonephritis.

Glomerulonephritis

The reasons

Manifestations of glomerulonephritis

Diagnostics

Treatment of individual morphological forms

Glomerulonephritis is an immune lesion of the kidney glomeruli.

By the nature of the course of glomerulonephritis is acute and chronic.

The reasons

  • Infections ( angina, scarlet fever, infective endocarditis, sepsis, pneumococcal pneumonia, typhoid fever, meningococcal infection, viral hepatitis B, infectious mononucleosis, epidemic parotitis, chickenpox , infections caused by Koksaki viruses, etc.)
  • Systemic diseases: systemic red   lupus , vasculitis, Schönlein-Genoha disease, hereditary pulmonary renal syndrome
  • Introduction of vaccines, serums
  • Toxic substances (organic solvents, alcohol, mercury, lead, etc.)
  • Irradiation, etc.

Glomerulonephritis manifests itself in 1-4 weeks. after exposure to a provoking factor.

Manifestations of glomerulonephritis

  • Blood in the urine – urine   colors “meat slop”
  • Swelling of the face (especially the eyelids), as well as feet and legs
  • Blood pressure increase
  • Decreased urine, thirst
  • Increased body temperature (rare)
  • Lack of appetite, nausea, vomiting,   headache weakness
  • Weight gain
  • Dyspnea

Depending on the various forms of glomerular lesion, one or other manifestations of glomerulonephritis may prevail.

Acute glomerulonephritis develops 6-12 days after the infection, usually  streptococcal (angina, tonsillitis, scarlet fever), including skin ( pyoderma, impetigo ).

The disease can also develop after other infections – bacterial, viral, parasitic, as well as after other antigenic effects – serum, vaccines, drugs.

In the classic cyclic course, acute glomerulonephritis is characterized by changes in urine (red urine due to blood admixture), swelling, and a decrease in the amount of urine released.

Diagnostics

  • General urine analysis. In the urine –   red blood cells,   white blood cells , cylinders,   protein
  • Urine specific gravity normal or elevated
  • Increased titer of antibodies to streptococcus in the blood ( antistreptolysin-O , antistreptokinase, antihyaluronidase)
  • Decrease in the content of the components of complement SZ, C4 in the serum with a return to the initial level in 6-8 weeks with post-streptococcal acute glomerulonephritis; with membranoproliferative glomerulonephritis, these changes persist for life
  • The content of total protein in serum is reduced, in the proteinogram – an increase in a1-and a2-globulins
  • Ultrasound of the kidneys
  • Radioisotope angiorenography
  • ECG
  • Ocular fundus
  • Renal biopsy allows to clarify the morphological form of chronic glomerulonephritis, its activity, to exclude kidney diseases with similar symptoms

Treatment of glomerulonephritis

  • Hospitalization in the nephrology department
  • Bed rest
  • Diet number 7a: restriction of proteins, salt limit edema,   hypertension

Antibiotics (for acute post-streptococcal glomerulonephritis or the presence of foci of infection)

Immunosuppressants and glucocorticoids are ineffective in post-infectious, post-streptococcal acute glomerulonephritis.

Immunosuppressive therapy – glucocorticoids and cytotoxic drugs – in case of exacerbation of chronic glomerulonephritis.

Glucocorticoids

shown in mesangioproliferative chronic glomerulonephritis and chronic glomerulonephritis with minimal glomerular changes. With membranous chronic glomerlonephritis, the effect is not clear.

With membranoproliferative chronic glomerulonephritis and focal segmental glomerulosclerosis, glucocorticoids are ineffective.

Prednisolone

administered on 1 mg / kg / day orally for 6-8 weeks, followed by a rapid decrease to 30 mg / day (5 mg / week), and then slow (2.5-1.25 mg / week) up to full cancellation.

Pulse therapy with prednisolone is carried out with a high activity of CGN in the first days of treatment – 1000 mg IV drip 1 r / day for 3 days in a row. After reducing the activity of chronic glomerulonephritis, monthly pulse therapy is possible until remission is achieved.

Cytostatics

  • cyclophosphamide at 2-3 mg / kg / day by mouth or intramuscularly or intravenously,
  • chlorambucil 0.1-0.2 mg / kg / day inside,

as alternative drugs:

  • Cyclosporine – 2.5-3.5 mg / kg / day, inside,
  • azathioprine 1.5-3 mg / kg / day inside)

they are indicated in active forms of chronic glomerulonephritis with a high risk of progression of renal failure, as well as in the presence of contraindications for the administration of glucocorticoids, inefficiency or complications when using the latter (in the latter case, they prefer the combined use of glucocorticoids).

Pulse therapy with cyclophosphamide is indicated for high activity of chronic glomerulonephritis, either in combination with pulse therapy with prednisolone (or against the background of daily administration of prednisolone), or in isolation without additional prescription of prednisolone; in the latter case, the dose of cyclophosphamide should be 15 mg / kg (or 0.6-0.75 g / m2 of body surface) i / v monthly:

Multicomponent treatment regimens

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Simultaneous use of glucocorticoids and cytostatics is considered more effective monotherapy with glucocorticoids. It is generally accepted to prescribe immunosuppressive drugs in combination with antiplatelet agents, anticoagulants – the so-called multi-component schemes:

  • 3-component scheme (without cytostatics): prednisone 1 – 1.5 mg / kg / day by mouth 4-6 weeks, then 1 mg / kg / day every other day, then reduced by 1.25-2.5 mg / week to cancellation + heparin in 5000 IU 4 p / day for 1 -2 months with a switch to phenyldione or acetylsalicylic acid in a dose of 0.25-0.125 g / day, or sulodexide in a dose of 250 ME 2 times / day orally + 400 mg dipyridamole / day inside or in / in. 
     
  • 4-component scheme Kinkayd-Smith: prednisone 25-30 mg / day orally for 1-2 months, then reduce the dose by 1.25-2.5 mg / week until discontinuation + Cyclophosphamide 100-200 mg for 1 – 2 months, then half dose to achieve remission (cyclophosphamide can be replaced with chlorambucil or azathioprine) + Heparin 5000 U, 4 p / day for 1-2 months with switching to phenyldione or acetylsalicylic acid, or sulodexide + Dipyridamole 400 mg / day inside or in / in. 
     
  • Ponticelli’s scheme: initiation of therapy with prednisolone – 3 days in a row at 1000 mg / day, the next 27 days prednisone 30 mg / day by mouth, the 2nd month – chlorambucil 0.2 mg / kg (alternation of prednisolone and chlorbutin). 
     
  • Steinberg scheme – pulse therapy with cyclophosphamide: 1000 mg IV monthly for a year. In the next 2 years – 1 time in 3 months. In the next 2 years – 1 time in 6 months.

Antihypertensive therapy: captopril 50-100 mg / day, enalapril 10-20 mg / day, ramipril 2.5-10 mg / day

Diuretics – hydrochlorothiazide, furosemide, spironolactone

Antioxidant therapy (vitamin E), however, there is no convincing evidence of its effectiveness.

Lipid-lowering drugs (nephrotic syndrome): simvastatin, lovastatin, fluvastatin, atorvastatin in a dose of 10-60 mg / day for 4-6 weeks with a subsequent decrease in dose.

Antiplatelet agents (in combination with glucocorticoids, cytostatics, anticoagulants; see above). Dipyridamole 400-600 mg / day. Pentoxifylline at 0.2-0.3 g / day. Ticlopidine 0.25 g 2 p / day

Plasma exchange   in combination with pulse therapy with prednisolone and / or cyclophosphamide is indicated for highly active chronic glomerulonephritis and the lack of effect of treatment with these drugs.

Surgery. Kidney transplantation in 50% is complicated by relapse in the graft, in 10% by graft rejection.

Treatment of individual morphological forms

Mesangioproliferative chronic glomerulonephritis

With slowly progressive forms, incl. with IgA nephritis, there is no need for immunosuppressive therapy. At high risk of progression – glucocorticoids and / or cytostatics – 3-and 4-component schemes. The effect of immunosuppressive therapy on the long-term prognosis remains unclear.

Membranous chronic glomerulonephritis

The combined use of glucocorticoids and cytostatics. Pulse therapy with cyclophosphamide 1000 mg IV monthly. In patients without nephrotic syndrome and normal renal function, they are ACE inhibitors.

Membranoproliferative (mesangiocapillary) chronic glomerulonephritis

Treatment of the underlying disease. ACE inhibitors. In the presence of nephrotic syndrome and reduced renal function, therapy with glucocorticoids and cyclophosphamide with the addition of antiplatelet agents and anticoagulants is justified.

Chronic glomerulonephritis with minimal changes

Prednisone 1 to 1.5 mg / kg for 4 weeks, then 1 mg / kg every other day for another 4 weeks. Cyclophosphamide or chlorambucil with the ineffectiveness of prednisone or the inability to cancel it due to relapses. With continuing relapses of nephrotic syndrome – cyclosporine 3-5 mg / kg / day (children 6 mg / m2) 6-12 months after achieving remission.

Focal segmental glomerulosclerosis

Immunosuppressive therapy is not effective enough. Glukokrkoikoid prescribed for a long time – up to 16-24 weeks. Patients with nephrotic syndrome are prescribed prednisone for 1–1.2 mg / kg daily for 3-4 months, then every other day for 2 months, then reduce the dose until canceled. Cytostatics (cyclophosphamide, cyclosporine) in combination with glucocorticoids.

Fibroplastic chronic glomerulonephritis

In the focal process, treatment is carried out according to the morphological form that led to its development. Diffuse form – a contraindication to active immunosuppressive therapy.

Treatment according to clinical forms is carried out when it is impossible to perform a biopsy of the kidneys.

  • Latent form of glomerulonephritis. Active immunosuppressive therapy is not indicated. When proteinuria> 1.5 g / day prescribed ACE inhibitors.
  • Hematuric form of glomerulonephritis. Intermittent effect of prednisone and cytostatics. Patients with isolated hematuria and / or small proteinuria are ACE inhibitors and dipyridamole.
  • Hypertensive form of glomerulonephritis. ACE inhibitors; target level of blood pressure – 120-125 / 80 mm Hg. For exacerbations, cytostatics are used as part of a 3-component scheme. Glucocorticoids (prednisone 0.5 mg / kg / day) can be administered as monotherapy or as part of a combination regimen.
  • Nephrotic form of glomerulonephritis – indication for the purpose of a 3-or 4-component scheme
  • Mixed form – 3 or 4-component treatment regimen.

Cirrhosis of the liver

The reasons

Manifestations of cirrhosis

Diagnostics

Treatment of cirrhosis

Diet for liver cirrhosis

Forecast

Prevention

Cirrhosis of the liver – a disease characterized by a violation of the structure of the liver due to the proliferation of connective tissue; manifested by functional liver failure.

The reasons

The main risk factors for cirrhosis are considered to be:

  • chronic alcoholism
  • viral hepatitis
  • toxic effects of industrial poisons, drugs (methotrexate, isoniazid, etc.), mycotoxins , etc.
  • venous congestion in the liver associated with prolonged and severe heart failure 
  • hereditary diseases – hemochromatosis , hepatocerebral dystrophy, deficiency of alpha- single- antitrypsin , galactosemia , glycogenosis, etc. 
  • prolonged damage to the biliary tract

In about 50% of patients with cirrhosis of the liver, the disease develops due to the action of several causal factors (more often the hepatitis B virus and alcohol).

Manifestations of cirrhosis

Complaints of weakness, fatigue, decreased performance and appetite, dyspeptic disorders (nausea, vomiting, bitter taste in the mouth, belching, intolerance to fatty foods, alcohol).

Characterized by a feeling of heaviness or pain in the abdomen, mainly in the right hypochondrium and the epigastric region. Among the signs of cirrhosis of the liver, so-called “liver signs” in the form of reddening of the palms, vascular “asterisks” (mainly on the skin of the upper half of the body) are important. Often there are hemorrhages in the skin, as well as increased bleeding of the mucous membranes.

Marked itching, pain in the joints, reduce hair in the armpits and pubis, reduce sexual desire. Body temperature rises moderately or remains within the normal range.

Often there is asthenic syndrome, manifested by weakness, increased fatigue, irritability, tearfulness, instability of mood. Patients are impressionable, often touchy, picky, suspicious, prone to hysterical reactions. Characterized by sleep disturbance – insomnia at night, sleepiness during the day.

For cirrhosis of the liver are caused by colds, a violation of the regime, the use of alcohol.

Diagnostics

The diagnosis of cirrhosis in the early stages presents significant difficulties, since the disease develops gradually and at first has no pronounced manifestations.

Ultrasound, X-ray and radionuclide methods of investigation are essential in recognizing cirrhosis . Quite accurate information about the state of the liver in cirrhosis can be obtained using computed tomography . 

Radionuclide study of the liver – scintigraphy is inferior in its information content to ultrasound and computed tomography, but unlike them, it also makes it possible to evaluate the function of the organ.

Crucial in the diagnosis of cirrhosis is the study of liver tissue obtained by puncture biopsy – blind or targeted, carried out under the control of ultrasound or during laparoscopy.

Treatment of cirrhosis

Limit mental and physical stress. With an overall good condition, therapeutic walking and therapeutic exercises are recommended. Women with active liver cirrhosis should avoid pregnancy.

Compensated inactive liver cirrhosis, as a rule, does not require medical treatment. In addition, you should generally limit the intake of medicines, especially soothing.

With sub – and decompensated forms, the choice of drug therapy is determined by the nature of the main manifestations of the disease. In the case of a low protein content in the blood, anabolic steroids are prescribed, transfusions of albumin and plasma. The presence of anemia is an indication for prescribing iron supplements. When edema and ascites limit fluid intake, exclude from the diet table salt, prescribe diuretics (hypothiazide, furosemide) in combination with aldosterone antagonists ( spironolactone ). Paracentesis is produced for health reasons, simultaneously releasing no more than 3 liters of liquid.  

The so-called hepatoprotectors are also used – vitamins of group B, orotic acid, extracts and hydrolysates of the liver, silibinin (legal), Essentiale , etc.

In the case of process activity, the same agents are used as with chronic active hepatitis, the main ones being hormones (prednisone) and immunosuppressants ( azathioprine , etc.). Their effectiveness is inversely related to the depth of the structural reorganization of the liver tissue and in far advanced stages of cirrhosis of the liver is close to zero.

To prevent infections in all patients with cirrhosis of the liver during any interventions (tooth extraction, rectoromanoscopy , paracentesis , etc.) prophylactically prescribed antibiotics. Antibacterial therapy is also indicated even in light infectious processes. 

General advice for patients with cirrhosis of the liver:

  • Rest as soon as you feel tired.
  • Do not lift weights (this can cause gastrointestinal bleeding)
  • Achieve stool frequency 1-2 times a day. Patients with cirrhosis of the liver to normalize the work of the intestine and the composition of the intestinal flora in favor of “beneficial” bacteria are encouraged to take lactulose ( duphalac ). Duphalac is prescribed in the dose that causes soft, half-shaped chair 1-2 times a day. The dose ranges from 1-3 teaspoons to 1-3 tablespoons per day, is selected individually. The drug has no contraindications, it can be taken even for small children and pregnant women.
  • To improve the digestion of patients prescribed multienzyme preparations. 
    With fluid retention (edema, ascites), it is necessary to limit the intake of salt to 0.5 g per day, fluids – up to 1000-1500 ml per day.
  • Daily measure body weight, the volume of the abdomen at the navel (an increase in the volume of the abdomen and body weight indicates fluid retention);
  • Daily read the fluid balance per day (diuresis): count the volume of all ingested fluid (tea, coffee, water, soup, fruit, etc.) and count all the fluid released during urination. The amount of released fluid should be about 200-300 ml more than the amount of fluid taken.
  • To control the degree of damage to the nervous system, it is recommended to use a simple handwriting test: write a short phrase every day, for example, “Good morning” in a special notebook. Show your notebook to relatives – if you change your handwriting, contact your doctor.

Diet for liver cirrhosis

Excluded from nutrition:

  • mineral waters containing sodium;
  • alcohol;
  • salt, food must be prepared without adding salt (salt-free bread, crackers, cookies and bread are used, as well as salt-free oil);
  • products containing baking powder and baking soda (cakes, biscuit cookies, cakes, pastries and plain bread);
  • pickles, olives, ham, bacon, corned beef, tongues, oysters, mussels, herring, fish and canned meat, fish and meat pate, sausage, mayonnaise, various canned sauces and all kinds of cheeses, ice cream.

It is recommended to use seasonings in cooking: lemon juice, orange zest, onion, garlic, salt-free ketchup and mayonnaise, pepper, mustard, sage, cumin, parsley, marjoram, bay leaf, cloves.

100 g of beef or poultry, rabbit or fish and one egg per day are allowed (one egg can replace 50 g of meat). Milk is limited to 1 cup per day. You can eat low-fat sour cream. You can eat boiled rice (without salt). Allowed any vegetables and fruits in fresh form or in the form of dishes prepared at home.

Sample menu for the day for a patient with liver cirrhosis:

  • Breakfast: cereal porridge (semolina, buckwheat, millet, barley, oatmeal) with cream and sugar or baked fruit. 60 g of salt-free bread, or loaves (slices), or salt-free crackers with unsalted butter and marmalade (jelly or honey), 1 egg, tea or coffee with milk.
  • Lunch: 60 g of beef or poultry meat or 90 g of white fish, potatoes, greens, fruit (fresh or baked)
  • Lunch: 60 g of salt-free bread or bread, unsalted butter, jam or tomato, tea or coffee with milk.
  • Dinner: soup without salt, beef, poultry meat or fish (as for lunch), potatoes, greens, fruit or jelly from fruit juice and gelatin, sour cream, tea or coffee with milk.

Forecast

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Life expectancy in liver cirrhosis depends on the degree of compensation process. Approximately half of patients with compensated cirrhosis (at the time of diagnosis) live more than 7 years.

With decompensated cirrhosis, after 3 years, 11–41% remain alive. With the development of ascites, only a quarter of patients experience 3 years. Even more unfavorable prognosis has cirrhosis, accompanied by damage to the nervous system, in which patients in most cases die within a year.

The main causes of death are hepatic coma and bleeding from the upper gastrointestinal tract. Patients with cirrhosis of the liver are partially able-bodied (group III disability), and with decompensated cirrhosis, the active forms of the disease and when joining complications are disabled (disability groups II and I).

Prevention

Prevention consists in the prevention and timely treatment of diseases leading to cirrhosis of the liver (primarily alcoholism and viral hepatitis ). 

Cholecystitis

Symptoms

Cholecystitis treatment

Food for cholecystitis

Folk treatment

Symptoms

For cholecystitis is characterized by pain or heaviness in the right hypochondrium after exercise, plentiful food intake, ingestion of fatty or fried foods, after excitement, with hypothermia. The pains may be dull, aching, or intense. Pain in cholecystitis can be given in the right hand, right shoulder blade.

Patients are also worried about nausea, empty belching, feeling of bitterness in the mouth. Possible increase in body temperature.

The development of acute and chronic cholecystitis predispose bile stasis and damage to the walls of the gallbladder.

Stagnant bile contribute to:

  • violation of the diet (long breaks between meals, food dry rations);
  • sedentary lifestyle;
  • constipation;
  • pregnancy;
  • metabolic disorders ( diabetes, obesity, atherosclerosis );   
  • obstacles to the flow of bile ( opistorhi , for example).

Damage to the walls of the gallbladder can be caused by:

  • bile with altered physicochemical properties;
  • stones;
  • pancreatic enzymes flowing into the bile duct;
  • gallbladder injuries.

Cholecystitis treatment

Bed rest is shown only during an exacerbation, accompanied by abdominal pain, temperature. Long-term restrictions in movements adversely affect the course of cholecystitis, as they contribute to the stagnation of bile.

During an attack of biliary colic, it is important to eliminate pain syndrome as soon as possible. To this end, you can apply no-silos, spasmolitin .

During an attack of pain, apply moderate heat to the area of ​​the right hypochondrium in the form of non-heated hot-water bottles, a warming compress.

The indication for the treatment of cholecystitis with antibiotics is an exacerbation of the inflammatory process in the biliary tract, accompanied by pain, temperature. The course of antibiotic therapy is non-durable (7-10 days). Antibiotics for cholecystitis should be used in combination with baktisubtil and always with vitamins (C, groups B, A).

They resort to broad-spectrum antibiotics – ampioks, amoxicillin, amoxiclav . If giardias are found in bile, treatment with antiglance agents is necessary.

Vitamin therapy (in the acute period, vitamins A, C, B1, B2, PP, and further courses of vitamins B6 and B12, B15, B5, E) should be a mandatory part of the treatment of patients with cholecystitis.

In the treatment of patients with cholecystitis, it is necessary to widely use cholagogue preparations, since, by reducing the stagnation of bile in the affected bladder, they also contribute to the more rapid elimination of inflammatory changes in it.

Most often combine magnesium sulfate as a 5% or 10% – of the solution according to the tea, dessert or tablespoon three times daily holosas (1 teaspoon three times a day), holagonom (tablets 2-3 times daily) or medicinal herbs.

Food for cholecystitis

One of the main factors in the treatment of patients with cholecystitis is diet . Some increase in meals is required (up to 4-6 times), as this will improve the flow of bile. 

Food enrichment with bran bread, cottage cheese, egg white, oatmeal, cod, and yeast drinks is desirable.

Patients with cholecystitis poorly tolerate fat, fatty meats, poultry, fish. From animal fats it is recommended to use only butter. Very useful vegetable oils (corn, sunflower, olive). The unsaturated fatty acids ( arachidonic , linoleic, linolenic) contained in them stimulate bile secretion, improve the functional state of the liver. Vegetable oils should be added to vinaigrettes, salads, sauerkraut or given in tea, dessert, tablespoon 2-3 times a day before meals. Of carbohydrates limit only foods that contain a lot of poorly digestible fiber (cabbage, turnip, etc.). The amount of fluid increases as it improves the flow of bile.

Patients with exacerbation of cholecystitis are recommended only vegetarian soups. Exclude fried dishes (especially breaded), very cold drinks and dishes (ice cream, products from the refrigerator), seasonings (vinegar, pepper, garlic, onions, roots, mustard, horseradish), mushrooms, all sausages, ham, smoked meats, canned food, short pastry, cream cakes, any fried pies, pancakes, coffee and cocoa.

Dairy, vegetarian and fruit soups are given to the patient, from second courses – boiled vegetables in any form, cereals, puddings, boiled fish and meat (with the exception of pork, lamb, game meat, brains, kidneys as rich in extractive substances). Drinks are allowed – weak tea, compote, fruit drink, jelly, juices (but unpreserved), milk, yogurt, kefir, “Snowball”, ryazhenka, white and black bread (better than yesterday), processed (but not snack) curds – “Friendship” , “Yantar”, “Sour-milk”, not sharp cheeses. Useful products containing a lot of magnesium salts: bread and bran confectionery (for example, Health bread), buckwheat and oatmeal; raw fruits, vegetables, berries. Useful radish (but not radish). Dietary treatment should be carried out at home for 3 years after the last exacerbation with cholecystitis and 1.5 years with biliary dyskinesia. 

Folk treatment

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Folk treatment of acute and chronic cholecystitis is the use of herbal decoctions.

The most widespread in cholecystitis was a collection according to N. G. Kovaleva:

  • Calendula officinalis (aboveground part)
  • garden dill (seeds) – 10 g, white birch (leaves) – 10 g,
  • forest sticks (grass) – 10 g,
  • juniper ordinary (fruits) – 10 g,
  • Chamomile (flowers) – 20 g,
  • wild strawberry (berries) – 20 g,
  • white rose (petals) – 20 g,
  • horsetail (shoots) – 30 g,
  • corn silk – 30 g,
  • wild rose brown (fruit crushed) – 40 g

5–6 g of collection are brewed with 500 ml of boiling water, infused and taken in 50–150 ml 3 times a day for 10–15 minutes. before meals. The taste is bitter, the smell is pleasant.

In recent years, they have found widespread use in the treatment of patients suffering from diseases of the gallbladder and biliary tract, preparations containing essential oils (in particular, German – rovauhol and enatin ). As a choleretic, you can use black radish juice and 1 tablespoon 3 times daily before meals for 10–20 days.

The choleretic effect of polyatomic alcohols (sorbitol, mannitol and xylitol) has been convincingly proven . Sorbitol stimulates the production of endogenous cholecystokinin , increases the bacterial synthesis of vitamins B1 and B2, enhances the absorption of vitamin B12. Sorbitol can be used in the form of a 10–15% solution of 50–75 ml 3 times a day instead of magnesium sulfate. Xylitol is also prescribed in the same dose.

In chronic cholecystitis, it is widely prescribed to drink mineral waters of low and medium mineralization with a predominance of hydrocarbonates, sulfates, chlorine, magnesium, sodium, and calcium. Thermal water (35–42 ° C) or hyperthermal (42–50 ° C) temperature is used. 

Mineral waters stimulate the secretion of bile, the excretion, the decrease in viscosity and its dilution. Drink water in the amount of 3 ml per 1 kg of body weight in small sips. Essentuki number 4, 17, 20, Smirnovskaya, Borzhom, Slavyanovskaya are used more often.

If cholecystitis is complicated by gastritis with high acidity, then mineral water is given 1–1.5 hours before meals, gastritis with normal or low acidity – 40 minutes. before meals. The course of treatment with mineral waters 1-1.5 months. with a break between the next course of 3-6 months.  

Gilbert ‘s syndrome

The reasons

Symptoms of Gilbert’s disease

Diagnostics

Treatment of Gilbert’s syndrome

Forecast

Syndrome Gilbert (disease Gilbert ) is a benign hepatic dysfunction, which consists in clearing it of indirect bilirubin , which is formed during the breakdown of hemoglobin.   

Gilbert ‘s syndrome is a hereditary constitutional feature, so this pathology is not considered by many authors to be a disease.

Such an anomaly is found in 3-10% of the population, especially it is often diagnosed among the inhabitants of Africa. It is known that men are 3-7 times more likely to suffer from this disease.

The main characteristics of the described syndrome include the periodic increase in blood bilirubin and the associated jaundice. 

The reasons

Gilbert ‘s syndrome is a hereditary disease caused by a defect in a gene located in the second chromosome that is responsible for the production of the hepatic enzyme glucoronyl transferase. Indirect bilirubin binds to the liver through this enzyme. Its excess leads to hyperbilirubinemia (increased bilirubin content in the blood) and, as a result, to jaundice.

The factors that cause the aggravation of Gilbert’s syndrome (jaundice) are highlighted:

  • infectious and viral diseases;
  • injuries;
  • menstruation;
  • violation of the diet;
  • starvation;
  • insolation;
  • lack of sleep;
  • dehydration;
  • excessive exercise;
  • stress;
  • taking certain medications ( rifampicin , chloramphenicol, anabolic drugs, sulfonamides, hormones, ampicillin, caffeine, paracetamol, and others);
  • alcohol consumption;
  • surgical intervention.

Symptoms of Gilbert’s disease

In a third of patients, the pathology does not manifest itself. Elevated levels of bilirubin in the blood are observed from birth, but it is difficult to diagnose this diagnosis in infants due to physiological jaundice of newborns. As a rule, Gilbert’s syndrome is determined in young men aged 20-30 years during the examination for another reason.

The main symptom of Gilbert’s syndrome is icteric (jaundice) of the sclera and, sometimes, the skin. Jaundice in most cases is periodic and has a mild severity.

About 30% of patients during the period of exacerbation note the following symptoms:

  • pain in the right hypochondrium;
  • heartburn;
  • metallic taste in the mouth;
  • loss of appetite;
  • nausea and vomiting (especially when eating sweet foods);
  • flatulence ;
  • feeling of full belly;
  • constipation or diarrhea.  

The signs characteristic of many diseases are not excluded:

  • general weakness and malaise;
  • chronic fatigue;
  • difficulty concentrating;
  • dizziness;
  • cardiopalmus;
  • insomnia;
  • chills (no fever);
  • muscle pain.

Some patients complain of emotional disturbances:

  • depression ;
  • propensity for antisocial behavior;
  • unreasonable fear and panic;
  • irritability.

Emotional lability is most likely not associated with elevated bilirubin, but with self-suggestion (constant testing, visits to various clinics and doctors).

Diagnostics

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Various laboratory tests help confirm or refute Gilbert’s syndrome :

  • complete blood count – reticulocytosis in the blood (elevated levels of immature red blood cells) and mild anemia – 100-110 g / l.
  • urinalysis – no abnormalities. The presence in the urine of urobilinogen and bilirubin indicates the pathology of the liver.   
  • biochemical analysis of blood – blood sugar is normal or slightly reduced, blood proteins are within normal limits, alkaline phosphatase, AST , ALT are normal, and the thymol test is negative.     
  • blood bilirubin – in general, the total bilirubin content is 8.5-20.5 mmol / l. In Gilbert’s syndrome, there is an increase in total bilirubin due to indirect.
  • blood clotting – prothrombin index and prothrombin time – within normal limits.
  • viral hepatitis markers are absent.  
  • Ultrasound of the liver.

Perhaps some increase in the size of the liver during an exacerbation. Gilbert ‘s syndrome is often combined with cholangitis, gallstones, chronic pancreatitis.  

It is also recommended to investigate the functions of the thyroid gland and conduct a blood test for serum iron, transferrin, total iron binding capacity (OZHSS).

In addition, special tests are conducted to confirm the diagnosis:

  • Trial with fasting. Fasting within 48 hours or caloric restriction of food (up to 400 kcal per day) leads to a sharp increase (by 2-3 times) in free bilirubin. Unbound bilirubin is determined on an empty stomach on the first day of the test and after two days. An increase in indirect bilirubin by 50-100% indicates a positive test. 

  • Test with phenobarbital. 
    Acceptance of phenobarbital in a dose of 3 mg / kg / day for 5 days helps to reduce the level of unbound bilirubin.
  • Test with nicotinic acid. 
    An intravenous injection of nicotinic acid in a dose of 50 mg leads to an increase in the amount of unbound bilirubin in the blood by a factor of 2-3 over the course of three hours.
  • Trial with rifampicin . The administration of 900 mg of rifampicin causes an increase in indirect bilirubin. 

Also confirm the diagnosis allows percutaneous liver puncture. Histological examination of punctate shows no signs of chronic hepatitis and cirrhosis of the liver . 

Another additional, but expensive, study is molecular genetic analysis (blood from a vein), which is used to determine defective DNA involved in the development of Gilbert’s syndrome.

Treatment of Gilbert’s syndrome

Specific treatment of Gilbert’s syndrome does not exist. The gastroenterologist (in his absence – the therapist) monitors the condition and treatment of patients.

Diet for syndrome

Lifetime is recommended, and during periods of exacerbation – especially careful, adherence to a diet.

Excluded:

  • sweet food;
  • bakery products;
  • fat creams;
  • chocolate.

In the diet should prevail vegetables and fruits, from cereals preference is given to oatmeal and buckwheat. Low-fat cottage cheese is allowed, up to 1 egg per day, not sharp hard cheeses, dry or condensed milk, a small amount of sour cream. Meat, fish and poultry should be low-fat varieties, the use of spicy foods or food with preservatives is contraindicated. Alcohol, especially strong, should be discarded.

Shows copious drinking. It is advisable to replace black tea and coffee with green tea and unsweetened sour berry juice (cranberries, lingonberries, cherries).

Meal – at least 4-5 times a day, in moderate portions. Fasting, like overeating, can lead to exacerbation of Gilbert’s syndrome.

In addition, patients with this syndrome should avoid exposure to the sun. It is important to inform physicians about the presence of this pathology so that the attending physician can select the appropriate treatment for any other reason.

Drug therapy

During periods of exacerbation, an appointment is scheduled:

  • hepatoprotectors ( Essentiale forte, Kars, silymarin, heptral);
  • vitamins (B6);
  • enzymes (festal, mezim);

Also shown are short courses of phenobarbital, which binds indirect bilirubin.

For the restoration of intestinal peristalsis and with severe nausea or vomiting using metoclopromide ( cerculated ), domperidone.

Forecast

The prognosis for Gilbert’s syndrome is favorable. If you follow the diet and rules of conduct, the life expectancy of these patients does not differ from the life expectancy of healthy people. Moreover, maintaining a healthy lifestyle contributes to its increase.

Complications in the form of chronic hepatitis and cirrhosis of the liver are possible with alcohol abuse, excessive passion for “heavy” food, which is quite possible in healthy people.

Liver cyst

Kinds

Manifestations of liver cyst

Diagnostics

Surgical treatment of liver whales

This is a cavity in the liver filled with fluid.

Liver cyst occurs in approximately 0.8% of the population. In women, it occurs 3-5 times more often than in men, mostly manifested between 30 and 50 years.

Kinds

Liver cysts are divided into true and false.

According to modern concepts, true cysts in the liver occur if during embryonic development there is no connection to the biliary tract system of individual bile ducts; the lack of reverse development of these passages is the cause of the development of liver cysts.

False cysts develop after a traumatic rupture of the liver. They can also be formed after the treatment of liver abscess, removal of echinococcus.

Manifestations of liver cyst

The contents of the liver cysts is a clear transparent or brown transparent liquid mixed with blood or bile. They are more common in the left lobe of the liver.

Manifestations of liver cysts are not specific. The most frequent symptoms are vague pains in the right hypochondrium and the epigastric region, abdominal asymmetry, the definition of a tumor-like mass in the right hypochondrium.

Diagnostics

The decisive factor in the diagnosis belongs to ultrasound and computed tomography of the abdominal cavity. 

Computed tomography allows to establish the presence of liver cysts in 100% of cases.

Surgical treatment of liver whales

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All surgical interventions in liver cysts are divided into radical, conditionally radical, palliative.

A radical operation is liver transplantation.

Conditional-radical operations:

  • husking a cyst with its shells;
  • removal of the affected part of the liver;
  • excision of the cyst wall.

Palliative surgery for liver cysts:

  • opening and emptying the cyst;
  • marsupialization of the cyst (the cyst is opened, its contents are removed, and the edges of the wall of the opened cyst are then sutured to the edges of the wound to form an artificial pocket)
  • cystoentero -, cystogastroanastomoz (i.e. creating a message of the cyst cavity with the intestinal cavity or the stomach).

Indications for surgical treatment:

Absolute:

  • suppuration,
  • gap,
  • bleeding.

Conditionally absolute:

  • giant cyst of any localization (more than 10 cm in diameter);
  • cyst with a central location in the gate of the liver (with compression of the choleretic tract and / or with symptoms of portal hypertension ); 
  • a cyst with pronounced manifestations (constant pain in the hypochondrium, digestive disorders, emaciation, etc.).

Relative:

  • large cysts (from 3 to 10 cm in diameter);
  • isolated cyst of III-IV segments;
  • recurrent liver cysts in case of failure of puncture treatment methods.

Patients with liver cysts with a diameter of 3 cm are subject to follow-up.

Gallstone disease

Risk factors

Symptoms of gallstone disease

Required examinations

Treatment of gallstone disease

Gallstone disease is a disease characterized by the formation of gallstones or bile ducts. Also known as cholelithiasis , gallstones.

Stone formation is a stage process with periods of active growth and remission.

Risk factors

There are several reasons for the occurrence of gallstone disease:

  • excess cholesterol secretion to bile
  • reduced secretion of phospholipids and bile acids to bile
  • bile stasis
  • biliary tract infection
  • hemolytic diseases.

Most gallstones are mixed. They contain cholesterol, bilirubin, bile acids, proteins, glycoproteins, various salts, trace elements. Cholesterol stones contain mainly cholesterol, have a round or oval shape, layered structure, diameter from 4–5 to 12–15 mm, are localized in the gall bladder.

Cholesterol- pigmented limes – multiple, have faces, the shape is different. Significantly vary in number – tens, hundreds and even thousands.

Pigment stones are small, multiple, rigid, fragile, perfectly homogeneous, black with a metallic tinge, located both in the gallbladder and in the bile ducts.

Calcium stones consist of various salts of calcium, a freakish form, have spiky processes, of light or dark brown color.

Symptoms of gallstone disease

Conventionally, there are several forms of the disease.

Latent form of gallstone disease. 
It should be considered rather as one of the phases in the course of gallstone disease. It can last for a very long time in the absence of manifestations.

Dyspeptic chronic form of the disease. 
Its manifestations:

  • uvstvo heaviness in the epigastric and right hypochondrium,
  • heartburn,
  • flatulence ,
  • unstable chair.

The appearance of pain provokes the use of fatty, fried, spicy foods, too large portions of food.

Painful chronic form of gallstone disease. 
This form of pronounced pain attacks are absent. The pains are aching in nature, localized in the epigastric and right subcostal areas, spread to the area of ​​the right scapula. There are weakness, malaise, irritability.

Biliary colic and chronic recurrent form. 
This is a sudden attack of intense pain in the right hypochondrium and the epigastric region. It is provoked by eating fats, spices, negative emotions, physical tension, pregnancy, menstruation.

Required examinations

  • Blood chemistry
  • Ultrasound
  • Pre dudenal sounding
  • X-ray

Treatment of gallstone disease

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Treatment of gallstone disease depends on the form of the disease and the degree of operational risk.

1. With single stones of the gallbladder with a diameter of more than 1-2 cm, multiple stones are removed gallbladder. The gold standard of surgical treatment is cholecystectomy – removal of the gallbladder. Radical surgery for cholelithiasis provides complete recovery in 95% of patients. In 10% of patients delaying the operation leads to a worsening of the course of the disease.

2. Dissolving or crushing of stones is shown in cases with small stones (up to 1 cm) and single stones.

Crushing is carried out using ultrasound or electromagnetic waves. Crushing of gallstones occurs as a result of the impact of a shock wave on a stone, which is formed by a spark discharge or excitation of piezocrystals and is focused on a stone with the help of a parabolic reflector. At the focal point, the wave energy reaches its maximum. In this case, a deformation occurs in the stone, which exceeds the strength of the stone. Not one, but a lot of shock waves enter the stone – from 1,500 to 3,500, depending on the composition of the stone. Such multiple shock waves destroy it into small fragments.

Small fragments, the size of which does not exceed the diameter of the cystic duct, leave the gall bladder through the cystic duct. Further, through the common bile duct, they enter the intestine and are removed from the body.

Larger fragments that cannot pass through the cystic duct remain in the gallbladder. Therefore, to increase the effectiveness of treatment, it is advisable to add bile acid preparations to extracorporeal lithotripsy.

The main disadvantage of this method is the high probability of recurrence, that is, the reappearance of gallstones. After 5 years, the recurrence rate is 50%.

3. Dissolution of gallstones is possible only with cholesterol stones.

To do this, apply ursodeoxycholic acid at 15 mg / kg per day in 2-3 doses, take about 2 years. Chenodeoxycholic acid, 15 mg / kg per day (1/3 doses in the morning and 2/3 in the evening), are taken for a year or more.

Contact dissolution of stones is carried out using methylbutyl ether: through the introduction of the drug into the lumen of the gallbladder.

4. Diet : food containing large amounts of plant fiber, vitamin C, reduced amounts of protein and fat. Food should be taken in small portions 5-6 times a day. 

Hepatitis C

Transmission method

Manifestations of hepatitis C

Diagnostics

Hepatitis C treatment

Hepatitis C is a viral liver disease that occurs with diffuse inflammation of the liver.

The genome is represented by RNA.

Transmission method

  • intravenously, intramuscularly (during transfusion of blood and its drugs, hemodialysis, injections, surgical and dental treatment);
  • sex with a person infected with a virus C.

Manifestations of hepatitis C

The incubation period is 20–90 days.

In most patients with chronic hepatitis C, the disease is asymptomatic. If complaints exist, then it is most often

  • weakness,
  • dull pain in the right hypochondrium,
  • nausea,
  • loss of appetite
  • itchy skin
  • pains in muscles and joints.

Hepatitis C is characterized by a wavy course; the probability of transition to the chronic form for the icteric form is 50%, for other acute forms it is approximately 85%.

Diagnostics

  • Blood chemistry;
  • General blood analysis;
  • PHK-HCV (PCR). RNA virus detected in serum after 1-2 weeks. after infection;
  • Anti-HCV (ELISA, Western blot turns ); antibodies to viral proteins; in test systems, IgM (activity markers) and IgG are determined.

Hepatitis C treatment

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Hepatitis C vaccine has not yet been created due to the high variability of the virus.

Interferon preparations

The main drug, whose effectiveness in the treatment of hepatitis C is proven, is interferon alpha (intron A). The optimal treatment regimen for chronic hepatitis C is currently a combination of intron A and ribavirin .

Recommended: 3 million IU of Intron A p / c or v / m 3 p / week . or every other day in combination with rebetol 1000–1200 mg / day . for 6 months, then examine the RNA of hepatitis C virus (HCV) in serum (twice). With a positive result, the continuation of treatment according to this scheme is of little prospect. In the absence of HCV RNA, treatment should continue for up to 12 months.

Use of PegIntron at a dose of 1.5 mcg / kg 1 time / week . instead of the usual interferon alpha, if necessary, reduce the dose of ribavirin to 800 mg / day.

With good tolerability of both drugs, the PegIntron combination at a dose of 1.5 µg / kg 1 time / week is optimal . and ribavirin at a daily dose of 13 mg / kg 2 mg / kg daily. Such a protocol allows achieving a stable response in more than 60% of cases, including 88% of cases in patients infected with HCV 2 or 3 genotypes.

Lamivudin is taken daily once in a dose of 100 mg orally without regard to meals. The combination of lamivudine with intron increases the effectiveness of treatment.

Hepatitis C Diet

Pevzner table number 5.

Meal 5 times a day in the crushed look.

  • vegetarian fruit, milk soups, cereal soups on vegetable broth,
  • boiled meat, poultry low-fat varieties, boiled lean fish,
  • milk, sour milk, kefir, acidophilus milk, cottage cheese up to 200 g per day,
  • cereal and flour dishes (except for baking), white bread, black stale,
  • ripe fruits, berries (except sour varieties), raw, baked, boiled,
  • vegetables and greens boiled and raw (especially carrots, beets),
  • jam, honey, sugar (up to 70 g per day),
  • vegetable, fruit juices in significant quantities,
  • tea is not strong with milk.

Restrict

  • fats (cream, butter up to 10 g, vegetable oil 20–30 g),
  • egg (one per day).

Excluded:

  • alcoholic beverages
  • liver, brains, fat,
  • legumes, mushrooms, spinach, sorrel, onions,
  • muffin
  • fatty meats, fish,
  • fried, spicy, smoked products,
  • extractives of meat, fish,
  • spices, vinegar, canned food,
  • ice cream, cocoa, carbonated drinks, chocolate, creams).

Hepatitis B

Forms

The reasons

Hepatitis B development mechanisms

Manifestations

Hepatitis B treatment

Complications

Prevention

Hepatitis vaccinations

Hepatitis B is a viral infection predominantly affecting the liver and leading to the chronic progressive form of the disease, carriage of the virus, the development of cirrhosis and liver cancer. 

The relevance of hepatitis B is high due to the possibility of its long latent course and transmission to other people.

Forms

The acute and chronic course of the disease is distinguished; in addition, the carriage of hepatitis B is distinguished by a separate variant.

The acute form may occur immediately after infection, occurs with severe clinical symptoms, and sometimes with fulminant development. Up to 95% of people are completely cured, the remaining part of acute hepatitis becomes chronic, and in newborns chronic disease occurs in 90% of cases.

Chronic form may occur after acute hepatitis, and may be initially without the acute phase of the disease. Its manifestations can vary from asymptomatic (carriage of the virus) to active hepatitis with the transition to cirrhosis.

The reasons

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Hepatitis B is caused by a particular virus that is fairly stable in the external environment. It is transmitted by parenteral route, that is, during sexual intercourse of all options, injections, blood transfusions or surgeries. Infection is possible during dentistry, manicure, shaving, tattooing, if the instruments are not properly treated and there is skin trauma.

The virus can be transmitted from an infected mother to a baby during childbirth, but the virus does not get into the milk when breastfeeding.

Domestic cases of hepatitis B infection are unlikely: it is impossible to get infected through common dishes and kisses, towels, handshakes and hugs, the amount of the virus is negligible. But the use of common razors or toothbrushes increases the likelihood of infection.

The virus is found in most human biological fluids – saliva, sweat, tears, urine, but its highest concentrations are found in the blood.

Hepatitis B development mechanisms

Hepatitis B virus when it enters the body spreads through the body and is fixed in the liver cells. The virus itself does not damage the cells, but the activation of protective immune systems recognizes the cells damaged by the virus and attacks them.

The more active the immune process is, the stronger the manifestations will be. With the destruction of damaged liver cells develops inflammation of the liver – hepatitis. It is the work of the immune system that determines the carriage and the transition to the chronic form.

Manifestations

Hepatitis B occurs in strictly defined stages, starting from an incubation period that lasts from 30–40 days to six months, but on average it is 60–90 days. During this time, the virus multiplies in the body and penetrates the liver tissue. This is followed by a prodromal ( anicteric ) period of the disease, with the appearance of common infectious manifestations, similar to most colds.

These include:

  • violation of health with loss of appetite, weakness, lethargy;
  • nausea and vomiting;
  • temperature increase to insignificant numbers;
  • muscle and joint pain;
  • headaches, feeling of weakness;
  • there may be respiratory manifestations (runny nose, cough, sore throat).

Gradually, the symptoms pass into the icteric period. They also appear in a certain sequence:

  • darkening of urine occurs , the color resembles dark beer; 
  • yellow sclera and mucous membranes of the mouth, especially if you raise the tongue to the sky;
  • stained hands and skin.

As jaundice appears, the general symptoms of intoxication decrease, and the condition improves. There may be pain or heaviness in the right subcostal area at the site of the projection of the liver. Sometimes there may be a cleansing of feces due to blockage of the bile ducts.  

On average, hepatitis lasts about three months, but changes in blood tests can still be quite long.

Severe and fulminant forms of hepatitis B are especially dangerous, since they flow hard and quickly enough. There are attacks:

  • sharp weakness, inability to get out of bed;
  • dizziness;
  • vomiting;
  • nightmares at night as signs of brain tissue damage;
  • fainting, collapse of consciousness;
  • bleeding gums, nasal bleeding; 
  • bruises appear on the skin, edemas on the legs.

When fulminant forms develop symptoms of coma and death is not uncommon.

In chronic hepatitis B, the onset of the disease is usually gradual, and the patient himself may not immediately notice the onset of the disease.

The first signs of chronic hepatitis:

  • fatigue, gradually increasing, weakness and drowsiness;
  • difficulty in waking up;
  • disturbed sleep and waking cycles, daytime sleepiness and sleeplessness at night;
  • anorexia, nausea, bloating, vomiting;
  • manifestations of jaundice occur: urine darkens, sclera and mucous membranes turn yellow (jaundice is usually persistent or manifested by waves).

Hepatitis B treatment

The use of therapies is aimed at combating viruses, at alleviating the patient’s condition, eliminating toxicosis and liver damage.

For the purpose of therapy they conduct:

  • special regime activities with the creation of peace – physical and psychological;
  • the appointment of a special “liver” diet with the exception of fatty, spicy and liver-loading products, alcohol, salt restriction; fractional meals and small portions;
  • treatment with antiviral agents from the interferon group;
  • immunostimulating treatment in order to activate its own immunity;
  • with the aim of eliminating intoxication, drip injection of solutions is prescribed – hemodez , polyglucin , glucose, saline;
  • preparations are added to the treatment to maintain the liver, enzymes to improve digestion, cholagogue;
  • Vitamin therapy is indicated for a tonic effect and speedy recovery of impaired metabolism.

In the future, in order to restore the immune system, it is necessary to conduct long-term courses of interferon to prevent the infection from becoming chronic.

Complications

Mostly they occur in weakened people with chronic pathology. The transition of hepatitis B to the chronic form is directly dependent on age. The younger the children, the higher their chances of a chronic process. Up to five years, the risk of liver damage by a chronic process is greatest.

Prevention

The basis of hepatitis prevention is a healthy lifestyle and loyalty to your sexual partner.

In addition, it is important to use disposable tools for any manipulations with skin puncture, dental treatment, careful processing of tools for haircuts and shaving.

Hepatitis vaccinations

Vaccination for hepatitis is carried out according to the national calendar.

Children are vaccinated three times, immediately after birth, after one month and six months from the first vaccination. Adults are vaccinated in the same way at any age. At the same time, immunity lasts up to 10–15 years.

First of all, people at risk are vaccinated:

  • doctors, people working with biological materials
  • nursing home patients prisoners
  • children of all ages
  • family members of hepatitis
  • patients receiving blood or hemodialysis
  • sexually active people
  • travelers
  • people with diseased liver and other hepatitis.

To date, hepatitis B vaccination is relevant to all.

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