Necrotizing nephrosis microspecimen is one of the serious pathologies of the kidneys, in which damage to organs is observed, including filtration functions. The origins of the disease are infectious and toxic in nature. Negative substances accumulate in the human body and are absolutely not removed from it. As a result, serious intoxication occurs, which requires immediate treatment. If therapy is not carried out in time, the patient may even die. Necronephrosis is characterized by pathological necrology, which develops in the epithelial tissues of the main sections of the renal tubules, which provokes a decrease in urine output and forms renal failure. In this article we will look at a macrodrug of necrotic nephrosis.
Causes of necrotic nephrosis
In necrotic nephrosis, acute organ damage occurs, which occurs with destabilization of blood movement.
In necrotic nephrosis, acute organ damage occurs, which occurs with destabilization of blood movement and the formation of disease in the epithelial tissues of the tubules of the renal organs. As a result of these processes, acute renal failure develops. In modern medicine, a micropreparation is often called a “toxic kidney,” since one of the main causes of the disease is severe chemical poisoning of the organ. At the same time, the body is oversaturated with negative toxic substances.
Complications of necrotic nephrosis can occur after a person has suffered from diseases such as malaria, sepsis or diphtheria. If the patient has experienced massive dehydration or significantly loses salt, then a microscopic specimen such as necrotizing nephrosis may form. The following reasons can also cause the formation of the disease:
- After an out-of-hospital abortion, a person may exhibit nephrotic nephrosis;
- Kidney microspecimens can form after sepsis;
- In some situations, the disease is observed after surgical intervention, especially of a urological nature.
Description of drugs in Lesson No. 29
Description of drugs in Pathological Anatomy in Lesson No. 29
- LESSON No. 29
kidney disease.
Microslide No. 218
“Intracapillary proliferative glomerulonephritis” - demonstration.
The size of the glomeruli is increased. Proliferation of endothelial and mesangial cells, infiltration of glomeruli with polymorphonuclear leukocytes and vascular congestion are pronounced. The epithelium of the proximal and distal tubules is in a state of hyaline-droplet dystrophy.
Macrodrug
“Subacute glomerulonephritis (large variegated kidney)” - description.
The kidneys are significantly enlarged in size, flabby, the cortex is wide, swollen, yellowish-gray, dull, well demarcated from the dark red medulla.
Microslide No. 81
“Extracapillary productive glomerulonephritis” - drawing
.
The inflammatory process is localized predominantly extracapillary and is represented by the proliferation of podocytes and nephrothelium with the formation of “crescents” characteristic of this type of nephritis. There is also damage (microperforation) to the basement membranes of capillaries, deposition of fibrin in the glomerulus, foci of fibrinoid necrosis and sclerosis, synechiae with a capsule. The epithelium of the proximal and distal tubules is in a state of hydropia, the stroma of the kidney is diffusely sclerotic, focally infiltrated with lymphohistiocytic elements.
Electronogram
“Membranous nephropathy” - description.
There is uneven thickening of the basement membrane of the glomerular capillaries and deposition of immune complexes (deposits) on its epithelial surface. Deposits of immune complexes are separated from each other by protrusions of the newly formed substance of the basement membrane, as a result of which it has the appearance of a ridge. The substance of the basement membrane is formed by podocytes.
Microslide No. 219
“Membranous nephropathy” - demonstration.
There is diffuse thickening of the basement membranes of the glomerular capillaries (no cell proliferation) and vacuolization of the tubular epithelium.
Macrodrug
“Chronic glomerulonephritis with outcome in wrinkling (secondary shriveled kidneys)” - description.
The kidneys are reduced in size, have a dense consistency, and the surface is fine-grained, which is due to the alternation of areas of sclerosis and hyalinosis of the glomeruli with areas of hypertrophied glomeruli. On the section, the cortex and medulla are thinned.
Microslide No. 125
“Secondary wrinkled kidneys” - description.
In some areas, there is atrophy of the glomeruli and tubules, their replacement with connective tissue: the glomeruli have the appearance of scars or hyaline balls. In other areas, the glomeruli are preserved, sometimes hypertrophied, the capillary loops are sclerotic, the lumen of the tubules is expanded, and the epithelium is thickened. Arterioles are sclerosed and hyalinized.
Macropreparation
"Kidney amyloid" - description.
The buds are enlarged in size, dense in consistency, their surface is pale gray or yellow-gray. On the section, the cortex is wide, waxy, the medulla is gray-pink, greasy, cyanotic. Such a kidney, characteristic of the proteinuric stage of renal amyloidosis, is called the “big sebaceous kidney.” In the nephrotic stage of amyloidosis, the kidneys become large, dense, white-yellow, waxy, (“large white amyloid kidney”).
Microslide No. 124
“Kidney amyloidosis” - description.
When stained with Congo mouth, amyloid stains dirty red in the mesangium and capillary loops of the glomeruli, under the endothelium of extraglomerular vessels, along the basement membrane of the tubules and reticular fibers of the stroma. In the epithelium of the convoluted tubules, protein and fatty degeneration is detected; drops of fat are colored orange by Sudan III.
Microslide No. 7
“Necrotic nephrosis” - description.
Necrosis involves the epithelium of the proximal and distal tubules and is focal. Edema, leukocyte infiltration of the stroma, and hemorrhages are pronounced. These changes are characteristic of the oligoanuric stage of the disease.
Macrodrug
"Hidronephrosis" - demonstration.
The kidney is sharply increased in size, its cortical and medulla layers are thinned and poorly distinguishable, the pelvis and calyces are stretched. A coral stone is visible in the cavity of the pelvis.
Macrodrug
“Fibrinous pericarditis”.
On the dull epicardium, fibrin threads are visible, enveloping it as if in hair (“hairy heart”).
Causes
The etiology of nephrosis is varied, but most often the disease is caused by poisoning or infection. Intoxication can lead to rapid progression of kidney damage.
The immediate causes of necrotic nephrosis are toxic substances that enter the body in large quantities.
These include:
- Uranus.
- Mercury.
- Lead.
- Bismuth nitrate.
- Sulfuric and hydrochloric acid.
- Chloroform.
- Antifreeze.
- Vinegar.
- Barbiturates.
- Arsenic.
- Sulfate preparations.
Poor circulation to the kidneys can also lead to serious injury, often accompanied by multiple organ dysfunction, dehydration, and severe intestinal obstruction.
Necronephrosis - symptoms and treatment of necronephrosis
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Necronephrosis (necrotic nephrosis) is a degenerative kidney disease characterized by necrotic changes in the epithelium of the renal tubules, most often of toxic and infectious origin.
The causes of necronephrosis can be:
- various intoxications (the so-called toxic kidney), poisoning with salts of heavy metals, mercury, bismuth, lead, uranium, chromium, gold, as well as arsenic compounds, cantharidin, carbon tetrachloride, antifreeze, acetic acid, barbiturates, sulfonamides, etc.;
- dehydration and desalination of the body - the so-called chloropenic kidney;
- massive hemolysis, incompatible blood transfusion – hemolytic kidney; kidney injuries – traumatic kidney;
- severe acute infections - sepsis, typhus, cholera, diphtheria and icterohemorrhagic leptospirosis;
- out-of-hospital abortions occurring with a picture of acute anaerobic sepsis and massive bleeding;
- urological and other surgical interventions;
- burns, as well as other conditions accompanied by shock, leading to disruption of intrarenal circulation, which leads to ischemia, and subsequently to necrotic changes, mainly in the epithelium of the renal tubules.
What is important in the occurrence of necronephrosis is, firstly, acute disruption of the renal circulation with the development of anoxia of various elements of the renal tissue, and secondly, direct damage to the elements of the renal nephron by toxic substances.
Symptoms of necronephrosis
There is an acute onset of the disease, primarily expressed by a decrease in urine output up to complete anuria. Protein appears in the urine, often in small quantities.
In the urine sediment, hyaline and granular casts, an abundance of epithelial cells, red blood cells, often in moderate quantities, and single leukocytes are found.
The specific gravity of urine, despite its small amount, is low (hyposthenuria).
The clinical picture of acute renal failure is rapidly developing. Symptoms of uremia appear: vomiting, general weakness, apathy, stupor, coma and hypothermia develop. nitrogenous waste in the blood quickly increases, often reaching huge numbers (urea 500 and 1000 mg%).
Along with the retention of nitrogenous wastes, there is also a retention of potassium, which is especially dangerous. Hyperkalemia can quickly reach 30-45 mg% (against the norm of 16-22 mg%).
Clinically, hyperkalemia is manifested by severe symptoms of intoxication from the nervous system in the form of paresthesia, decreased tendon reflexes, paralysis of the limbs, bradycardia, and arrhythmia.
In this case, changes in the electrocardiogram characteristic of hyperkalemia are observed in the form of disappearance or deformation of the P wave, conduction disturbances (lengthening of the PQ and QRS), a decrease in the voltage of the R wave and the appearance of high pointed T waves.
The course of necronephrosis is characterized by several stages characteristic of acute renal failure.
Despite the severe anatomical and clinical picture, necronephrosis can result in complete recovery with restoration of the morphological structure and function of the kidneys.
Often, in the anuric stage, death from acute uremia may occur. There is no transition to a chronic form. However, long-term disturbances in the concentration function of the kidneys may occur.
Liver abscess macro specimen description
Liver abscesses can be single or multiple, their size varies. Amoebic liver abscesses are mostly single; with pylephlebitis of appendicular origin they are usually multiple. With any abscess, except for a small centrally located one, the size and configuration of the liver changes.
Changes in the liver parenchyma depend on the type, size and phase of development of the abscess, the number of abscesses. In the initial phases of the development of amoebic processes in the liver, as a rule, gray-brown necrotic areas are found, around which there is a zone with an increased number of dilated vessels. Changes in the parenchyma of these areas are the result of the toxic effects of the amoeba. Subsequently, softening develops in the center and an abscess forms.
The long-term existence of an abscess causes reactive inflammation along the periphery and the development of a connective tissue membrane. With amoebic liver abscesses, the pus is chocolate-colored, odorless, thick, creamy in consistency, usually sterile.
During microscopic examination, no microorganisms are found in it, but liver cells and even pieces of liver tissue are found, i.e., essentially pus consists of decay products of liver tissue. When an abscess persists for a long time, a thick layer of connective tissue usually develops around it. Pathological changes in pyogenic liver abscesses develop in the following sequence: first, there is a pronounced hyperemia of the lesion, then focal hepatitis develops with central softening and the formation of an abscess, the walls of which are covered with granulation tissue.
Solitary pyogenic abscess
Acute liver abscesses that develop as a result of pylephlebitis of appendicular origin are characterized by a severe septic course and quickly lead to death from sepsis or peritonitis, so a connective tissue capsule usually does not have time to develop around them. In most cases, abscesses are located in the right lobe of the liver, but some multiple pyogenic abscesses are also located in the left lobe.
Pyogenic liver abscesses are often multiple. In some cases, with pylephlebitis, the liver is literally stuffed with a large number of abscesses of different sizes. The contents of pyogenic abscesses do not differ from the contents of ordinary abscesses. With low virulence of the microflora and the chronic course of the abscess, the liquid part of the pus is absorbed and takes on the appearance of a curdled disintegration.
“Guide to purulent surgery”, V.I. Struchkov, V.K. Gostishchev,
3. hyperplasia of melanocytes in the basal layer of the epidermis at the border with the dermis
4. in the dermis there are macrophages that collect melanin (melanoforms)
5. Local acquired melanosis, possible degeneration into malignant tumors - melanoma.
15. Microslide Ch/31 – hyaline glomerulosclerosis.
1. the walls of the arterioles are thickened due to the deposition of hyaline of homogeneous eosinophilic masses under the endothelium
2. multiple hyalinized glomeruli
3. between the hyalinized glomeruli, the tubules atrophied and were replaced by connective tissue
4. Mechanism of hyaline formation. Destruction of fibrous structures and increased tissue-vascular permeability (plasmorrhagia) in connection with angioneurotic (dyscirculatory), metabolic and immunopathological processes. Plasmorrhagia is associated with the impregnation of tissue with plasma proteins and their adsorption on altered fibrous structures, followed by precipitation and the formation of hyaline protein. Hyalinosis is the result of plasma impregnation, fibrinoid swelling, inflammation, necrosis, sclerosis.
16. Microslide O/87-fibrinous pericarditis.
1) Structure and color of fibrinous deposits on the epicardium: red-pink color, in the form of intertwined threads.
2) The epicardium is infiltrated with leukocytes.
3) The strength of the connection of the film with the underlying tissues: the weak connection of the thin fibrinous film with the underlying tissues is easily removed; upon separation, surface defects are formed.
4) The vessels of the epicardium are full of blood.
5) The type of fibrinous inflammation on the epicardium is lobar.
6) What diseases can cause fibrinous pericarditis:
rheumatism, uremia, sepsis, transmural myocardial infarction.
17. Microslide Ch/140 – diphtheritic cystitis
.
1. transitional epithelium is completely necrotic and saturated with fibrin,
2. necrosis partially extends to the submucosa,
3. diffuse inflammatory infiltration in the submucosa.
4. the muscle layers and serous membrane of the bladder are preserved,
5. name the possible outcomes of this type of fibrinous inflammation: ulcers followed by substitution. With deep ulcers - scars, sepsis, bleeding.
18. Microslide O/20 – kidney abscess.
1) The presence of a cavity in the kidney.
2) The composition of the purulent exudate contained in the cavity: purulent, creamy mass. Tissue detritus from the inflammation site, microbes, viable and dead granulocytes, lymphocytes, macrophages, neutrophils, leukocytes.
3) Pyogenic membrane at the border with the kidney tissue.
4) Structure of the pyogenic membrane: granulation tissue shaft. Pyogenic capsule is granulation tissue delimiting the abscess cavity. As a rule, it consists of 2 layers: the inner layer consists of granulations, the outer layer is formed as a result of the maturation of granulation tissue into mature SDT. The outer layer may be missing.
5) Abscess along the course: acute, in exacerbation of chronic pyelonephritis, accompanied by purulent discharge.
19. Microslide O/135 – Cellulitis of the skin.
1) The epidermis is partially necrotic.
2) Diffuse leukocyte infiltration in the dermis and subcutaneous tissue.
3) Serous exudate, hemorrhages in the hypodermis.
4) Phlegmon
is
a purulent, non-demarcated diffuse inflammation, in which purulent exudate permeates and exfoliates the tissue.
Treatment
If poisoning is important in the etiology of the disease, then treatment of the body is aimed at eliminating poisons and toxins in the body. As a necessary method of therapeutic therapy.
You can achieve the removal of toxins and poisons from the body using gastric lavage. Of course, this procedure is designed for medical personnel. It is not recommended to rinse the stomach on your own!
Saline laxatives have a good effect. The use of antidotes and absorbents is also appropriate. Absorbents help remove toxic substances from the body. These include activated carbon.
If urination stops, then normalization of the electrolyte balance of the blood is used in the treatment of necronephrosis. This promotes the removal of nitrogen metabolism products. Hemodialysis can be widely used.
Blood transfusion is used in the most severe cases. Transfusion is very effective for this disease. Especially with unacceptable values of nitrogen content in the blood.
If this disease is caused by heavy bleeding, then it is necessary to stop it. To achieve this, various techniques are used to stop bleeding. But it is also necessary to eliminate the blood deficiency in the body.
Most often, patients are under the necessary medical supervision. They are seen by a nephrologist. What helps them cope with this disease. And in case of long-term impairment of kidney function, it allows you to monitor and prescribe specific treatment.
Necrotizing nephrosis - clinical picture and treatment methods
Nephrosis includes diseases accompanied by dystrophic changes in the kidneys. The clinical picture of this pathological condition includes various anomalies of the excretory function of the body. Necrotizing nephrosis is an acute disease and can lead to serious complications if timely treatment is not started.
- What is this
- Causes
- Clinical picture
- Diagnostics
- Treatment methods
What is this
Necronephrosis is an acute toxic or infectious, shockogenic disease, which is accompanied by impaired blood flow through the blood vessels of the kidneys and ischemia of this organ. As a result of the death of the epithelium of the renal tubules, acute renal failure develops - uremia.
In necrotizing nephrosis, the phenomenon of nephrogenic shock occurs because the degree of damage to the blood and lymphatic flow can be very high. A person has various symptoms of intoxication.
Causes
The etiology of nephrosis is varied, but most often the disease is caused by poisoning or infection. Intoxication can lead to rapid progression of kidney damage.
The immediate causes of necrotic nephrosis are toxic substances that enter the body in large quantities. These include:
- Uranus.
- Mercury.
- Lead.
- Bismuth nitrate.
- Sulfuric and hydrochloric acid.
- Chloroform.
- Antifreeze.
- Vinegar.
- Barbiturates.
- Arsenic.
- Sulfate preparations.
Poor circulation to the kidneys can also lead to serious injury, often accompanied by multiple organ dysfunction, dehydration, and severe intestinal obstruction.
Clinical picture
At the very beginning of the disease, the symptoms are subtle and do not cause concern. At the first stage of development (1-2 days), patients may present signs of shock, poisoning and intoxication.
The olierinurin stage (up to 6 days) is characterized by a significant decrease in the amount of urine excreted per day. Up to 400 ml is secreted , later anuria (cessation of the secretion of biological fluid).
At the same stage, myoglobinuria, proteinuria syndrome (the presence of protein in the urine) is added. Renal failure increases, the blood becomes saturated with nitrogen-containing substances, acidosis and hyperkalemia develop.
The clinical picture is characterized as follows:
- Swelling appears around the eyes.
- Swelling spreads throughout the body.
- Fluid accumulates around internal organs.
- Stretch marks form on the skin.
- The patient may experience muscle pain.
- Joints are affected.
The nature of the pathological changes depends on the influence of chemical and bacterial toxins on the epithelial cells of the kidneys. Also, the patient’s condition may worsen if there were previously problems with this organ and new symptoms appear. For example, vomiting, dizziness, stupor, uremic coma, apathy.
The polyuric stage is characterized by an increase in the amount of urine excreted to 3 liters per day. The liquid is light. In the absence of complications, renal function begins to recover gradually, and the blood composition returns to normal.
Rehabilitation of the patient lasts from 3 to 12 months. The patient is recovering, kidney function is improving. In the end, the organ works again without failures, but further observation by a doctor is required.
Diagnostics
Diagnosis is made based on symptoms, physical examination, and test results.
To make a diagnosis, do the following:
- Taking general blood, urine and stool tests.
- The patient's diuresis (urine volume) is measured daily, so the patient's stay in a medical facility is mandatory.
- A Zimnitsky test is performed. The test determines the ability of the kidneys to concentrate and excrete urine under normal conditions.
- A patient with suspected necrotizing nephrosis will have to donate blood to determine the amount of nitrogen. This test reveals kidney failure. With it, the nitrogen in the patient’s blood will be higher than normal. The condition is called azotemia.
- Blood to detect creatinine levels. This test can also detect kidney failure. Typically, an increase in creatinine occurs in parallel with an increase in azotemia.
- Mandatory examinations include the Rehberg test . This analysis is necessary for the differential diagnosis of functional and tissue damage to the kidneys. The Rehberg test will tell you about the condition of the organ, and will also reveal necrotic nephrosis at an early stage.
Diagnosis is also carried out using instrumental examination methods. These include ultrasound and ECG. Ultrasound examination reveals enlarged kidneys.
Treatment methods
The earlier the disease is identified and treated, the better the prognosis. The goal of therapy is to eliminate the cause that led to the development of necrotizing nephrosis.
The first step in treatment is gastrointestinal lavage . This procedure is necessary to speed up the elimination of toxins and poisons. Washing is carried out using saline solutions, laxatives and sorbents.
If a patient is poisoned by mercury or lead, special antidotes . In each case, the antidote is different, taking into account the patient’s age, chronic and acute diseases, as well as weight.
Next, necrotic nephrosis is treated with teas that have a diuretic effect. Patients are prescribed corticosteroid drugs in combination with immunosuppressants.
Throughout the entire therapy, the patient must adhere to a drinking and eating regimen. Dietary nutrition is only a small part of complex treatment, which also allows the patient to recover faster.
Along with the diet and diuretic teas, the patient is prescribed the use of diuretic drugs. The dosage and duration of use is determined by the attending physician. The best diuretic medications are Novazurol , Lasix , Salirgan .
If side effects occur, do not be afraid to go for a second appointment. Their occurrence can lead to serious complications. Not only kidney failure may develop, but also problems with the heart.
Source: https://pochkizdorov.ru/nekroticheskij-nefroz-klinicheskaya-kartina-i-metody-lecheniya/
