Treatment of chronic hepatitis B presentation. Chronic hepatitis, Department of Faculty and Hospital Therapy, Faculty of General Medicine and Internal Diseases, Medical and Preventive Faculty, Chronic. Cystic variant of CP

Presentation on the topic: "Pyelonephritis in children. Etiology, pathogenesis, clinical picture, diagnosis, treatment, prevention. " - Transcript:

1 Pyelonephritis in children. Etiology, pathogenesis, clinical picture, diagnosis, treatment, prevention.

2 Lecture plan 1. Etiology, pathogenesis of pyelonephritis. 2. Classification of pyelonephritis in children. 3. Clinical and diagnostic criteria for pyelonephritis. 4. Treatment, prevention of pyelonephritis in children.

3 Pyelonephritis is a microbial-inflammatory disease of the kidneys with damage to the calyx-pelvic system, interstitial tissue of the renal parenchyma and tubules

4 Microbial-inflammatory diseases of the kidneys and urinary tract rank first in the structure of nephropathy in children. These diseases (cystitis, urethritis, pyelonephritis) are 19.1 per 1000 children. In adults, in% of cases, the disease begins in childhood In adults, in% of cases, the disease begins in childhood

5 Acute pyelonephritis - most have one type of microorganism. Chronic pyelonephritis - microbial associations in 15% of patients Chronic pyelonephritis - microbial associations in 15% of patients

6 Etiological structure of pyelonephritis in children 1. E. coli - 54.2%. 2. Enterobacter spp - 12.7%. 3. Enterococcus spp - 8.7%. 4. Kl. Pneumoniae - 5.0%. 5. Proteus spp - 4.5%. 6. P. aeruginosa - 4.4%. 7. Sfaphylococcus spp - 4.3%.

7 Pathogenesis 1. Violation of urodynamics - anomalies of the urinary tract, vesicoureteral reflux. 2. Bacteriuria both in acute illness and due to the presence of chronic foci of infection. 3. Previous damage to the interstitial tissue of the kidneys as a result of metabolic nephropathy, past viral diseases, drug damage and others. 4. Violation of the body's reactivity, in particular immunological. - The ascending (urinogenic) route of infection is the leading one in getting the pathogen into the pelvis, tubules of the interstitium

8 Chronic pyelonephritis. Specific immune inflammation - Infiltration of the kidney interstitium with lymphocytes and plasma cells - Intensive synthesis of immunoglobulins - Formation of immune complexes and their deposition on the basement membranes of the tubules - Release of biologically active lymphokines - Increased destruction - Enhanced synthesis of collagen fibers with the formation of scars in kidney tissue and nephrosclerosis

12 Classification (A.F. Vozianov, V.G. Maidannik, I.V. Bagdasarova, 2004) Clinical forms: 1) Non-obstructive pyelonephritis. 2) Obstructive pyelonephritis: against the background of organic or functional changes in hemo- or urodynamics, metabolic nephropathy, dysembryogenesis

13 The nature of the process 1) Acute 2) Chronic: - wavy - wavy - latent - latent Activity 1) Active stage (I, II, III degrees) (I, II, III degrees) 2) Partial clinical and laboratory remission. 3) Complete clinical and laboratory remission

14 Stage of the disease 1) Infiltrative 2) Sclerotic State of renal function 1) Without impaired renal function 2) With impaired renal function 3) Chronic renal failure

15 Criteria for determining the activity of pyelonephritis in children Signs Degree of activity ІІІІІІ - Body temperature - Symptoms of intoxication - Leukocytosis, x 10 9 / l - SHEE, mm / h - C-reactive protein - B-lymphocytes - CEC, us. units N or subfebrile Absent or insignificant Up to 10 Up to 15 No / + 38.5 о С Significantly expressed 15 and\u003e 25 and\u003e +++ / and\u003e 0.20 and\u003e 38.5 о С Significantly expressed 15 and\u003e 25 and\u003e +++ / ++++ 40 and\u003e 0.20 and\u003e "\u003e

16 An example of a diagnosis: 1. Non-obstructive acute pyelonephritis, grade II activity, infiltrative stage without impaired renal function. 2. Obstructive chronic pyelonephritis, undulating course, activity of the II degree, sclerotic stage, without impaired renal function. Metabolic nephropathy: oxaluria 2. Obstructive chronic pyelonephritis, undulating course, activity of the II degree, sclerotic stage, without impaired renal function. Metabolic nephropathy: oxaluria

10% in »title \u003d» Criteria for determining the stages of pyelonephritis in children Signs Infiltrative stage Sclerotic stage - Hodson's symptom - Kidney area - Renal-cortical index - Hodson's index - Effective renal plasma flow Absent Increased\u003e 10% in »class \u003d» link_thumb »\u003e 17 Criteria for determining the stages of pyelonephritis in children Signs Infiltrative stage Sclerotic stage - Hodson's symptom - Kidney area - Renal-cortical index - Hodson's index - Effective renal plasma flow Absent Increased\u003e 10% age N Increased N Positive Decreased\u003e 10% of the age norm Increased 10% Decreased \u003e 10% of age N Increased - - N Positive Decreased\u003e 10% of the age norm Increased Decreased Decreased »\u003e 10% in» title \u003d »Criteria for determining the stages of pyelonephritis in children Signs Infiltrative stage Sclerotic stage - Hodson's symptom - Kidney area - Renal-cortical index - Index Hodson - Effective renal plasma flow Absent Increased\u003e 10% in »\u003e 10% in» title \u003d »Criteria for determining the stages of pyelonephritis in children Signs Infiltrative stage Sclerotic stage - Hodson's symptom - Kidney area - Renal-cortical index - Hodson's index - Effective renal plasma flow Absent Increased\u003e 10% in »\u003e

18 Clinic 1. Pain syndrome - pain in the lower back and abdomen. 2. Dysuric disorders. 3. Intoxication syndrome: increased body t with chills, headache, weakness, lethargy, pallor. 4. Urinary syndrome: - Proteinuria - up to 1 g / l - Proteinuria - up to 1 g / l - Neutrophilic leukocyturia - Neutrophilic leukocyturia - Microhematuria - Microhematuria - Increased cellular epithelium. - Increase in cellular epithelium.

). Determination of the functional state of the kidneys: - Zimnitsky's test - clearance for endogenous creatinine. 6. Bioch "title \u003d" Diagnostics General urine analysis in dynamics Test according to Nechiporenko Urine cultures Determination of the degree of bacteriuria (in 1 ml of urine 100,000 microbes and\u003e). Determination of the functional state of the kidneys: - Zimnitsky's test - clearance of endogenous creatinine. 6. Bioch "class \u003d" link_thumb "\u003e 19 Diagnostics General analysis of urine in dynamics Test according to Nechiporenko Urine cultures Determination of the degree of bacteriuria (in 1 ml of urine of microbes and\u003e). Determination of the functional state of the kidneys: - Zimnitsky's test - clearance of endogenous creatinine. 6. Biochemical blood test (creatinine, urea, total protein, cholesterol, sialic acids, C-reactive protein).). Determination of the functional state of the kidneys: - Zimnitsky's test - clearance for endogenous creatinine. 6. Bioh "\u003e). Determination of the functional state of the kidneys: - Zimnitsky's test - clearance of endogenous creatinine. 6. Biochemical blood test (creatinine, urea, total protein, cholesterol, sialic acids, C-reactive protein). "\u003e). Determination of the functional state of the kidneys: - Zimnitsky's test - clearance for endogenous creatinine. 6. Bioch "title \u003d" Diagnostics General urine analysis in dynamics Test according to Nechiporenko Urine cultures Determination of the degree of bacteriuria (in 1 ml of urine 100,000 microbes and\u003e). Determination of the functional state of the kidneys: - Zimnitsky's test - clearance of endogenous creatinine. 6. Bioh "\u003e). Determination of the functional state of the kidneys: - Zimnitsky's test - clearance of endogenous creatinine. 6. Bioch "title \u003d" Diagnostics General urine analysis in dynamics Test according to Nechiporenko Urine cultures Determination of the degree of bacteriuria (in 1 ml of urine 100,000 microbes and\u003e). Determination of the functional state of the kidneys: - Zimnitsky's test - clearance for endogenous creatinine. 6. Bioch "\u003e

Chronic pyelonephritis in children

Chronic pyelonephritis is an inflammatory disease that contributes to the destruction of the calyx and renal parenchyma. This disease can affect people of various ages, from children to people of age. But, most often, children under 5-7 years old suffer from pyelonephritis (this is facilitated by the peculiarities of the urinary system), as well as girls aged 17-30 years (several factors are the cause of the development of this disease: the onset of sexual activity, pregnancy and childbirth). Older men can also suffer from this disease (adenoma of the prostate gland contributes to this).

Today, doctors believe that the main reason for the development of chronic pyelonephritis is inadequate treatment of the acute process. After premature termination of therapy, unexpected transformations of the causative agent into the L-form may occur.

If doctors observe relapses of the disease, they begin to conduct various urine tests for the most accurate identification of the pathogen. Also, other diseases can contribute to the development of pyelonephritis from an acute to a chronic form: sinusitis, gastritis, colitis, pancreatitis, tonsillitis and diabetes mellitus. Influence on the development of pyelonephritis can have hemodynamic and hormonal disorders, as well as nephrolithiasis of the kidney.

Doctors divide chronic pyelonephritis into several stages: primary and secondary, as well as one and two-sided.

In turn, the activity of this disease is assessed using three phases:

Latent course of the disease Acute inflammatory process Remission

How is chronic pyelonephritis

Anemic

Latent

Hypertensive.

Recurrent... This type of disease is undulating: frequent changes of episodic exacerbations destroy the latent passage of the disease

Note the fact that the presence of all variants of the course of the disease in one person is quite common.

And the doctors divided the whole process of the disease into several stages:

In medicine, it is not uncommon for patients to develop all of the above stages at the same time. It is believed that such a combination of events can become quite dangerous for the body of every person.

The main symptoms

The symptoms of chronic pyelonephritis in children are quite varied, and sometimes it can be quite difficult to detect them. It is possible to detect this disease only if moderate pain or leukocyturia occurs. Chronic pyelonephritis is quite often characterized by acute relapses, which contribute to the spread of pathological changes to new areas of the renal parenchyma. It happens that the disease is detected during autopsy.

Patients most often describe their condition with the following points:

Features of pyelonephritis

Chronic pyelonephritis in children can develop after suffering an acute form of the disease.

Several factors may contribute to this transition:

But, you should pay attention to the fact that pyelonephritis in children can occur as the first disease. Then, the general picture of this disease is very similar to pyelonephritis in adults. One of the features of this disease is the manifestation of hypertension as a symptom of pyelonephritis in children.

Treatment of chronic pyelonephritis in children

Of course, only the attending physician can exhaustively answer this question, because first you need to carry out all the tests. But, the most important point in the treatment of this disease is the elimination of all the causes that interfere with normal blood circulation and kidney passage. Treatment of chronic pyelonephritis in children with drugs always accompanies surgery and continues after it. Drug therapy is carried out in a complex and strictly individual way. If the therapy is carried out individually, the progression and occurrence of inflammatory processes almost always occurs.

In turn, complex treatment should be:

Also, during treatment, it is recommended to take the following drugs: derivatives of nitrofuran and natrifidine, Oxyquinolines, phenols, antibiotics and others. When using them, you must carefully follow all instructions and rules of antagonism and synergy of drugs.

The method and timing of treatment of the disease depends on the nature and severity of the inflammatory process. It must be remembered that nephrotic drugs are intended to be used in exceptional cases. The course of treatment begins only after the diagnosis of urine culture and antibiotics. In the course of treatment, it also happens that microorganisms quickly change their biological properties, which leads to an increase in resistance to some drugs. In this case, it is necessary to carry out an empirical type of treatment: the gradual replacement of past drugs with new, stronger ones. If leukocyturia develops, it is necessary to use drugs of a wide range of actions.

Treatment with folk remedies

Doctors do not welcome the treatment of pyelonephritis with folk, the poet should not tempt fate. Quite often, such treatment ends with various complications and relapses. Today, medicine believes that long-term antibiotic therapy is considered the most effective. Moreover, it is recommended to combine drugs with various anti-inflammatory drugs, which will achieve the maximum effect. Diuretics are often used, which increase the concentration of antibacterial drugs.

Presentation on the topic: "Acute and chronic pyelonephritis Completed by: V. Gavrilova" - Transcript:

1 Acute and chronic pyelonephritis Completed by: V.S. Gavrilova

2 Pyelonephritis is an inflammatory kidney disease of predominantly bacterial etiology, characterized by damage to the renal pelvis, calyx and renal parenchyma.

3 CLASSIFICATION OF PYELONEPHRITIS Primary (non-obstructive) Secondary (obstructive) Pyelonephritis (unilateral or bilateral) Acute Serous Purulent Apostematous kidney abscess Kidney carbuncle Phase of active inflammation Phase of latent inflammation Phase of remission Renal shrinkage or pyonephrosis Chronic

4 Etiology, pathogenesis: Most often, pyelonephritis is caused by intestinal escherichia, enterococcus, Proteus, staphylococci, streptococci. In 1/3 of patients with acute pyelonephritis and in 2/3 of patients with chronic pyelonephritis microflora is mixed. During treatment, the microflora and its sensitivity to antibiotics change, which requires repeated urine cultures to determine adequate uroantiseptics.

5 It is necessary to remember about the role of protoplasts and L-forms of bacteria in the occurrence of recurrent pyelonephritis. If the infection in the kidney is supported by protoplasts, then urine culture will not detect them. The development of pyelonephritis largely depends on the general state of the macroorganism, a decrease in its immunobiological reactivity.

6 Infection enters the kidney, pelvis and its calyx by hematogenous or lymphogenous route, from the lower urinary tract along the wall of the ureter, along its lumen - in the presence of retrograde refluxes. Of great importance in the development of pyelonephritis are urinary stasis, disorders of venous and lymphatic outflow from the kidney. Pyelonephritis is often preceded by latent interstitial nephritis.

7 Acute pyelonephritis Symptoms, course: The disease begins acutely, there is a high (up to 40 ° C) temperature, chills, torrential sweat, pain in the lumbar region; on the side of the affected kidney - tension of the anterior abdominal wall, sharp pain in the costal-vertebral angle; general malaise, thirst, dysuria or pollakiuria. The accompanying headache, nausea, vomiting indicate a rapidly growing intoxication.

8 Neutrophilic leukocytosis, aneosinophilia, pyuria with moderate proteinuria and hematuria are noted. Sometimes, when the condition of patients worsens, leukocytosis is replaced by leukopenia, which serves as a poor prognostic sign. Pasternatsky's symptom is usually positive. With bilateral acute pyelonephritis, signs of renal failure often appear. Acute pyelonephritis can be complicated by paranephritis, necrosis of the renal papillae.

9 Diagnosis: An important role in the diagnosis is played by indications in the history of a recent acute purulent process or the presence of chronic diseases (subacute septic endocarditis, gynecological diseases, etc.). Characterized by a combination of fever with dysuria, pain in the lumbar region, oliguria, pyuria, proteinuria, hematuria, bacteriuria with a high relative density of urine

10 It should be remembered that pathological elements in the urine can be observed in any acute purulent disease and that pyuria can be of extrarenal origin. The plain radiograph shows an increase in one of the kidneys in volume, with excretory urography - a sharp restriction of the mobility of the affected kidney by aspiration, the absence or later appearance of the shadow of the urinary tract on the affected side. Compression of the calyx and pelvis, amputation of one or more calyces indicate the presence of a carbuncle.

11 TREATMENT: - Most cases - conservative (hospital) - Bed rest, diet - Symptomatic therapy - Antibiotic therapy taking into account sensitivity

12 ANTIBACTERIAL THERAPY: - Fluoroquinolones, cephalosporins, aminoglycosides (antibioticogram) - anti-inflammatory, detoxification, therapy - drugs that improve blood supply

13 Chronic pyelonephritis May be a consequence of untreated acute pyelonephritis or primary chronic, that is, it can proceed without acute symptoms from the onset of the disease. In most patients, chronic pyelonephritis occurs in childhood, especially in girls

14 Symptoms, course: Unilateral chronic pyelonephritis is characterized by dull persistent pain in the lumbar region on the side of the affected kidney. Dysuric phenomena are absent in most patients. During the period of exacerbation, only 20% of patients have a fever. In the urine sediment, the predominance of leukocytes over other formed elements of urine is determined.

15 However, as the pyelonephritic kidney shrinks, the severity of urinary syndrome decreases. The relative density of urine remains normal. Detection of active leukocytes in urine is essential for diagnosis.

16 In the case of a latent course of pyelonephritis, it is advisable to conduct a pyrogenal or prednisolone test (30 mg of prednisolone dissolved in 10 ml of isotonic sodium chloride solution, injected intravenously for 5 minutes; after 1; 2; 3 hours and a day after that, urine is collected for research ). The prednisolone test is positive if, after the administration of prednisolone, more leukocytes are excreted in urine in 1 hour, a significant part of which are active

17 The detection of Sterneimer-Malbin cells in urine only indicates the presence of an inflammatory process in the urinary system, but does not yet prove the existence of pyelonephritis.

18 The functional state of the kidneys is examined using chromocystoscopy, excretory urography, clearance methods (for example, determination of the coefficient of purification of endogenous creatinine by each kidney separately), radionuclide methods

19 The diagnosis is often very difficult. In differential diagnosis with chronic glomerulonephritis, the nature of the urinary syndrome is important (the predominance of leukocyturia over hematuria, the presence of active leukocytes and Sternheimer-Malbin cells, significant bacteriuria in pyelonephritis), data from excretory urography, radionuclear renography.

20 Treatment of chronic pyelonephritis should be continued for a long time. Treatment should begin with the appointment of nitrofurans (furadonin, furadantin), nalidixic acid (nefam, nevifamon), 5-NOC, sulfonamides (urosulfan, atazol, etc.), alternating them alternately. With the ineffectiveness of these drugs, exacerbations of the disease, broad-spectrum antibiotics are used.

21 The appointment of an antibiotic each time should be preceded by a determination of the sensitivity of microflora to it. For most patients, monthly 10-day courses of treatment are sufficient. However, in some patients with this therapeutic tactic, virulent microflora continues to be sown from the urine.

22 In such cases, long-term continuous antibiotic therapy with a change of drugs every 5-7 days is recommended. With the development of renal failure, the effectiveness of antibiotic therapy decreases (due to a decrease in the concentration of antibacterial drugs in the urine).

Similar presentations: Chronic pyelonephritis. Urinary tract infection in children. Pyelonephritis is an inflammatory kidney disease of predominantly bacterial etiology, characterized by damage to the renal pelvis, calyces and parenchyma of the kidney.

The causative agents of the disease are E. coli, streptococcus, staphylococcus, proteus, viruses. Microbes enter the kidney tissue by hematogenous and ascending route.

With frequent exacerbations of pyelonephritis, the generally accepted approach is to prescribe monthly preventive courses of antibiotic therapy. Test on the topic: TAX ON ADDED. Download this presentation. Description of the presentation for individual slides: 1 slide.

Pathogenesis: pathogens are group A beta-hemolytic streptococcus, staphylococcus, viruses. Most kidney stones are composed of calcium salts (phosphates, oxalates, carbonates) X-ray of the kidneys Contrast urography Urine culture Ultrasound Scan of the kidneys Chromocystoscopy of opium. Be healthy. Thanks for attention.

Similar presentations: Chronic pyelonephritis. Urinary tract infection in children. Pyelonephritis is an inflammatory kidney disease of predominantly bacterial etiology, characterized by damage to the renal pelvis, calyces and parenchyma of the kidney. Download a free presentation on 'Pyelonephritis. Pyelonephritis is an infectious and inflammatory disease of the urinary tract mucosa and tubulo-interstitial tissue of the kidneys 1. Pyelonephritis. '' In .ppt format (PowerPoint). Slide 5 from the presentation "Prevention of kidney diseases" to medicine lessons on the topic "Diseases of the urinary system". Inflammation of the kidneys Pyelonephritis. In general, women prevail among patients with pyelonephritis. Presentation on the topic 'Pyelonephritis'. Download presentation (0.09 Mb). Annotation for the presentation. The presentation ‘Pyelonephritis’ talks about one of the human kidney diseases. The presentation contains all the basic information about pyelonephritis: -Etiology. Classification, etiology, clinical picture, diagnosis Urinary tract infections Acute pyelonephritis Chronic pyelonephritis. Download this presentation. Get the code Our banners. Presentation on topic: Pyelonephritis. Download this presentation.

Presentation on the topic 'Pyelonephritis'. These diseases (cystitis, urethritis, pyelonephritis) are 19.1 per 1000 children. In adults, in 50-70% of cases, the disease begins in childhood. Presentation on the topic 'Pyelonephritis' in medicine. Slide text: Pyelonephritis.

Growth trends persist (2. In the Republic of Belarus - 1. In the structure of the IMP about 6.

The ratio of sick women and men 2. 1. Description of the slide: Etiology Pyelonephritis is caused by: Intestinal Escherichia, Enterococcus, Proteus, Staphylococci, Streptococci. L-forms of bacteria (recurrence of pyelonephritis) Mycoplasma. Leptospira. Fungi In 1/3 of patients with acute pyelonephritis and in 2/3 of patients with chronic pyelonephritis microflora is mixed. In 3.0% of cases, the pathogen is not sown - this does not exclude an infectious process. Slide description: Predisposing factors: 1.

Sex - 2 - 3 times more often in women, 7. Women have 3 critical periods: a) childhood: girls during this period get sick 6 times more often than boys: b) the beginning of sexual activity: c) pregnancy. Hormonal imbalance: glucocorticoids and hormonal contraceptives. Exchange violations. diabetes mellitus, gout. Abnormalities of the kidneys and urinary tract. Slide description: Ways of infection spread: Hematogenous or lymphogenous (descending) Urinogenic (ascending) Slide description: More often pyelonephritis develops as a result of the ascending spread of infection.

The reasons. They are characterized by inflammatory infiltration by neutrophils and plasma cells, interstitial fibrosis. At the next stage, cell infiltration and shrinkage of the glomeruli, periglomerular fibrosis appear. Typical lesions of the tubules in the form of generalized atrophy, dystrophy of the epithelium.

Productive endarteritis with perivascular sclerosis is common. Slide description: Classification of pyelonephritis - acute and chronic - rapidly progressive - recurrent - latent. Slide description: Latent form - 2.

Most often, there are no complaints. Weakness, increased fatigue, less often subfebrile condition may be noted.

Women during pregnancy may have toxicosis. A functional study does not reveal anything, unless there is rarely an unmotivated increase in blood pressure, slight pain when tapping on the lower back. The diagnosis is made by laboratory.

Repeated tests are of decisive importance: moderate leukocyturia, no more than 1 - 3 g / l proteinuria + Nechiporenko test Stengheimer-Malbin cells are doubtful, but if there are more than 4. Active leukocytes are rarely detected. True bacteriuria *****\u003e 1. Description of the slide: Recurrent form - almost 8. Alternation of exacerbations and remissions. Features: intoxication syndrome with fever, chills, which can be even at normal temperature, in the clinical analysis of blood leukocytosis, increased ESR, shift to the left, C-reactive protein.

Pain in the lumbar region, often 2-sided, in some of the type of renal colic: the pain is asymmetric! Dysuric and hematuric syndromes. There may be micro and gross hematuria. The most unfavorable combination of syndromes: hematuria + hypertension -\u003e chronic renal failure after 2-4 years. Slide description: Acute pyelonephritis. The classic triad is fever, dysuria, and back pain. Severe chills Increase in body temperature to 4.

Pouring sweat, Pain in the lumbar region (on one side or on both sides of the spine) “+” A symptom of tapping. On the side of the affected kidney, tension of the anterior abdominal wall, Sharp soreness in the costal-vertebral angle, Symptoms of severe intoxication - general malaise, thirst, nausea, vomiting, dry mouth, muscle pain. Dysuric manifestations. Slide description: Acute pyelonephritis. Laboratory manifestations. In the urine is determined: mild proteinuria (up to 1 g / l), leukocyturia, leukocyte (white) casts of bacteria. The diagnosis is confirmed by bacteriological examination.

A large number of leukocytes and microbes are found in the urine. The presence of more than 1. 00. In the analysis of blood neutrophilic leukocytosis, aneosinophilia. Sometimes, when the condition of patients worsens, leukocytosis is replaced by leukopenia, which is a poor prognostic sign. Slide description: Acute pyelonephritis. Diagnostics. Anamnesis (a recent acute purulent process or the presence of chronic diseases) Characterized by a combination of fever with dysuria, pain in the lumbar region, oliguria, pyuria, proteinuria, hematuria, bacteriuria with a high relative density of urine. It should be remembered that pathological elements in the urine can be observed in any acute purulent disease and that pyuria may be of extrarenal origin (prostate gland, lower urinary tract). The plain radiograph shows an increase in one of the kidneys in volume. With excretory urography, a sharp restriction of the mobility of the affected kidney during breathing, the absence or later appearance of the shadow of the urinary tract on the side of the lesion.

Compression of the calyx and pelvis, amputation of one or more calyces indicate the presence of a carbuncle. Slide description: Chronic pyelonephritis Among the causes of chronicity, it should be noted: urodynamic disorders, focal infection, inadequate treatment. Chronic pyelonephritis is the cause of chronic renal failure in 1. In most patients, chronic pyelonephritis occurs in childhood, especially in girls. Slide description: Chronic pyelonephritis. For many years, it can pass latently (without symptoms) and is detected only when urine is examined (latent period, period of remission).

Frequent headaches Characterized by a dull, persistent pain in the lumbar region on the side of the affected kidney. Dysuric phenomena are absent in most patients. For an exacerbation of chronic pyelonephritis, the same symptoms are characteristic as for acute pyelonephritis. During the period of exacerbation, only in 2. If treatment is not started in time, then a serious complication - renal failure may occur. Slide description: Chronic pyelonephritis. Changes in urine tests: In the urine sediment, the predominance of leukocytes over other blood cells is determined.

However, as the kidney shrinks, the severity of the urinary syndrome decreases. The relative density of urine remains normal. Detection of active leukocytes in urine is essential for diagnosis. With an exacerbation of the process, bacteriuria can be detected. If the number of bacteria in 1 ml of urine exceeds 1.

Description of the slide: The functional state of the kidneys is investigated using: chromocystoscopy, excretory urography, clearance methods (for example, determination of the coefficient of purification of endogenous creatinine by each kidney separately), radionuclide methods (renography with hippuran, kidney scan). With infusion urography, a decrease in the concentration of the kidneys, a delayed release of a radiopaque substance, local spasms and deformities of the cups and pelvis are determined. Subsequently, the spastic phase is replaced by atony, the cups and pelvis expand. Then the edges of the cups take on a mushroom shape, the cups themselves come closer. Infusion urography is informative only in patients with blood urea levels below 1 g / l. In diagnostically unclear cases, renal biopsy is used.

Slide description: Laboratory criteria. A) During the period of exacerbation, the following are characteristic: - decrease in the relative density of urine; - proteinuria with a daily loss of protein not exceeding 1.5 - 2 g; - leukocyturia; - bacteriuria over 1. B) During the period of exacerbation there are relatively common: - microhematuria; - cylindruria; - positive acute phase reactions; - acidosis. C) During remission, isolated leukocyturia is more often (but not always) determined.

The use of samples with a quantitative count of urine sediment cells (Nechiporenko, Kakovsky - Addis) helps to reveal latent leukocyturia. Slide description: Pyelonephritis.

In the acute period Bed rest (for the period of fever), appoint a table. During the period of convalescence (after 4 - 6 weeks), the regimen expands.

Unlike other urinary tract infections, the antibiotic should produce high serum concentrations, given the high percentage of bacteremia in pyelonephritis. Slide description: Empirical antibiotic therapy. Slide description: Antibacterial therapy Currently, aminopenicillins (ampicillin, amoxicillin), 1st generation cephalosporins (cephalexin, cefradine, cefazolin), nitroxoline cannot be recommended for the treatment of pyelonephritis, since the resistance of the main causative agent of pyelonephritis to these drugs is about 2 ...

Description of the slide: With frequent exacerbations of pyelonephritis, the generally accepted approach is to prescribe monthly preventive courses of antibiotic therapy. The prophylactic use of antibacterial agents should be treated with extreme caution. There is no reliable data indicating the effectiveness and appropriateness of prophylactic antibiotics for pyelonephritis. Slide description: Pyelonephritis. Anti-relapse treatment.

After achieving remission of chronic pyelonephritis, maintenance therapy is prescribed lasting up to 6 - 1. It includes 7 - 1. NOC and others), herbal medicine. Slide description: Pyelonephritis. Ryabov's scheme during the period of remission: First week: 1 - 2 tab. Second week: uroseptic of plant origin: birch buds, lingonberry leaf, chamomile. Third week: 5- NOC 2 tab.

Fourth week: chloramphenicol 1 tab. After that, the same sequence, but change the drugs to similar ones from the same group. Description of the slide: Non-drug measures for the prevention of exacerbations of pyelonephritis include an adequate drinking regimen of 1.2-1.5 liters daily (with caution in patients with impaired heart function), the use of herbal medicine.

Herbal medicine helps to improve urination and does not lead to the development of serious adverse events. Slide description: When choosing drugs for herbal medicine, consider: Diuretic effect, depending on the content of essential oils, saponins, silicates (juniper, parsley, birch leaves) Anti-inflammatory effect associated with the presence of tannins and arbutin (lingonberry and bearberry leaves) Antiseptic effect due to phytoncides (garlic, onion, chamomile). Slide description: Nephrolithiasis.

Etiology. Enzymopathy (tubulopathy) with disturbance in the distal and proximal tubules. Climatic conditions. Ambient temperature, humidity, mineral composition of water - lead to the concentration of the stone substrate. Difficulty in the outflow of urine.

Hyperfunction of the parathyroid glands.

Slide 1

Chronic pain in oncology: modern methods of pharmacotherapy, MD, professor P.B. Zotov Tyumen Regional Oncological Dispensary Oncology presentations

Slide 2

Frequency of pain in cancer 25-45% - in early stages 80-95% - with advanced disease 10-30% of patients continue to experience pain despite ongoing therapy1 1Cancer Pain. From Molecules to Saffering. Paice J.A., Bell R.F., Kalso E.A., Soyannwo O.A. - IASP Press. Seattle, 2010 .-- 354p. No pain There is pain There is pain

Slide 3

Reasons for poor treatment effectiveness Lack of knowledge about the pathophysiology of pain. Lack of knowledge about pain control methods. Difficulty in handling recommended opiates. Refusal of the patient from taking analgesics or non-compliance with the recommended regimen. Lack of a proper assortment of analgesics. Price characteristic of the analgesic. ! !

Slide 4

What is chronic pain syndrome characterized by? Pathological algic system (Kryzhanovsky G.N., 1997) dysregulation Vegetative disorders. Dysregulation of the endocrine system. Psycho-emotional disorders. Circadian rhythm disorder. Pain behavior, personality change

Slide 5

"Pain behavior" "Restrictive behavior" - avoidance of situations that contribute to the recurrence or intensification of pain. Desire to get the maximum and quickest analgesic effect. Restriction of physical activity, food intake, reduction in sleep duration Inadequate choice of analgesic. Incorrect choice of the form of introduction. Non-compliance with the reception regimen. Unjustified change of drugs and regimens. Polyprogas. Increased pain

Slide 6

"Painful behavior" 3. Mood disorders: increased anxiety, depression. 4. Doubts about the correctness of the treatment, the competence of the doctor, medical institution. Aggressiveness towards others and yourself (suicidal behavior). Refusal or ignorance of the medical tactics recommended by the doctor. Increased pain

Slide 7

What should a doctor know to choose a treatment regimen? The intensity of the pain (weak, medium, strong, very strong / unbearable). Duration (acute, prolonged, chronic). Leading mechanism of pain (pain: nociceptive, neuropathic, psychogenic). The effectiveness and extent of previous therapy.

Slide 8

Verbal Rating Scale (VER) - 5-point: 0 - no pain 1 - mild pain 2 - moderate (moderate) intensity 3 - severe (severe) 4 - the most severe (unbearable) pain IMPORTANT: present the patient with the recommended criteria Subjective scales

Slide 9

Pain 1 2 3 Strong opioids Weak opioids ± non-opioid analgesics ± adjuvants Non-opioid analgesics ± adjuvants Pain persists or increases PAIN WHO. Cancer pain relief, 2nd ed. Geneva, WHO, 1996 ± non-opioid analgesics ± adjuvant drugs Pain persists or increases Three-step pain management regimen (WHO, 1986)

Slide 10

Dominant principle Maximum correspondence of the analgesic to the type of pain (tropism to the leading pathogenetic mechanism of pain).

Slide 11

Types of pain Peripheral component (nociceptors) Neurogenic component Psychological component DORSAL HORN Type of pain: 1. Somatogenic pain. 2. Neurogenic pain. 3. Psychogenic pain.

Slide 12

Peripheral analgesics - the basic stage for pain of varying intensity Analgin (metamizole) action is aimed at blocking inflammatory mediators (prostaglandins, kinins, etc.) Combined analgin preparations are still relevant in general practice: Tempalgin, Pentalgin, Baralgin Modern - have a longer duration (8-12 hours ) and a strong analgesic effect: 1. Ksefokam (lornoxicam) - tablets, injections 2. Flexen (ketoprofen) - suppositories, gel, capsules, ampoules 3. Perfalgan (paracetamol) - solution for intravenous infusion

Slide 13

For severe pain: the appointment of non-invasive prolonged forms of MCT-continus - tablets 10, 30, 60 and 100 mg Active substance: morphine Duration of action: 12 hours Experience of use in TOOD - since 1997. Disadvantages: cannot be used in case of dysphagia; decreased effectiveness in malabsorption syndrome

Slide 14

Comparison of opioid analgesics in terms of analgesic potential 100 The conditional analgesic potential of morphine is taken as 1

Slide 15

Fendivia: transdermal therapeutic system (TTS) Fendivia - patch Dose: 12.5; 25; 50; 75 and 100 mcg / h Active ingredient: fentanyl Duration of action: 72 hours Advantages: - gastrointestinal tract is not involved - duration of action - exclusion of breakthrough pain

Slide 16

Fendivia provides stable and non-invasive pain relief for the entire treatment period, thanks to the transdermal therapeutic system (TTS) ... Formation of fentanyl depot within the first 17-24 hours Achievement of the maximum analgesic effect after 24 hours. cm Fentanyl release per hour: 25, 50, 75 and 100 mcg

Slide 17

ONCE APPLICATION OF THE TRANSDERMAL THERAPEUTIC SYSTEM * Miser et al, 1989 4 3 2 1 0 0 12 24 36 48 60 72 Plasma concentrations of fentanyl (ng / ml) Time after application (h) Fendivia 100 μg / h

Slide 18

Ascending signal Descending signal Sensation of pain Spinal cord Peripheral nociceptors Pathological fracture of the vertebral body with metastases of breast cancer Neuropathic pain occurs in 30-60% of patients with advanced cancer Injury (compression) of the nerve + osteoporosis

Slide 19

Clinic of neurogenic pain Symptoms described by the patient: - prolonged, burning pain, shooting, piercing pain - pain similar to an electric discharge - paresthesia Symptoms determined by the doctor: - hyperalgesia - allodynia - dysesthesia - hyperpathy

Slide 20

Drugs used (for neurogenic pain) Anticonvulsants Muscle relaxants Antidepressants Neuroleptics Antiarrhythmics Local anesthetics Non-drug drugs (transcutaneous electroneurostimulation, physiotherapy, relaxation, biofeedback methods, etc.). Adjuvant Therapy (Three-Step Pain Management Scheme, WHO, 1986, 1992, 1996) Drug of choice for neuropathic pain: Lyrica (pregabalin)

Slide 21

Pathogenetic (targeted) drugs for the treatment of neuropathic pain syndrome Pregabalin (Lyrica) Gabapentin Oxcarbazepine Carbamazepine Amitriptyline Lamotrigine Local anesthetics (lidocaine patch)

Slide 22

Action Lyrica (pregabalin) Kavoussi R. Eur Neuropsychopharmacol. 2006; 16 Suppl 2: S128-133. Danilov A.B., Davydov O.S. Neuropathic pain. 2007 .-- S. 10-12. Pregabalin regulates the work of overly excitable neurons: Target - a2-d subunit of voltage-gated calcium channels2 Reduces excess release of excitatory mediators2 This mechanism of action explains its analgesic, anticonvulsant, and anxiolytic activity1,2 Pregabalin prevents excessive release of excitatory mediators1

Slide 2

Slide 3

Chronic pancreatitis (CP) is a long-term inflammatory disease of the pancreas, manifested by irreversible morphological changes that cause pain and / or a persistent decrease in function

Slide 4

The prevalence of chronic pancreatitis according to autopsy data is from 0.01 to 5.4%, on average 0.3-0.4%. The detection rate of chronic pancreatitis is 3.5-4 per 100,000 population per year. The disease usually begins in middle age (35-50 years).

Slide 5

usually people who take 150-200 ml of pure alcohol per day for an average of 10 years or more Heredity Hyperparathyroidism Congenital malformations of the pancreas

Slide 6

Pathogenesis

1. Obstruction of the main pancreatic duct with calculi, inflammatory stenosis or tumors 2. In alcoholic pancreatitis, damage to the pancreas is associated with an increase in the protein content in the pancreatic secretion, which leads to the appearance of protein plugs and obstruction of the small ducts of the gland 3. Change in the tone of the sphincter of Oddi: its spasm causes intraductal hypertension, and relaxation promotes reflux of duodenal contents and intraductal activation of pancreatic enzymes.

Slide 7

4. Calcification of the pancreas occurs in both alcoholic and non-alcoholic pancreatitis most often after traumatic injury in hypercalcemia, islet cell tumors.

Slide 8

Damage to the exocrine pancreas Disorders of food digestion, manifestations of lipase deficiency occur, which are manifested by impaired absorption of fats, fat-soluble vitamins A, D, E and K Damage to the endocrine pancreas Diabetes mellitus - impaired glucose tolerance hypoglycemic reactions to insulin ketoacidosis

Slide 9

Classification of chronic pancreatitis / Ivashkin V.T., 1990 /

1. by etiology Biliary-dependent Alcoholic Dysmetabolic Infectious Drug Idiopathic 2. By the nature of the clinical course Rarely recurrent Often recurrent With constantly present symptoms 3. By morphological signs Interstitial-edematous Parenchymal Fibro-sclerotic (indurative) Hyperplastic (pseudo-sympathetic) Hyposecretory Asthenoneurotic Latent Combined

Slide 10

Clinical picture:

Pain in the epigastric region after eating, radiating to the back, which can last for hours or several days Symptoms of dyspepsia (nausea, vomiting) Weight loss (in 30-52% of patients) Jaundice (in 16-33% of patients) Portal hypertension (rare)

Slide 11

Syndrome of insufficiency of exocrine function (with a decrease in the volume of the functioning parenchyma to 10% of the norm, signs of malabsorption appear - polyfeces, fatty stools, loss of body weight).

Slide 12

Diabetes mellitus develops in 10-30% of patients with CP, more often - impaired glucose tolerance (thirst, polyuria, pruritus, tendency to infectious processes)

Slide 13

Slide 14

Complications

cholestasis, infectious complications (inflammatory infiltrates, purulent cholangitis, septic conditions), subhepatic form of portal hypertension, erosive esophagitis, Mallory-Weiss syndrome, gastroduodenal ulcers, chronic duodenal obstruction, pancreatic cancer and abdominal ischemic syndrome.

Slide 15

Examples of wording a diagnosis

Chronic pancreatitis, biliary-dependent, rarely recurrent, acute phase (interstitial-edematous), complicated by obstructive jaundice. Chronic pancreatitis, alcoholic etiology, often recurrent course, exacerbation phase (with a predominant tail lesion, cystic, complicated by portal hypertension).

Slide 16

Laboratory diagnostics

UAC, OAM Biochemical blood test: bilirubin, LDH3, cholesterol, alkaline phosphatase, AST, ALT Determination of blood amylase, urine, serum lipase, serum trypsin and trypsin inhibitor concentration. Examination of blood sugar and urine

Slide 17

Assessment of exocrine pancreatic insufficiency. 1. Coprological examination (gray tint, offensive odor, polyfecal matter, oily appearance, steatorrhea) 2. Functional tests: direct tests of pancreatic secretion. Collect and study pancreatic juice or duodenal contents after stimulation of pancreatic secretion by exogenous hormones or hormone-like peptides (secretin-pancreozymin test);

Slide 18

Laboratory diagnostics (continued)

indirect tests - the study of duodenal contents after food stimulation (Lund test); oral tests - performed without cannulating the pancreatic duct or introducing a probe (bentiramine test - PABK - test); fluoresceindilaurate or pancreatolauril test; respiratory tests with a substrate labeled with radioisotopes), a double Schilling test (substrate-complex vitamin B12 - R-protein, control substance - _ vitamin B12 - internal Castle factor; / _ - low. method for the determination of pancreatic enzymes in feces (trypsin, chymotrypsin, elastase, lipase) The sensitivity and specificity of the elastase test in patients with severe and moderate exocrine pancreatic insufficiency are close to those of the secretin-pancreosimin test, while the sensitivity of the method is 63% if mild.

Slide 19

Imaging techniques in the diagnosis of chronic pancreatitis

Radiography of the pancreas area Transabdominal ultrasound (duct dilation, pseudocysts, calcification, dilation of the common bile duct, portal, splenic vein, ascites) Endoscopic ultrasound ERCP (changes in the structure of ducts, pseudocysts) Computed tomography (with intravenous contrast) Scintigraphy with the introduction of 99 granulocytes, or labeled 111Ip

Slide 20

Ultrasound

Slide 21

Pancreatic cyst

Slide 22

K T

Slide 23

Normal Pancreas Calcifications

Slide 24

Treatment

refusal to drink alcohol adherence to a diet low in fat (up to 50-75 g / day) and frequent small amounts of food pain relief enzyme replacement therapy fight against vitamin deficiency treatment of endocrine disorders

Slide 25

Treatment of an attack of chronic pancreatitis

intravenous administration of solutions of electrolytes and colloids, fresh frozen plasma or albumin fasting diet analgesia aspiration of stomach contents through a nasogastric tube. preparations of digestive enzymes (creon) heparin, plasma, platelet-activating factor antagonist Lexipafant (60-100 mg / day) surgical treatment of obstructive pancreatitis (papillosphincterotomy, dilatation or stenting of the pancreatic duct).

Slide 26

Long-term therapy for CP

I. Relief of chronic pain antispasmodics and anticholinergics (duspatalin, papaverine hydrochloride i / v or i / m 2 ml of 2% solution 2-4 times a day, platifillin i / v or i / m 4 mg 1 to 2 times a day) non-narcotic analgesics : paracetamol, tramadol (up to 800 mg / day or more) antidepressants (amitriptyline inside 75 - 150 mg per day) narcotic drugs (promedol) pancreatic enzymes in large doses (creon, mezim)

Slide 27

blockers of H2-histamine receptors (famotidine 20 mg 2 times a day) or proton pump inhibitors: omeprazole 20 mg 2 times a day (or esomeprazole or rabeprazole in the same dose) or lansoprazole (30 mg 1 time per day octreotide surgical treatment (lateral pancreatojejunostomy) , distal pancreatectomy, Whipple operation) endoscopic treatment (drainage of pseudocysts, solar plexus neurolysis)

Slide 28

Long-term therapy for CP (continued)

II. Relief of exocrine pancreatic insufficiency: preparations of extracts of the pancreas (creon) antacids 30 minutes before and 1 hour after meals or antisecretory drugs (H2 blockers, proton pump inhibitors) for flatulence - adsorbents (simethicone, dimethicone) or use combined enzyme preparations, containing adsorbents (pancreoflat). 4. in severe steatorrhea - fat-soluble vitamins (A, D, E, K), B vitamins. III. Treatment of endocrine disorders in CP

View all slides

dystrophic liver damage with

preservation of its lobular structure.

Slide 3

The disease can develop at any age.

Duration not less than 6 months.

Slide 4

Classification of hepatitis:

by etiology:

chronic viral hepatitis B, C, D.

autoimmune hepatitis.

alcoholic hepatitis.

toxic or drug-induced

Slide 5

2. according to the degree of activity of the process:

moderate.

Slide 6

Reasons for development:

The main reason is the acute viral hepatitis B, C, D. transferred in the past.

Transmission ways:

parenteral

from mother to fetus

Slide 7

2) Medicinal liver damage:

Cytostatics

Salicillates

Anabolic

Antidiabetic drugs

Slide 8

The toxic effects on the liver are:

Alcohol

Chlorinated hydrocarbons

Metals (lead, mercury, arsenic, phosphorus)

Benzene and its derivatives

Slide 9

Pathogenesis.

The chronic course and progression of the disease is explained by two processes:

1) Persistence of the virus in the body of patients against the background of a weakened immune system.

Slide 10

2) Development of autoimmune processes, when, under the influence of various factors, the hepatocytes themselves acquire antigenic properties.

Slide 11

Clinic.

Depends on the form of hepatitis, on the combination and severity of clinical syndromes. With all hepatitis, liver function is impaired in all types of metabolism, its external secretory capacity and detoxification function change.

Slide 12

With hepatitis, the liver increases in size, moderately dense with a pointed edge, painful on palpation. As a result, there is a feeling of heaviness, distention in the right hypochondrium.

Slide 13

Clinical syndromes:

Asthenovegetative - weakness, severe fatigue, nervousness, weight loss.

Dyspeptic - nausea, vomiting, loss of appetite, belching, heaviness in the epigastrium, flatulence, constipation.

Slide 14

3. Syndrome of immune inflammation - fever, swollen lymph nodes, joint pain, splenomegaly.

4. Cholestatic - jaundice, pruritus, skin pigmentation, santelasma, darkening of urine.

Slide 15

5. Syndrome of small liver failure - weight loss, jaundice, liver odor from the mouth, “liver” palms, “liver” tongue, vascular asterisks on the body, fingers in the form of drumsticks, nails in the form of watch glasses, santelasma appear on the skin.

Slide 16

6. Hemorrhagic - bleeding from the gums, nosebleeds, hemorrhages on the skin.

7. Syndrome of hypersplenism - enlargement of the spleen.

Slide 17

Diagnostics:

KLA - anemia, thrombocytopenia, leukopenia, increased ESR.

Biochemical blood test - hyperbilirubinemia, dysproteinemia, due to an increase in the amount of globulins. An increase in the level of sedimentary samples - sublimate, thymol. Increased level of transaminases - Al-At, Ac-At, and alkaline phosphatase.

Slide 18

3. OAM - proteinuria, microhematuria, bilirubin in the urine.

4. Immunological analysis.

5. Markers of viral infection.

Slide 19

Instrumental research:

Ultrasound of the liver and gallbladder (uneven liver tissue is detected, an increase in size).

Computed tomography of the abdominal organs.

Gastroscopy.

Slide 20

4. Colonoscopy.

5. Puncture liver biopsy, followed by histological examination, can be performed during laparoscopy or percutaneously. It allows you to judge the activity of the process and is an important differential criterion for distinguishing chronic hepatitis from liver cirrhosis.

Slide 21

Treatment regimen. Work with physical and psycho-emotional stress is excluded. Shows a short rest during the day. Hepatotoxic drugs, physiotherapy and balneotherapy are excluded. During the period of exacerbation - bed rest.

Slide 22

2. Health food - diet number 5.

Excluded: fatty meats and fish, fried foods, smoked meats, salty and spicy snacks, legumes, sorrel, spinach, fresh fruit, strong coffee, alcohol, carbonated drinks.

Slide 23

3. Antiviral treatment: carried out with hepatitis in the phase of virus multiplication and prevents the development of cirrhosis and liver cancer. Interferons for 6 months (Interferon A, Velferon, Roferon).

4. Pathogenetic treatment: corticosteroids, cytostatics.

Slide 24

5. Immunomodulating therapy has a stimulating and normalizing effect on the immune system: Timalin, D-penicillin, Timogen, T-activin.

Slide 25

6. Metabolic and coenzyme therapy is aimed at improving metabolic processes in the liver cells. Multivitamin complexes: Decamevit, Undevit, Duovit, vitamin E, Riboxin, Essentiale.

7. Hepatoprotectors: Korsil, Legalon, Katergen.

Slide 26

8. Detoxification therapy: Gemodez intravenously, 5% glucose. Enterosorbents - Laktofiltrum, Filtrum, Enterosgel.

9. Treatment of edematous-ascitic syndrome in cirrhosis, first - Veroshpiron, Aldikton, and then in combination with Uregit, Hypothiazid, Furosemide.

9. Treatment of bleeding from varicose veins.

Slide 27

Prevention of chronic hepatitis and liver cirrhosis:

Primary: prevention of viral hepatitis, effective treatment of acute viral hepatitis, rational nutrition, control over the intake of medications, the fight against alcoholism, drug addiction.

Secondary: prevention of exacerbations of the disease. Restriction of physical activity, proper employment. Nutritional therapy, treatment of concomitant gastrointestinal diseases.

Slide 28

Completed: student of the 141st group of Tretyakov A.

Teacher: Stepanishvili N.N.

View all slides

Content
Baseline tests
Clinical anatomy and physiology of the pancreas
Innervation and blood supply of the pancreas
Exocrine pancreatic function.
Secretion phases
Humoral and nervous regulation of the pancreas
RV hormonal function
Definition
Epidemiology
Etiology
Pathogenesis
Classification of chronic pancreatitis
Classification of CP by severity
Imaging techniques in the diagnosis of chronic pancreatitis:
Complications
Treatment
Final level tests

Clinical anatomy and physiology of the pancreas

Pancreas (PZh) - the gland of the digestive system,
producing pancreatic juice and having at the same time
endocrine function. Located in the upper abdomen, in
retroperitoneal space at the level of I-II lumbar vertebrae,
behind the back wall of the stomach. Has the form of a flattened strand, in
which distinguish between the head, body, tail. RV length is 14-23
cm, width 3-7.5 cm (in the head area), body width 2-5 cm, tail
0.3-3.4 cm, weight 65-105 g. Most of the pancreatic parenchyma (exocrine
part) secretes enzymes necessary for digestion. They
enter the pancreatic duct, often merging into the final
parts with a common bile duct and opening into the descending
section of the duodenum at the apex of the nipple of Vater
(large papilla of the duodenum). Vater papilla
has a sphincter of the hepato-pancreatic ampulla (sphincter of Oddi),
regulating the flow of pancreatic juice and bile into
duodenal
intestine.
Lesser
part
(endocrine)
grouped in the form of the smallest islets (islets of Langerhans)
and is interspersed into the parenchyma of the exocrine gland. Islets
Langerhans are formed by groups of secretory cells (insulocytes).

Allocate
four
cell type: α-cells,
generating
glucagon, β-cells,
generating
insulin,
γ-cells,
generating
somatostatin;
pcells producing
no pancreatic
polypeptide.
Much bigger
pancreatic
islets located in
tail of the pancreas.

Innervation and blood supply of the pancreas

The nerves innervate the pancreas,
going
from
hepatic,
splenic, celiac and
superior mesenteric plexus
and branches of the vagus nerve.
IN
them
composition
are included
sensitive
and
secretory fibers.
Blood supply
Pancreas
provide mainly
branches of the common hepatic,
top
mesenteric
and
splenic
arteries.
Venous blood flows through
eponymous
veins
in
portal vein. Lymphatic drainage
carried out
in
regional lymphatic
nodes.

Exocrine pancreatic function.

Exocrine
function
Pancreas
consists
in
elaboration
cells
exocrine pancreatic gland
juice containing the necessary enzymes
for the digestion of proteins (proteases), fats
(lipase)
and
carbohydrates
(glycosidase).
The main
of
them
(trypsinogen,
chymotrypsinogen)
secreted
in
inactive form and are activated only in
duodenum, turning
under the influence of enterokinase into trypsin and
chymotrypsin. Along with enzymes with
pancreatic juice enters water,
electrolytes and, above all, hydrocarbons
and plenty of protein. Bicarbonate
gives the pancreatic juice alkaline
reaction,
necessary
for
enzymatic breakdown of nutrients.
Branch
pancreatic
juice
carried out due to the pressure difference in
proximal and distal
duct
PZh,
and
also
and
in
duodenum and occurs
periodically, increasing when exposed
conditioned reflex (type and smell of food) and
unconditional reflex
irritants
(chewing and swallowing).

Secretion phases

Distinguish
3
phase
secretions
pancreatic juice:
-complicated reflex,
happening
under
influence of the
above irritants;
-gastric, which
associated with stretching
stomach
at
filling it with food;
-intestinal, having
humoral nature.

Humoral and nervous regulation of the pancreas

Humoral
regulation
carried out
in
basically
intestinal
polypeptide
hormones
secretin
and
pancreozymin. They stand out
special hormone-producing
cells
mucous
shell
duodenum with
entering it from the stomach
hydrochloric acid, as well as products
partial digestion of protein. On
RV secretion is also affected
pituitary hormones, thyroid
glands, adrenal glands and some
others.
Nervous
center,
regulatory
secretion
pancreatic juice, is in
medulla oblongata.

RV hormonal function

Hormonal
function
carried out by islets
Langerhans,
which
secrete hormones (insulin
and glucagon), regulating
carbohydrate metabolism, and
somatostatin
and
pancreatic
polypeptide,
being
hormonal
regulators
some
functions of the digestive
systems. On defeat
islets of Langerhans in
first of all violated
carbohydrate
exchange
is developing
sugar
diabetes.

Definition

Chronic pancreatitis (CP)
- long-term inflammatory
disease
pancreas
glands,
manifested
irreversible
morphological
changes,
which
cause pain and / or persistent
decreased function. With CP
morphological
changes
pancreas
glands
persist after termination
impact
etiological
factor a.

Epidemiology

Prevalence
chronic
pancreatitis according to
autopsies are from
0.01 to 5.4%, on average
0,3-0,4%.
Frequency
identifying
chronic
pancreatitis is
3.5-4 per 100,000
population
in
year.
Disease
usually
starts on average
age (35-50 years old).

Etiology

The most common cause of illness is alcohol consumption
(up to 90% of adult patients); people usually get sick
taking 150-200 ml of pure alcohol per day on average in
for 10 years or more, however, the timing of the onset of pancreatitis in
different people can vary significantly. Besides,
possible hereditary pancreatitis is a disease inherited
autosomal dominant type with 80% penetrance.
Hereditary pancreatitis is associated with a mutation in the gene encoding
synthesis of trypsin, which causes a violation of the defense mechanism against
intracellular activation of trypsin. Pancreatitis occurs in 3%
patients with hyperparathyroidism, with duct obstruction
pancreas (PZh) (stenosis, calculi, cancer),
congenital anomalies: annular pancreas, bifurcated pancreas
(pancreas divisum), with duodenal diverticula.
Rarely, chronic pancreatitis is due to stenosis
a duct that has arisen in acute, in particular biliary,
pancreatitis.

Pathogenesis

Several factors play a role in the pathogenesis of chronic pancreatitis.
factors. One of the main ones is obstruction of the main
pancreatic duct with calculi, inflammatory stenosis
or
tumors.
When
alcoholic
pancreatitis
damage
pancreas is associated with increased protein content in
pancreatic secretion, which leads to the appearance of protein
plugs and obstruction of small ducts of the gland. Another factor
involved in the pathogenesis of alcoholic pancreatitis, is
the change
tone
sphincter
Oddi:
him
spasm
causes
intraductal hypertension, and relaxation promotes reflux
duodenal
content
and
intraductal
activation
pancreatic enzymes.

Calcification
pancreas
glands
arises
as
at
alcoholic,
So
and
at
non-alcoholic pancreatitis more often
Total
after
traumatic
damage with hypercalcemia,
tumors
islet
cells.
A significant role in this is played by
pancreatic calculus protein
glands,
inhibitory
precipitation
oversaturated
solution
carbonate
calcium,
quantity
of this
squirrel
in
pancreatic
secret
deterministically
genetically.
Observed
some
phases
calcifications
pancreas
glands: growth, stable
phase that comes through
several years and a decrease in degree
calcification (observed in 30%
sick),
despite
on
progressive
decline
exocrine organ function.

Destruction
exocrine
parts
pancreas
glands
causes
progressive decrease in secretion
bicarbonates and enzymes, however
clinical manifestations of the disorder
food digestion develop
only with destruction of more than 90%
organ parenchyma. Firstly
arise
manifestations
lipase deficiency, which
are manifested by impaired absorption
fats, fat-soluble vitamins
A, D, E and K, which is infrequent
bone damage, disorders
clotting
blood.
When
HP
due to
deficit
proteases
violated
split
connections
vitamin B12 is an R-protein and decreases
secretion of cofactors that determine
absorption of vitamin B12, however
clinical
symptoms
of this
are rare.

In 10-30% of patients with CP
diabetes mellitus develops,
usually in the later stages
diseases, much more often
observed
violation
glucose tolerance. For
such patients are characterized by
development of hypoglycemic
reactions
on
insulin,
malnutrition or
alcohol intake. Ketoacidosis
is developing
seldom,
what
associated with simultaneous
decline
products
insulin and glucagon.

Table 1. Etiopathogenesis of chronic pancreatitis (according to P. Layer and U. Melle 2005)

Alcoholic
Mutations in SPINK1 (serine protease inhibitor kazal type1), trypsinogen gene or CFTR (cystic fibrosis
transmembran regulator) genes.
Caused by smoking
Hereditary
Trypsinogen gene mutation.
Autoimmune
Metabolic / nutritional.
Hypercalcemia
Hyperparathyroidism
Acquired or hereditary hypertriglyceridemia
Tropical (SPINK1 mutations)
Tropical calculous pancreatitis
Fibrocalculous pancreatogenic diabetes
Idiopathic
Early onset (SPINK1 mutations)
Late start
Obstructive.
Mild HSP obstruction
Traumatic stricture
Post-necrosis stricture
Stenosis of the sphincter of Oddi
Sphincter of Oddi dysfunction
Stones
Duodenal obstruction (diverculus, duodenal wall cysts)
Malignant stricture of the pancreas duct.
Pancreatic, ampullar and duodenal calcinoma

Classification of chronic pancreatitis

Currently, the classification of chronic pancreatitis proposed by Ivashkin is used.
V.T., Khazanov A.I. et al. (1990), based on the proposed in Marseille in 1983 and in Rome in 1989
g.
1. Variants of chronic pancreatitis by etiology
Biliary dependent
Alcoholic
Dysmetabolic
Infectious
Drug
Idiopathic
2. Variants of chronic pancreatitis by the nature of the clinical course
Rarely recurrent
Often relapsing
With persistent symptoms
3. Variants of chronic pancreatitis by morphological characteristics
Interstitial-edematous
Parenchymal
Fibrosclerotic (indurative)
Hyperplastic (pseudotumorous)
Cystic
4. Variants of chronic pancreatitis by clinical manifestations
Painful
Hyposecretory
Asthenoneurotic
Latent
Combined

The most difficult section of the classification is the division of CP by morphological characteristics. The authors based these principles on the given

Interstitial edematous CP

on
height of exacerbation (according to ultrasound
and CT) is characterized by moderate
increase
sizes
PZh.
Due to edema of the gland itself
and
parenchymal
fiber
contours
Pancreas
visualized
indistinct, its structure is presented
heterogeneous, there are areas
both increased and decreased
density; there is a mixed
echogenicity. As it subsides
exacerbation, the size of the pancreas becomes
normal, clear contours. IN
contrast to acute pancreatitis
part of morphological changes
turns out to be stable (more
or less persist
areas of the gland seal). Have
most patients expressed
no changes in the duct system
discovered.

Parenchymal variant of CP

For parenchymal variant
HP
characteristic
significant
duration
diseases,
alternation of periods of exacerbation and
remission. Pain during exacerbation
less pronounced, amylase test
turns out to be positive less often and
the increase rate is less. More
than
at
half
sick
are recorded
symptoms
exocrine
pancreatic insufficiency: steatorrhea,
polyfecal matter, tendency to diarrhea,
which the
relatively
easily
stops
enzyme
drugs. According to ultrasound and CT
the size and contours of the pancreas exist
not changed, stable
uniform compaction is noted
glands. Duct changes in
the majority
sick
not
comes to light.

Fibrosclerotic variant of CP

- long-term history - more than 15
years old. In almost all patients
fixed
exocrine
pancreatic insufficiency, intense pain,
not inferior to drug therapy.
The clear line between
exacerbation and remission. Amylazny
the test in half the cases is
negative. Complications are frequent, but
character
them
depends
from
preferential localization of the process
(in the head - bile passage disorders, in
tail-breaking
passability
splenic vein and subhepatic
form of portal hypertension). By
data
Ultrasound
and
CT dimensions
pancreas
glands
reduced,
parenchyma of increased echogenicity,
significantly compacted, clear contours,
uneven,
quite often
come to light
calcification. In some patients, the enlargement of the ductal system of the gland.

Hyperplastic variant of CP

- occurs in approximately
5%
sick.
Disease
takes a long time (usually
more than 10 years). Pains wear
expressed
character
and
constant
as
usually
fixed
failure
exocrine pancreatic function.
Sometimes
Pancreas
can
palpate; amylase test
positive in only 50%
sick. According to ultrasound and CT
The pancreas or its individual parts sharply
increased.
IN
plan
differential diagnosis with
pancreatic tumor
it is advisable to conduct a sample
with lasix, as well as repeated
blood serum test for
tumor markers.

Cystic variant of CP

- occurs 2 times
more often than hyperplastic. It stands out in
a separate option, since it is characterized
a kind of clinical picture - pain
moderate, but almost constant, amylase test,
generally positive and persists
long time. According to ultrasound and CT-RV
increased, there are liquid formations, areas
fibrosis and calcification, ducts usually
expanded. Exacerbations are frequent and do not always have
"Visible" reason.
Reactive pancreatitis is a reaction of the pancreas
glands for acute pathology, or exacerbation
chronic organ pathology, functionally,
morphologically
related
from
pancreas
iron. Reactive pancreatitis ends when
elimination of exacerbation of the underlying disease, but
its statement requires medical and
preventive measures aimed at
prevention of the development of chronic pancreatitis.
As a chronic form of the course, reactive
pancreatitis does not exist and the diagnosis is made to be
can not.

Classification of CP by severity

An easy course of the disease. Rare (1-2 times a year) and short
exacerbations, quickly relieving pain syndrome. RV functions are not
violated.
Outside
exacerbations
well-being
sick
quite
satisfactory. There was no decrease in body weight. Indicators
coprograms within normal limits.
Medium severity. Exacerbations 3-4 times a year with typical prolonged
pain syndrome, with the phenomenon of pancreatic hyperenzymemia,
detected by laboratory research methods. Violations
exocrine and endocrine pancreatic function
moderate (change in the nature of feces, steatorrhea, creatorrhea according to
coprograms, latent diabetes mellitus), with instrumental
examination - ultrasound and radioisotope signs of damage
pancreas.
Heavy current. Continuously recurrent course (frequent
prolonged exacerbations), persistent pain syndrome, severe
dyspeptic disorders, "pancreatic diarrhea", sharp
violation of general digestion, profound changes in exocrine
pancreatic functions, development of pancreatic diabetes mellitus, pancreatic cysts.
Progressive exhaustion, polyhypovitaminosis, extrapancreatic
exacerbations (pancreatogenic effusion pleurisy, pancreatogenic
nephropathy, secondary duodenal ulcers).

Clinical picture:

Pain in the epigastric region after eating, radiating to
back that can last for hours or
several days.
Nausea, vomiting.
Weight loss (in 30-52% of patients).
Jaundice (in 16-33% of patients). Edema and development of pancreatic fibrosis can
cause compression of the bile ducts and surrounding vessels.
Transient jaundice occurs due to pancreatic edema during exacerbations
chronic pancreatitis, persistent-associated with obstruction of the general
bile duct due to fibrosis of the pancreas head. With lighter
obstruction, only the level of alkaline phosphatase is increased.
During an attack of chronic pancreatitis, fatty
necrosis, often the subcutaneous tissue on the legs is affected, which manifests itself
painful nodules that can be mistaken for nodular
erythema.
Inflammation and fibrosis of the peripancreatic tissue can lead to
compression and thrombosis of the splenic, superior mesenteric and portal veins,
however, an extensive picture of portal hypertension is rare.
Formation of pseudocysts due to ruptured ducts of the pancreas, in situ
previous tissue necrosis and subsequent accumulation of secretions. Cysts
may be asymptomatic or cause pain in the upper half
abdomen, often manifested by compression of adjacent organs.

Exocrine insufficiency syndrome

With a prolonged course of the disease as
destruction of the pancreatic parenchyma intensity of pain
attacks
becomes
less
(but
continued drinking can cause
persistence of pain), and with a decrease in volume
functioning parenchyma up to 10% of the norm
signs of malabsorption appear - polyfecal matter,
fatty stools, weight loss. In patients with
alcoholic pancreatitis signs of malabsorption
occur on average 10 years after the appearance
first clinical symptoms.
Diagnosis is based on characteristic
pain syndrome, signs of insufficiency
exocrine pancreatic function in a patient,
regularly drinking alcohol. Unlike
acute pancreatitis, in chronic rare
there is an increase in the level of enzymes in the blood
or urine, so if this happens, you can
suspect
formation
pseudocysts
or
pancreatic ascites Steadily increased
the level of amylase in the blood allows you to
the assumption of macroamylasemia (in which
amylase forms large complexes with proteins
plasma not filtered by the kidneys and in urine
normal amylase activity is observed) or
extra-pancreatic sources of hyperamilasemia.

Table 2. Extra-pancreatic sources of hyperamilasemia and hyperamylazuria (according to W. B. Salt II, S. Schtnkor):

Renal failure
Diseases of the salivary glands:
parotitis
calculus
radiation sialadenitis
Complications of Maxillofacial Surgery
Tumor hyperamilasemia:
lung cancer
esophageal carcinoma
ovarian cancer
Macroamylasemia
Burns
Diabetic ketoacidosis
Pregnancy
Kidney transplant
Brain trauma
Drug treatment:
morphine
Diseases of the abdominal organs:
biliary tract diseases (cholecystitis, choledocholithiasis)
complications of peptic ulcer - perforation or
penetration of ulcers
bowel obstruction or infarction
ectopic pregnancy
peritonitis
aortic aneurysm
postoperative hyperamilasemia

Imaging techniques in the diagnosis of chronic pancreatitis:

X-ray of the area
PZh.
Transabdominal ultrasound
(expansion
ducts,
pseudocysts,
calcification, expansion
common bile duct,
gate,
splenic
veins, ascites).
Endoscopic ultrasound.
ERCP
(the change
structures
ducts,
pseudocysts).
CT scan
(from
intravenous
contrasting)
Introduction scintigraphy
granulocytes,
tagged
99mTc or 111Ip.

Plain radiography in 30-40% of cases
reveals
calcification
pancreas
glands or intraductal stones, especially
when examining in oblique projection. it
takes off
need
{!LANG-205d049c4cee4831277f5b1dd2474d91!}
{!LANG-1dffdbf9b111ade2c6f945deb479911e!}
{!LANG-86a8981704b1b564ad24dd370604092b!}
{!LANG-840c5dd9822c183110821273a4cf33d5!}
{!LANG-f5d2729e6840276113cbb5bc83e7c63f!}
{!LANG-929351e41ed976747d8a8052a4ea583a!}
{!LANG-12707e2c0324b55b264040255521586c!}
{!LANG-bb404560314a9ae0674b98c431512dbe!}
{!LANG-89e2e950e346e47e51c728bda9bd395b!}
{!LANG-9e2d5e25f98402a480015234007d2d6e!}
{!LANG-bc29a28ceefddb4495e324ccb53634cc!}
{!LANG-0783bfd10adeda0c8880574bdde888de!}
{!LANG-a37c4e56ffef4aaf65f2febb19702de2!}
{!LANG-0d7e34057eed8345a8efc6168b4fba35!}
{!LANG-fcdfb6fec969c144b4836278c63825b4!}
{!LANG-0e40674109dff95225f3ecf9f3b88223!}
{!LANG-a55784fb91966e13337eb37dba02fafc!}
{!LANG-3f718263ed6b24f1f10aafa588f430b1!}
{!LANG-54bbfb4faffaf32c5f918b4bff0c66e0!}
{!LANG-b270815307ab3b42e29d2b3b53864d40!}
{!LANG-e168b086734e28e0ed16f3bafa140d7e!}
pancreas
glands
from
{!LANG-331d302d1fc0d8e083532e8db6612e0e!}
{!LANG-10468f6ca80d13b5977179c936bfb4f4!}

{!LANG-00972427d213a9c22a417fa71e4a3eeb!}
{!LANG-6f4c4e4e8c3efe6d30559053f0ac66e8!}
{!LANG-2c623697b04adbddc904402cc018eb33!}
{!LANG-84963ffd22ba3154c403a9d614a54d25!}
{!LANG-cfb247f3ebbe653308a0006473c3aa14!}
exocrine
{!LANG-0eff2b22c6d76705e7a6d94f71d53a75!}
{!LANG-a2c6f74dd5e87c96f484dd2aca388119!}
{!LANG-71f80b7569517d99fbe29bb1ba8d5e34!}
{!LANG-9bd8bf2d4fec791f9843c22a87c3439b!}
{!LANG-c07992974e35e3da76daf322a5a13d45!}
{!LANG-29821405b3a6e145901a026950e6cf44!}
{!LANG-b6f28b666e074fadadca7335713c50f6!}
{!LANG-df84eea175fbe5b46bbfe8c28fc53323!}
{!LANG-492bfc08e4ea8598cd5e7b7347cf7591!}
{!LANG-d3daf21012ed3ea57d7d78c0ec6fddaf!}
{!LANG-2d0245c72503727671f8f0ee5a7dc4b0!}
{!LANG-72c99d3645a11e5c36fc346a7a24a270!}
{!LANG-d06aec0c05bad97f73ba569f5fc115e5!}
{!LANG-2b979c16e32f6ea34654328a437418c8!}
{!LANG-27fa38b40e866efbd0ec0e894270cc04!}
exocrine

{!LANG-418f2ed861ec1274164090f6410178a1!}
{!LANG-920b3e452b0da0903a628f4dd9f87f74!}
{!LANG-01dc09205c0e63a3ee5ff8ec03a5b2a5!}
{!LANG-160a9b956f6de72c2cfdb291d09ce5c7!}
{!LANG-e5c9234d1c3e317a9c32472acd3f2646!}
{!LANG-ec990a4a0caf08ee3cb967fb2d482096!}
{!LANG-0684ee7ba150a2fe5a0be40221f4bd9f!}

{!LANG-ec5e3fcf12c6060e3b4ff5966cdfbdca!}

{!LANG-48e454a1607aa826035e392666fad491!}
{!LANG-66dd41340032031c3a208156da3f2398!}
{!LANG-691ece3335b7c728d95200589b55f362!}
Pancreas
{!LANG-275d28c9e01e1139bbc224a29420cf91!}
hormones
or
{!LANG-613f702665e5201bfa06a55081440561!}
{!LANG-3cfb81b02aa2ceb3267a1b1d4fbdbc11!}
{!LANG-9bcfd4cb54167eabc70e89d45854ce58!}
{!LANG-163841677368dc8b935375488eaf26bd!}
{!LANG-e09168ad4d29d57f0d58cb9a7e483d9e!}
{!LANG-92c41e5920839333f814cd1e5a807ba2!}
{!LANG-5faa7eb66b5a9ec5922ba078fa93ba3d!}
{!LANG-3540aabbcef15f4bf345a823f6cbf98d!}
{!LANG-fe6caea3b0e43fde930af49c26f30a57!}
{!LANG-f993b6628f911a62e0f171e512db27e8!}
{!LANG-9bcfd4cb54167eabc70e89d45854ce58!}
from
{!LANG-03116366fe9234f341c0734b365f97f1!}
{!LANG-8cfad4a160e8cdd13eb9fad573a06462!}
{!LANG-384bf861b01a904a2effaa82f4ca00b3!}

{!LANG-4c687ce172461f3a06f5eeb9dfbac48e!}
{!LANG-19cbd81d4e33ef3e0009eccb46ad1c3e!}
{!LANG-6f4c4e4e8c3efe6d30559053f0ac66e8!}
{!LANG-0dd42ba04220ecac8cb86047c3f2cffd!}
{!LANG-6b1a18079e9b2f9893ffc827797deaa5!}
{!LANG-2531932a4cd11b2f75518f6f184b530e!}
{!LANG-b13d3915f7ea09e499beb3ccb0529050!}
exocrine
{!LANG-bfeee57878762624ae2600a32ebb5e1a!}
{!LANG-dcb2a17176c54bd0bc5f9859e33162ed!}
{!LANG-84190a725ac01b5b8ee0de429ac2afe5!}
{!LANG-ba8f17222b521e830d96b7438f2eb874!}
{!LANG-9959bb82cb41d0960b8961effb36d505!}
{!LANG-e6b267feba7d0e4f976aba0b01f1bff8!}
{!LANG-ae38ce19a9fc62022d52493a51738ca0!}
as
{!LANG-25a4865d2f164d79fdec79bec3729427!}
{!LANG-3f8dd1510d352da9cbc33d263cf22936!}
{!LANG-bc070df52a6ac9db543c02d2fe95e73b!}
{!LANG-9747e96884353c8ce0e4f8d35d418b91!}
{!LANG-25a4865d2f164d79fdec79bec3729427!}
{!LANG-b51b4934db707d8d0efdd32b1e32d942!}
{!LANG-23a13b1662d305ca82a38859f31ff24c!}
{!LANG-07f850a48c4d4c6a1eab80c4b7d7990c!}
{!LANG-2f5f681068c2d107e9c1f7c3e7f50076!}
(<90
{!LANG-fe61ed109325c031bb006b0755301dae!}
{!LANG-02b71575bf900e9753aa608bc4975d7b!}
{!LANG-16df69af1108011871cdc9e6ece43102!}
(>2
{!LANG-a54370922e443eefe0e012a942b723a5!}
{!LANG-a29ea55145e80d2576c2931901b5e30d!}
secretions
at
{!LANG-009a0760356de77644a78294af4ee83d!}
{!LANG-07f850a48c4d4c6a1eab80c4b7d7990c!}
{!LANG-2f5f681068c2d107e9c1f7c3e7f50076!}
and
{!LANG-5cc04b67b58e432233518143692f2c1f!}
pancreas.

{!LANG-4d93a48c70d3c6a7a3776bbb66a0d90d!}

{!LANG-b5df3ab7f4258da7728b4afce29507ad!}
{!LANG-b378490da3d1b71c0dbbe9d46969776e!}
{!LANG-910aadaf689c12aae4a82fcff1cf0bfe!}
{!LANG-11cc49eec9ad6a1467beda9852e7ec55!}
{!LANG-34b61a4666ee2c6f4ad6ab7e794dfc3b!}
{!LANG-4c4a73bdca64302d607b73f7f3ad32e2!}
{!LANG-73306d5c650b60de951f7de357e420ad!}
{!LANG-c52d070fa86c72a7c5f0ec16588d0234!}

{!LANG-651bbb3a3846436b04c589a86fc4528b!}

{!LANG-07ea06ae6944aca970cce33c805dcc98!}
{!LANG-27ad0f387591d80ac1d230cdd0a6e10c!}
{!LANG-72123b2ff416af0ec8f42b935fb071b0!}
{!LANG-30ca134730c534a7280fe31a68c10d77!}
{!LANG-4e79c454409f5f569f50c50d99e5999c!}
pancreatic
{!LANG-01546b3b0703750450b34faa72d12972!}
{!LANG-851e4683d9056b1f3f7551e5d5ef2335!}
Total
{!LANG-2df0ac49cd405be1181adf5f605555c0!}
{!LANG-ecd91aa3b45eaf1c406202f0fc1db9d9!}
{!LANG-b2c027cb7d93f7bb699df461a59f93c1!}
{!LANG-7d12c8a2d9baeb5284f958b98aac1199!}
{!LANG-fbaee65a237edc7b6881ebf8f10406dc!}
{!LANG-714fbf56248a65db98771389ecf7a4e4!}
{!LANG-354e3c05947987a8c1475293875a765e!}
{!LANG-69dd68b9d91c9900d1934a7b719435cd!}
and
{!LANG-fe8be85f3cc200e0062701bb0ee00408!}
sick
from
exocrine
{!LANG-5024c04aeb925c8b52d15c065a5510cf!}
{!LANG-7115fdf579cebb1e95b9fd2f06cabaff!}
and
{!LANG-e1efbe756c2b403c4ea41cd12c55b487!}
{!LANG-568b3fe5b1727f06e056f32116e9f7fb!}
{!LANG-a5eef58dbf4a51cac58c55f80f91e752!}
{!LANG-568b3fe5b1727f06e056f32116e9f7fb!}
exocrine
{!LANG-4ea84f7fd9f62da7fca44f74d130d552!}
{!LANG-49e5678daab713dc97c917438a1faa92!}

{!LANG-1bf36c45cca8150f47519f017f41b955!}

{!LANG-6db4f53eda205ba3c80a9c1780155890!}

{!LANG-4281dff0b5a678fdc921e7c6bee601b4!}

{!LANG-9d9859548836d1e638d12ad9ff882077!}
{!LANG-697f4787a16ec976f679e47f817eab3c!}
{!LANG-cc795fd88744c1b57b8e4d2afef9d6c0!}
{!LANG-b02126e0ce581ad3858fc0029e64b916!}
4
{!LANG-9bc496ecab1e174964d04d71f5b550fb!}
4
{!LANG-6c4990c583a585ac3f0ddb59823ca4a1!}
{!LANG-a504d41add0219331c8bdcf8ba922ffa!}
3
{!LANG-468d48ea3d2298178d22d886a22f2040!}
2
{!LANG-a5ee70224dd162ad58ce5a5ba71441b3!}
2
{!LANG-6998d7d60f0ed038d56bd8048324a437!}
1

{!LANG-4404c03853cc294a36d42031ba2446a0!}

{!LANG-73b6bda73c921e206fafb968cc2bb2d8!}
ERCP
{!LANG-2632a9695b546fa88b0f756c9c6d1b4e!}
{!LANG-68edcaf6fb446dece413e2573ac6909e!}
{!LANG-19776fce337ce1fa28cf432cccb328d9!}
{!LANG-396e328e506bb3ce832033d48ab83698!}
{!LANG-f798204788a6c2695e6047450dcb1c7d!}
{!LANG-dc345dee1bfcd7e54a9573a6ad2cb88d!}
{!LANG-0e03c856bcc51fb6c1f2bd59859803ca!}
{!LANG-fd95e0ec7ab2169464df8faeab869c1f!}
{!LANG-6b2a2c44e3fe4f92e1fb25593c0e1e41!}
{!LANG-e08e07e282898747ed5f99ab045f9ab3!}
{!LANG-77f212bbe8f75d57e449e1e4f1171615!}
{!LANG-7714cdd0e0fd7560900fe271b0a8d8c0!}
{!LANG-e84a7af418f9dc5922252a07269040d5!}
{!LANG-920a190fdd452253db90f288c58dd01d!}
{!LANG-ed9f256cf8f160a25d3fccf8feddfd69!}
{!LANG-5d9bdbf806ec170d79e35ce89383b722!}
{!LANG-77f212bbe8f75d57e449e1e4f1171615!}
{!LANG-571f80c52f1224466b6d42ba2a021b91!}
{!LANG-41e64ed9afd0f7d0bf1838a0c86eb1ce!}
{!LANG-3603ba4aca6b43a63221b1a4b8e50bbc!}
{!LANG-1a5a20215c370678d30a6a11e3158701!}
{!LANG-b0d1b1b15d06818ff19970b14851b2d8!}
{!LANG-86ab03bc3319cd82d2952010899047a9!}
{!LANG-3ff02da31dd7944218ae204a6dc27903!}
{!LANG-51049ab253b30666022e29b05c49e73c!}
{!LANG-2a3b735137bb47a4891f2ed9326aa165!}
{!LANG-f5791cb3eb7bbbe86d04641a26a2f23e!}
{!LANG-933bc1fa494b0dd3d6816a5063f5cb4a!}
{!LANG-f72e52b2ebb1b9d386ffadca115d18bc!}
{!LANG-451ff0fd183108251dc09bbf26660d7b!}
{!LANG-7b40ec60747068f70105b93bceec67d1!}
{!LANG-844ef61ba228067fa34d9c95f81356ed!}
{!LANG-e00c7f765117efbe454f75cbed7f6d8e!}
{!LANG-909f01e11346347848335e9bd577895a!}

{!LANG-1c45091f80b8e1fdce034641bdab9a75!}

{!LANG-e05d9caa9686eee8b32781973fa4c8e8!}
{!LANG-f6a33c56bbdd30fddf19eed8f2da8237!}
{!LANG-83d6a1e8f0c7b17d5531ee8b64600fdc!}
{!LANG-00e5cde4c6686a2d64a10e1b726376ae!}
{!LANG-99f867149dfa4b7592769e7877193cf4!}
{!LANG-0a0640de0983e419b579ceaa434a7b21!}
{!LANG-be1a1654ad68bde6d696e4e807222aa2!}
{!LANG-d8b680c60658fd549a20bbecce768b2c!}
{!LANG-07a9fb4b08c33e137999ac60822dbc73!}
{!LANG-305b81c3c38504ef13f39ed79af717a1!}
{!LANG-49aa640ada6033d97b32735ade02861b!}
{!LANG-4e69ec2f3c5ebbb0c1446642661f6826!}
{!LANG-6e55e88a7b1a2aabc4524e5b02e8b062!}
{!LANG-6ce170aad7b672e8f09c884b4feea88c!}
{!LANG-465ea4b557626fdbee24c0c6b4143c8d!}
{!LANG-c2dcaced6e307027fc0d9e4fbefda479!}
{!LANG-2bc63fe60162894f8c8306b0d7c02813!}
{!LANG-d9508056e5b2674759b5ed594b0b5eb8!}
{!LANG-adf0b8f741bf4fb9af2ea78cd315151c!}
{!LANG-baa83c788311c03a52ae23cbae19031b!}
decline
products
{!LANG-7c656843715531a49b307a64e71e03fa!}
{!LANG-8cbb58ac8d1a4fef8e501a704ea75c13!}
{!LANG-9aae0587cbcc05e8a2683221e5bf1c1a!}
Pancreas
and
{!LANG-d27d7e8de12cd7528cc56c55d5eeba1a!}
{!LANG-01c77aa4dca8a931b8afee8b4e593377!}

{!LANG-3b2905fd9bc26bf73252efebe98fe04a!}

{!LANG-d22f739b906ceddf6ab0006dd1411d52!}
{!LANG-ecf752230610f6d856a99f2e99c61aea!}
{!LANG-f1055efb9413424a3d0d5bd1ad5a166a!}
{!LANG-ed288d2b890f9f0bcb43290660e39b19!}
{!LANG-7e316b9f2bfaaa8886d37715f94bbce4!}
{!LANG-d87b1a1b6a864e46f2140cb1bd5bfaa0!}
{!LANG-da9ba91e30b8f48485898e6c15d6d857!}
{!LANG-f588e4b39dd5dcb9ba2ac10044994f45!}
{!LANG-ef61193da909b432605083f11f6bda74!}
{!LANG-c948dd3eb42a5be6d7d7ef5d331614af!}
{!LANG-fbd926dcd4038e43dc368b1437bcefb5!}
{!LANG-b7e1017457d9954b798abfea91a7d45d!}

{!LANG-1e27badbe0570aec128b993e5cc30972!}

{!LANG-0fa13abab639d978c3d74d42d226c53a!}
from
{!LANG-4055ad2f7e5a210ab286223310a10b3d!}
{!LANG-11e6f27c85415d771dd790f900a81172!}
{!LANG-51d151cca37593c153cf22758e1c97c4!}
{!LANG-5214935f3aef8f19bc6ede10bcc3b0a6!}
from
{!LANG-3424009f115e2ce1cc78e2aa8c3ac913!}
{!LANG-820c436aa60f44b9fa46dcf20d6505a9!}
{!LANG-0570db860b342f1d22eb6566297e1351!}
{!LANG-f93261c861ab0eb731c1bb5577936846!}
{!LANG-4bb00b231fa132c6867020e2ce3a494b!}
{!LANG-1641a1ae8c8ec12f4f34de793c7dd7ef!}
{!LANG-94b4cc7f416ca10a8c77f229055eda96!}
{!LANG-1521239cfbfe41709b703b11e0017f58!}
{!LANG-f8e618df8043792c5ccf9f1f3c625753!}
{!LANG-bbde1620cf1b6d527d43d36134b0c8f0!}
{!LANG-e72a5c9a804a41d2fc0dd5caad2b46c3!}
{!LANG-9e675009927df5e870223c8b8a145f7f!}
{!LANG-1ad160ea370eec5cf9bbbf7cfbaa5237!}
{!LANG-af8f672181ee53532ece0f76c8c0f51d!}
{!LANG-60404aaae78792bc42bcd2ae7c66d6e1!}
{!LANG-37e4cd280427c01925cce754b627064f!}

{!LANG-8fa19d79556df1c5201efe22adaf62a8!}

{!LANG-492f10f283c4395a48424b737304f9ee!}
{!LANG-11ac0401736147873dc0c1ae324b2fa2!}
{!LANG-e79bc7cfe69dbaab073c8adc1469ab57!}
{!LANG-6978a596ec1ab1e1d7d5f71e7d848587!}
{!LANG-e886c48968a30c12f4ee965d21b01e80!}
{!LANG-48055437075bede1c61c8e845d89fdbc!}
{!LANG-0d2c75f78d6f7f495e5af0cb13abf39f!}
{!LANG-e1f0cbd258ccf39bd8b871ad83047bbf!}
{!LANG-fa232802e9488821525e1817feb5a649!}
{!LANG-eea5f79623a25051f9a5cfb53e48f6c9!}
and
{!LANG-fa053fe669874d81b31eca4b2a7ed27a!}
{!LANG-87ef71bd20684f443f0bff049c3d397c!}
{!LANG-305300cad53a55270f0d9302dbf03078!}
{!LANG-9aac06e6d46fb6631d6d1fc082063f28!}
{!LANG-901f1b87113dbc3ee1af2dba360b7b5c!}
{!LANG-d84ddcb3a34d17e64fe4d842efaa1836!}
{!LANG-0842bab3cb436b3884184a2210181549!}
{!LANG-c2f289c18f9c0c917e78dbe3efc37d46!}
{!LANG-984653e65b1a0b26cc4a4b90a313bc17!}
{!LANG-e5adbf5627fa57a4a5e25254a83020cb!}
{!LANG-ffc63c5d9cfe54c99ed492eeb5327f37!}
{!LANG-e8149938235b17d43b553e4b6bbbd3e7!}

{!LANG-6b26dd485022aba87e7f72825930ecaa!}

{!LANG-3b73ad45407ef44a2d10dda782c43f20!}
{!LANG-9b736ed5c2ca62623fe9e29e8953d2b2!}
{!LANG-6ea85a829a780c1d2c7f37aafc0ff838!}
{!LANG-53a7369b92fc2d2d1ddcdab8c5c76876!}
{!LANG-a13558045aa2e08348b1aad80719c7b6!}
{!LANG-dadee09a1d8f5287e768a10144bc49d6!}
{!LANG-de475432abb56ddabcd01a3127c5c468!}
{!LANG-1c4df50b7ea0c9c6a9ddab402b628a09!}
{!LANG-70cc57b7a205685e1fe1eba0767dadf1!}
{!LANG-de0b83a35cd9fee6a8e06adf91a50575!}
{!LANG-e3930cea59aa6fb47979d51ac4937062!}
{!LANG-686953cf5e9f9e4c543d6896a8645684!}
{!LANG-75982b2745c232568b34244182b287d1!}
{!LANG-d2f6d7989769f7d9ec68c9c112c702fc!}
{!LANG-6e38a53bb4b684e31673be3d8fa5a633!}
{!LANG-6d98714c53ac7f7749717beb6af19c22!}
{!LANG-be6158549166e43a896e5bb9f4e55683!}
{!LANG-d4782d7865024341bbc868cde0afbd4d!}
{!LANG-2ad456de9cb0f27546c5086bf365351d!}
{!LANG-41a10b72e518ac0c88a96fd89b83a344!}
{!LANG-5faf87ab3b2ed55f4dcdb3c888dd45a8!}
{!LANG-e360ea995a7ec7dbe2fa19b59ecd62c3!}
{!LANG-83b5b2a1236b8600c07b56d5c1bd8336!}
{!LANG-0684e04da7a637e5cd11cd91eeb9a8f7!}
{!LANG-3e5188879c5928159c090e2da15070e1!}
{!LANG-21de43ef355aaf1dbaf82b2fce0a606d!}

{!LANG-5858923f6f6cefb87268624ffa26dff7!}
pancreatic
{!LANG-e87a0d4694c14d6aabab74513c775fc8!}
{!LANG-229bf868d54e52edc2404c8578e18c7c!}
{!LANG-889dcc0b7b74e394f9480ed3dd3d8b69!}
{!LANG-3ece696934a03d3f46e22209ecf18d66!}
{!LANG-7321d416179bdf02d9fee5e498b3f56c!}
{!LANG-6790979bd50a9bc5c0f250400efb54c3!}
{!LANG-5f411215ac9482afd3665800f279e95f!}
{!LANG-f9e0ec2f8176b4fae439bdc1e1b03ff2!}
{!LANG-3d525645465788928f09c66f05fd427b!}
{!LANG-ba11ebc9c1e122202d665159703fe01c!}
{!LANG-676c6a934ad821fc99786793eb49b419!}
{!LANG-759de569358fdb3fb0f5f24ef82538c7!}
{!LANG-c8a91a94af335fad66fdcfd2aa77df77!}
{!LANG-55353c59b2d6e59766c20886ca10058c!}
{!LANG-7d3b1f8585933b003a9e1aacba3b660e!}
{!LANG-cd54ce748db6816742e3abfe4e402e17!}
{!LANG-6b553488458213776b28b8859c75d2f8!}
{!LANG-396e6c569f10c8e80d9705a65de9327d!}
{!LANG-ca43462f593390486f19082bbe213237!}
{!LANG-9286bba2a90082ca152ae0153db3cac7!}
{!LANG-ab2af3210114b43d11283e0bff04418d!}
{!LANG-f6d409462d61237cb551c538a78df6e8!}
{!LANG-3769effa2d789b2975d988d58d9a8fec!}
{!LANG-28360b6820e31470f9a3090aeb91977c!}
{!LANG-ebe449ab620977fbdb308e0c3b981026!}
{!LANG-4eff588502fef7671beed2c3464ade7d!}
{!LANG-5a6eb48bfcde27625de1bac0efba2d09!}
{!LANG-7fff14626d886abe33b1d3cf753c9b1c!}
{!LANG-347bb5ab4baa24413ef90f51807ff53d!}
in
{!LANG-e9416771d6477e16623e6a51469be887!}
{!LANG-204c806d883e7923e07933660d292a22!}
{!LANG-b6a777762fcafcaf2b688e8cf5cc8d2b!}
{!LANG-f4cac981d445846cbc03bf519108779e!}
{!LANG-26f326290327345f715f64dfeaebc50b!}
{!LANG-b15ab68574b41c1b60dff3973642c9ea!}
{!LANG-21e1258ee64040f40a866c3835f697d9!}
{!LANG-0f87f7a10ecb5379a518ff12175ea0c9!}

{!LANG-8fd42515d09593445fd54b22d26c9435!}
at
{!LANG-a3d54faa8097fc934d9ad3120c405adc!}
{!LANG-71130c3200a6c7fa68b6cf7f04a28674!}
{!LANG-f515fd68068fbde5bbb4e46638a7ee86!}
sick
{!LANG-5725333bf4e80a5f3327721c2313823a!}
can
{!LANG-5cc41d41101eb29b06e4b243725b5762!}
{!LANG-e07b62f06cf2a771f45573fb622333d9!}
{!LANG-c94d0311a980b0538098d4b734e637b9!}
{!LANG-cae6832e9e6d29b4d78e2e195eedb95b!}
pancreatic
{!LANG-e35bc59124e9563e7e553513048d2506!}
not
{!LANG-ac5e0225a85ae08e9dd974e6e037342f!}
{!LANG-a48d30f450d88a095c42987a11aebdb6!}
{!LANG-9aff654a916c7898a7b4cea382402333!}
{!LANG-2c458951f8f18c8a582101e758d112d7!}
{!LANG-df566997d65dcf374d29f22342b26949!}
{!LANG-157a6512e9ddcfff402fcee9fc8d9065!}
{!LANG-4662d4f823943d284d3040fd19d01ec3!}
{!LANG-f0e30a9f9424924590058e65ccae032b!}
{!LANG-b8d6541c444cc350549947182eedc673!}
{!LANG-1b4fc11e2564de7ed3eb3a5fa5ac5cb5!}
{!LANG-fca9ab2facea407f7d651243b56921d3!}
{!LANG-e54ee5bc679ff8271883df7d064cb973!}
{!LANG-e4089ae26ea57b97d359cd36345d8284!}
{!LANG-02589f80e79b0f6509b7ee0ac840c4e3!}
{!LANG-94275cd349b863b0e5951beeeb002647!}
{!LANG-bcd5a8cb7297c42641bf5576535476b0!}
{!LANG-c3a8468c2109272b5b2ca281a6917c2c!}
{!LANG-6f4c4e4e8c3efe6d30559053f0ac66e8!}
{!LANG-22b98291c25fd787866bbbc6f0f61de1!}
{!LANG-af8f672181ee53532ece0f76c8c0f51d!}
under
{!LANG-71578e8912d2b1ff559f34d5212d5759!}
{!LANG-5d56db35be10737aa3bd879d3fcec650!}
Ultrasound
{!LANG-54e65659e104934ab98cd1091b819ca0!}
{!LANG-735ca79900d5b3aacadcfbcfeaaba29b!}
{!LANG-854adc154478c5adef8754d559f4e483!}

{!LANG-89c84c355bd0d6c15b81490edcf54f7c!}

{!LANG-a1d76f5604343ac3dee4a4adcbfbb853!}
{!LANG-9d39442d4ec672b7ecbad997639c428b!}
{!LANG-e1d730bc02b452dfc4fb3f2fc38f0d09!}
{!LANG-43a0c3e82878b8a223dc5f24078021b4!}
{!LANG-e4ba33fcec456abf6a7eb75b814b9b6e!}
{!LANG-1a87f0997a34d9c3c021dd66105ba335!}
{!LANG-7ebbe809d42f75acb9ad02d3128b47bb!}
{!LANG-7d61507f3925d43c19a2332cd036a413!}
{!LANG-b0da1061ab08145114c34688ae18e250!}
{!LANG-f7ea85e5231d4d5f3f1892e1496b3a86!}
{!LANG-02db194705c23c3d6debe56b67671d08!}
{!LANG-06318ee9b790fd679d071bfeda510f51!}
{!LANG-fbebd361cc15fff2a466a2c279bf4251!}
{!LANG-1d5cbfde3024f3b5a3851f9d0a5da22b!}
{!LANG-4e747831a7a9bacbe49338b8f8701479!}
{!LANG-903fc1328d8226e07e9ae1c0bc43fece!}
{!LANG-e44f6dd8b3e500666383d833542107e2!}
{!LANG-ea2549f7484c66955df654ca8d6bdb0f!}
{!LANG-eb2fe57a2c20df4b44c4160fbbbf4ea5!}
{!LANG-d709d54e864a7c28fb28d7e878a582b6!}
{!LANG-ab3f1cf5e604f6580e50db78e368784a!}
{!LANG-19e9c5405d30195d8f145085a9496331!}
{!LANG-baac24bb4777c743fbdf9fb93fa6c936!}
{!LANG-8c753b140052476d20e2d2672e1db6de!}

{!LANG-1c51dfa22cd88af7dc0e78cbdf273f8f!}
{!LANG-c00e05865d5ffaa572485315c9573ad1!}
{!LANG-003ed48c98ea83e2e82dbbaa2fc7fb10!}
{!LANG-83fbf11a3075cb381ca363247cce3495!}
{!LANG-9fde4663380cc77a08b48c9d2791d3de!}
{!LANG-4a2f70e21ab1afa9bbe7c1ce0fcddabc!}
{!LANG-a6f387676fc1583531dd075ae916fe02!}
{!LANG-5f02ab207af6d1d76143951dbbb5b258!}
{!LANG-3a095d3905fba45bf2ca40e743072e51!}
{!LANG-cbfebc30758d583e2bb52126a029fab8!}
{!LANG-4b9ae624e5b6708b7279632bb8cf4e95!}
{!LANG-78cfaa0b6f63d80d53cdbaa42440582a!}
{!LANG-5bc6e23c4031dd2f245108d11599429d!}
{!LANG-dfd90c446ac191eccf866f25fabdf564!}
{!LANG-0e53b4eb2b58d66c4a1422e987f41c58!}
{!LANG-e10c98afbb32e3e5cffea017eeccb989!}
{!LANG-495c2f2bd7be1093cb05d90bb2017c71!}
{!LANG-732d1f35e8a156605e5e979fde9a73e2!}
{!LANG-3b9dab0a5f557f23782724a9ae1844b8!}
{!LANG-af126c47c08e8b831c6cfc7c0a56cd36!}
{!LANG-bb818d4cf9954536508063f5ef6dcf2b!}
{!LANG-b71cc1e8ea81e41159a7667ab50fca66!}
{!LANG-4dcaf8f9dd25d4ba30f0ee61fc00a46e!}
{!LANG-2a4637d452304327cd15b6630d32d5c7!}
or
{!LANG-62fea308e8d9fd16b909045d7cb8762c!}
{!LANG-52e1218371fab3fd0494c33960aa9a38!}
{!LANG-5a7692e4c9306d17186c84490e73984d!}
{!LANG-1d62650682cefd42749740c40a4b4558!}

{!LANG-f22b3f2b02b9dc013d1decf268332ac0!}
{!LANG-4c40a66d382b5ad4706ead8c2c006127!}
{!LANG-5dd13ecf2be6168dbe0b21de02c735bf!}
{!LANG-5de0bc81466a341dced62ba671db14c6!}
{!LANG-310d2e032fce4fe03d156812bfefef35!}
{!LANG-d605d08e6e0a8fd27e912714c4c7c91e!}
{!LANG-958451580d48bc8eaedb7c95291b8612!}
{!LANG-31557576409e7438b81102de6557bbf3!}
{!LANG-730460712c90ee4320f0b75be9cf95f6!}
{!LANG-369aaaa2d37fca141992cadd3bed5a8f!}
{!LANG-a4fd85a3168b236951c49cb57db855ae!}
secretions
{!LANG-664b591d1dcf60df1c76fad330c172eb!}
{!LANG-51e4854029ba54d40fe27d571cfd74e4!}
{!LANG-e2dc2cce1538d5a6dc06f89cb124b3ce!}
{!LANG-89d1a5f5baff2d54d5a0325e309412be!}
{!LANG-a91ed9eb54bab769804b6fe1db930fac!}
{!LANG-56c04514b320ab2a7aaaeef119ddd832!}
{!LANG-9999e12e3e441331ef52bf4d845d007e!}
in
{!LANG-3eea470e93e767f3fdc6a728458504b1!}
{!LANG-7c2b14c4cbfc80959000883b7846efac!}
{!LANG-106301eb64aec44c3eb3550eaa86ab34!}
{!LANG-dcb5185b13ce1d53cd2ddf54689d427f!}
{!LANG-710b4fca820a243b59c478bf6eb3d112!}
causes
{!LANG-eee67c25dbcadb808ad718ce2a9ea874!}
{!LANG-e06022c0ebea4a1a383ffded3a6da327!}

{!LANG-2dc20a15aeae1e35d73fced96bfe9cf2!}
{!LANG-135caa937adece37772be51cde0d6d70!}
for
{!LANG-d85b0886d54dde45b1b438d3ee109951!}
{!LANG-f8927b986b8e5f6fd7f8dd0f4b2149f5!}
{!LANG-7326f6ac4479b585d9af28d10e3f895a!}
{!LANG-4a13e8e8f62d79107a27334ff301dd14!}
{!LANG-d45e6edf9766bbb5f96398aad53a4205!}
{!LANG-ed75a8813c645c50d9362fa2b82e7155!}
{!LANG-efd298c2a4595c9b00bc4a4e3bd1e87b!}
{!LANG-8c8aa737d709825ceb13a858ece1b66e!}
{!LANG-5ff6b62a22a8bce05542e00ce9ff8c15!}
{!LANG-4122e663e36a3679e2f23c326827edfd!}
{!LANG-7ebbe809d42f75acb9ad02d3128b47bb!}
{!LANG-da06a67259c81b22c6d8f1b6f22d0770!}
{!LANG-f12bfe7d0900833acf240106bd255b36!}
{!LANG-d4b91488d7beea0e5d0569ba9dc8d42f!}
{!LANG-24a7c344d462b78636164802cb3a2382!}
from
{!LANG-991c4a610bd2993a740763db87e9af03!}
{!LANG-5ea2a2502788b1035b5ef46989cda7a2!}
{!LANG-815327e59c1826701201f31d7997b626!}
{!LANG-455b66c0d6637de7ffbf896570092a23!}
{!LANG-d85d5d8a3ab6f9ee95c13bf9a54a108e!}
{!LANG-ee5ef503dc3369b0d34938ae97b6c412!}
{!LANG-5b43893b341016e63fc187a350531cd9!}
{!LANG-c8bbdd5227a7b79117ca03d490b192f4!}
{!LANG-5e359a73e22a4e348e40cb5cc91b704b!}
{!LANG-fc6fac1508d254d1e2187a9496c3e54d!}

{!LANG-f8a52895e1b8da35e586727a78e4ab83!}
{!LANG-b13d3915f7ea09e499beb3ccb0529050!}
at
HP
{!LANG-e084114d706f75b765f41084ebf6c44f!}
{!LANG-20ace8e3075652336b2738546e975623!}
{!LANG-3d9cc88cd22f9be9350230142bf45886!}
{!LANG-2ba974801622b413ef20fd97b38689de!}
{!LANG-72b9fc49bdfbe1311c1d209695395d8d!}
{!LANG-a1908b6d8842ea9237b25b4884183760!}
{!LANG-ed15983c12b0fa296b798007bfc341c9!}
and
{!LANG-0afb04656dfabcf337d75174b48c3834!}
failure
{!LANG-7b819d3f91b1bfca05792b943dfda16c!}
{!LANG-8b83faf81a64c1779eb3eeb2597fbcb2!}
{!LANG-0b7ba613db5f85f3a6698e4f845df364!}
carbohydrates
in
{!LANG-e223f0810e31ee09f0a157da1daf5a34!}
{!LANG-73147cdfa9e8e8843736ecca15ff4f80!}
{!LANG-be44eeca349f98502ffcd14d26f924ec!}
{!LANG-87fae77c6613cc3a366996227dc81ff2!}
{!LANG-7ff541fee94cead82692ef2d3df20b8b!}
at
{!LANG-abdb72bb7f9bbbdde20da4e6603601bd!}
{!LANG-7701ca4fddc5a3b948cca730cdb09d9c!}
{!LANG-8c0111aac1a4bc75433692b302e881d8!}
{!LANG-3d94b40f3b83185e9a1b36945de8f381!}
{!LANG-d41f4e30adc56702a5d5bd89523dc09a!}
and
{!LANG-943ee5c15c6cc6cb17790dacc28a7b16!}
{!LANG-194c3afdc15b5b8fc3d9de94b0542511!}
{!LANG-eaa9db51b47a313257c1db23239aa52e!}
{!LANG-a3326ac5ee8e781f21c0b891c867237f!}
{!LANG-539395626a9478bc5dcc026353e97282!}

{!LANG-48449eb766d2ef0e71a965d0d212c0d5!}

{!LANG-d100304345d1e56b77db8ee6757937dc!}
{!LANG-908bb01cdf60eaf09b6af82b1963a358!}
{!LANG-1f0d8f60f8ed2ddacfd4f2f6ae2fc8df!}
{!LANG-36713ad2ca929cbc21c5aeb07138c610!}
{!LANG-ec92d93636571cbf2d7635ade1280134!}
{!LANG-3933cc851e596d1b99464f9f204d4882!}
{!LANG-34a991722cdcb8d2e8845a44529e2874!}
{!LANG-4de0971d2607308bdb36f65b4977f43d!}
{!LANG-653015033c37c22fa237cc89b719b573!}
{!LANG-449ad41e9798998974a72c7848ea304a!}
{!LANG-82edeafa00fb546ce28cecb1db33f901!}
{!LANG-12521df1151a3dc94075328b36ddbcf6!}
{!LANG-1a8d087d8b05b9180d4905527c15855e!}

{!LANG-9fb6f1af1ccb7e14bdcf069254fef905!}
{!LANG-7841d102fd1a7a15f06f846b3651eb1d!}
{!LANG-2e50b456c12ac6c13a9b50f2f9cc9d5e!}
or
{!LANG-bef95e8c7bf5dc1b776a15e55df9e003!}
{!LANG-002ffed617760d643cc7b0fe02aeef34!}
{!LANG-eab5548ffb81524fa4dd16dcb8b0b225!}
{!LANG-765a216baa60c8c8b85cc98a3907d0c9!}
or
{!LANG-67429b9594507311e6d90b1880fc0915!}
{!LANG-13e0e13d906553f80132b0198fc9ae6c!}
{!LANG-8b913f8a2043ecaa7c9e55d0551d1bd3!}
{!LANG-4d8523597eb1aec21360ce82d3b924f0!}
and
{!LANG-be3dc454b384df626be9415be8015f1a!}
{!LANG-040e834cf419695d3efc0404d107fc32!}
{!LANG-ef454b0374758f6623582ce105a01ce2!}
{!LANG-e80468d10069c4b2768cd552306ca205!}
{!LANG-2ead22fd478ca3b5d8e9a9ae0e19b2e4!}
{!LANG-759514f6c926e236031ad620a0c03428!}
{!LANG-bb85c2d2e6787b0cfda5a4bb2270fc5d!}
{!LANG-4d8523597eb1aec21360ce82d3b924f0!}
{!LANG-5d91ff89098ca133983cf28c26b2ed35!}
{!LANG-be7cd21a05d3f91d09a23609604436e6!}
and
{!LANG-e08f3778c6db7f5cf7a49d369b1a9af5!}
{!LANG-ff84b8fe805414fb8332ea9323df4901!}
under
{!LANG-7d25b92a0d81fa58b2112ad5c940ebb5!}

Treatment of chronic hepatitis B presentation. Chronic hepatitis, Department of Faculty and Hospital Therapy, Faculty of General Medicine and Internal Diseases, Medical and Preventive Faculty, Chronic. Cystic variant of CP

Presentation on the topic: "Pyelonephritis in children. Etiology, pathogenesis, clinical picture, diagnosis, treatment, prevention. " - Transcript:

Chronic pyelonephritis in children

How is chronic pyelonephritis

The main symptoms

Features of pyelonephritis

Treatment of chronic pyelonephritis in children

Treatment with folk remedies

Presentation on the topic: "Acute and chronic pyelonephritis Completed by: V. Gavrilova" - Transcript:

Similar presentations: Chronic pyelonephritis. Urinary tract infection in children. Pyelonephritis is an inflammatory kidney disease of predominantly bacterial etiology, characterized by damage to the renal pelvis, calyces and parenchyma of the kidney.

Pathogenesis

Classification of chronic pancreatitis / Ivashkin V.T., 1990 /

Clinical picture:

Complications

Examples of wording a diagnosis

Laboratory diagnostics

Laboratory diagnostics (continued)

Imaging techniques in the diagnosis of chronic pancreatitis

Ultrasound

Pancreatic cyst

K T

Treatment

Treatment of an attack of chronic pancreatitis

Long-term therapy for CP

Long-term therapy for CP (continued)

Classification of hepatitis:

Reasons for development:

Pathogenesis.

Clinic.

Clinical syndromes:

Diagnostics:

Instrumental research:

Prevention of chronic hepatitis and liver cirrhosis:

Clinical anatomy and physiology of the pancreas

Innervation and blood supply of the pancreas

Exocrine pancreatic function.

Secretion phases

Humoral and nervous regulation of the pancreas

RV hormonal function

Definition

Epidemiology

Etiology

Pathogenesis

Table 1. Etiopathogenesis of chronic pancreatitis (according to P. Layer and U. Melle 2005)

Classification of chronic pancreatitis

The most difficult section of the classification is the division of CP by morphological characteristics. The authors based these principles on the given

Interstitial edematous CP

Parenchymal variant of CP

Fibrosclerotic variant of CP

Hyperplastic variant of CP

Cystic variant of CP

Classification of CP by severity

Clinical picture:

Exocrine insufficiency syndrome

Table 2. Extra-pancreatic sources of hyperamilasemia and hyperamylazuria (according to W. B. Salt II, S. Schtnkor):

Imaging techniques in the diagnosis of chronic pancreatitis:

{!LANG-ec5e3fcf12c6060e3b4ff5966cdfbdca!}

{!LANG-4d93a48c70d3c6a7a3776bbb66a0d90d!}

{!LANG-651bbb3a3846436b04c589a86fc4528b!}

{!LANG-1bf36c45cca8150f47519f017f41b955!}

{!LANG-4281dff0b5a678fdc921e7c6bee601b4!}

{!LANG-4404c03853cc294a36d42031ba2446a0!}

{!LANG-1c45091f80b8e1fdce034641bdab9a75!}

{!LANG-3b2905fd9bc26bf73252efebe98fe04a!}

{!LANG-1e27badbe0570aec128b993e5cc30972!}

{!LANG-8fa19d79556df1c5201efe22adaf62a8!}

{!LANG-6b26dd485022aba87e7f72825930ecaa!}

{!LANG-89c84c355bd0d6c15b81490edcf54f7c!}

{!LANG-48449eb766d2ef0e71a965d0d212c0d5!}

{!LANG-6bc8d2fe18abb67700153bb7a0d2a733!}

You need to know