Treatment of chronic hepatitis in presentation. Inflammation
Patient B., 27 years old, nursing mother. 3 weeks after birth, pain appeared in the area of the right breast. Feeding from the right breast became painful. On the 3rd day of the disease, the patient developed chills, body temperature increased to 39o C. Objectively: The condition is not satisfactory. Forced body position, the patient is inclined to the right. The right mammary gland is externally stagnant - swollen, palpation of the gland is painful. Enlarged regional lymph glands in the armpit are also painful on palpation. Laboratory testing revealed: leukocyte count – 12.4x109 /l; ESR – 35 mm/h. Questions: Are there any signs indicating the inflammatory nature of the disease in a woman? Indicate local and general signs of inflammation, their pathogenesis. What is meant by the term “hematological syndrome” during inflammation, its pathogenesis The role of the immune system in the development of inflammation Pathogenesis of the development of a febrile reaction during inflammation
dystrophic liver damage with
maintaining its lobular structure.
Slide 3
The disease can develop at any age.
Duration of at least 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 process activity:
moderate.
Slide 6
Reasons for development:
The main reason is acute viral hepatitis B, C, D in the past.
Transmission routes:
parenteral
from mother to fetus
Slide 7
2) Drug-induced liver damage:
Cytostatics
Salicylates
Anabolic steroids
Antidiabetic drugs
Slide 8
Toxic effects on the liver are caused by:
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) The 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 functions in all types of metabolism are disrupted, its external secretory ability and detoxification function change.
Slide 12
With hepatitis, the liver increases in size, is moderately dense with a pointed edge, and is painful on palpation. As a result, there is a feeling of heaviness and fullness 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. Immune inflammation syndrome - increased body temperature, swollen lymph nodes, joint pain, splenomegaly.
4. Cholestatic - jaundice, skin itching, skin pigmentation, santhelasma, darkening of urine.
Slide 15
5. Minor liver failure syndrome - weight loss, jaundice, liver odor from the mouth, “liver” palms, “hepatic” tongue, spider veins on the body, fingers in the form of drumsticks, nails in the form of watch glasses, santelazmas on the skin.
Slide 16
6. Hemorrhagic – bleeding from the gums, nosebleeds, hemorrhages on the skin.
7. Hypersplenism syndrome – enlarged spleen.
Slide 17
Diagnostics:
CBC – anemia, thrombocytopenia, leukopenia, increased ESR.
Biochemical blood test - hyperbilirubinemia, dysproteinemia, due to an increase in the amount of globulins. Increased level of sediment samples – sublimate, thymol. Increased levels 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 studies:
Ultrasound of the liver and gallbladder (unevenness of the liver tissue and an increase in size are revealed).
Computed tomography of the abdominal organs.
Gastroscopy.
Slide 20
4. Colonoscopy.
5. A puncture biopsy of the liver followed by histological examination can be performed during laparoscopy or percutaneously. Allows one to judge the activity of the process and is an important differential criterion for distinguishing chronic hepatitis from cirrhosis of the liver.
Slide 21
Treatment regimen. Work with physical and psycho-emotional stress is excluded. A short rest during the day is indicated. Hepatotoxic drugs, physiotherapy and balneotherapy are excluded. During an exacerbation - bed rest.
Slide 22
2. Medical nutrition – diet No. 5.
Excluded: fatty meats and fish, fried foods, smoked foods, salty and spicy snacks, legumes, sorrel, spinach, fresh fruit, strong coffee, alcohol, carbonated drinks.
Slide 23
3. Antiviral treatment: carried out for hepatitis during the multiplication phase of the virus 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. Immunomodeling therapy has a stimulating and normalizing effect on the immune system: Timalin, D-penicillin, Thymogen, T-activin.
Slide 25
6. Metabolic and coenzyme therapy is aimed at improving metabolic processes in liver cells. Multivitamin complexes: Decamevit, Undevit, Duovit, vitamin E, Riboxin, Essentiale.
7. Hepatoprotectors: Corsil, Legalon, Katergen.
Slide 26
8. Detoxification therapy: Hemodesis intravenous drip, 5% glucose. Enterosorbents – Laktofiltrum, Filtrum, Enterosgel.
9. Treatment of edematous-ascitic syndrome in cirrhosis, first - Veroshpiron, Aldikton, and then in combination with Uregit, Hypothiazide, Furosemide.
9. Treatment of bleeding from dilated veins.
Slide 27
Prevention of chronic hepatitis and liver cirrhosis:
Primary: prevention of viral hepatitis, effective treatment of acute viral hepatitis, balanced nutrition, monitoring the intake of medications, combating alcoholism and drug addiction.
Secondary: prevention of exacerbations of the disease. Limiting physical activity, proper employment. Nutritional therapy, treatment of concomitant gastrointestinal diseases.
Slide 28
Completed by: student of group 141 Tretyakova A.
Teacher: Stepanishvili N. N.
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Slide 1
Chronic pain in oncology: modern methods of pharmacotherapy, MD, Professor P.B. Zotov Tyumen Regional Oncology Center Presentations on oncologySlide 2
The frequency of pain in cancer is 25-45% - in the early stages 80-95% - with an advanced process 10-30% of patients continue to experience pain despite the 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 the low effectiveness of treatment: Lack of knowledge about the pathophysiology of pain. Lack of knowledge about pain control methods. Difficulty in obtaining recommended opiates. The patient’s refusal to take analgesics or failure to comply with the recommended regimen. Lack of proper range of analgesics. Price characteristics of the analgesic. ! !
Slide 4
What is chronic pain syndrome characterized by? Pathological algic system (Kryzhanovsky G.N., 1997) dysregulation Autonomic disorders. Dysregulation of the endocrine system. Psycho-emotional disorders. Disturbance of circadian rhythms. "Pain behavior", personality change
Slide 5
“Pain behavior” “Restrictive behavior” - avoidance of situations that contribute to the resumption or intensification of pain. The desire to get the maximum and fastest pain-relieving effect. Limiting physical activity, food intake, reducing sleep duration Inadequate choice of analgesic. Incorrect choice of administration form. Failure to comply with the dosage regimen. Unjustified changes in medications and regimens. Polypromasia. Increased pain
Slide 6
“Pain behavior” 3. Mood disturbances: increased anxiety, depression. 4. Doubts regarding the correctness of the treatment, the competence of the doctor, the medical institution. Aggression towards others and oneself (suicidal behavior). Refusal or ignoring the treatment tactics recommended by the doctor. Increased pain
Slide 7
What should a doctor know to choose a treatment regimen? Intensity of pain (weak, medium, strong, very strong / unbearable). Duration (acute, long-term, chronic). Leading mechanism of pain (pain: nociceptive, neuropathic, psychogenic). Efficacy and extent of previous therapy.
Slide 8
Verbal Rating Scale (VRS) – 5-point: 0 – no pain 1 – mild pain 2 – moderate (moderate) intensity 3 – severe (pronounced) 4 – severe (unbearable) pain IMPORTANT: present the recommended criteria to the patient Subjective scales
Slide 9
Pain 1 2 3 Strong opioids Weak opioids ± non-opioid analgesics ± adjuvant agents Non-opioid analgesics ± adjuvant agents Pain persists or worsens PAIN WHO. Cancer pain relief, 2nd ed. Geneva, WHO, 1996 ± non-opioid analgesics ± adjuvant agents Pain does not go away or increases Three-step pain treatment 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 step for pain of varying intensity Analgin (metamizole) action is aimed at blocking inflammatory mediators (prostaglandins, kinins, etc. In general practice, combined analgin preparations are still relevant: Tempalgin, Pentalgin, Baralgin Modern ones have a longer duration (8-12 hours) ) and a strong analgesic effect: 1. Xefocam (lornoxicam) - tablets, injections 2. Flexen (ketoprofen) - suppositories, gel, capsules, ampoules 3. Perfalgan (paracetamol) - solution for IV infusion
Slide 13
For severe pain: prescribing non-invasive prolonged forms of MCT-continus - tablets 10, 30, 60 and 100 mg Active ingredient: morphine Duration of action: 12 hours Experience of use in TOOD - since 1997 Disadvantages: cannot be used for dysphagia, decreased effectiveness in malabsorption syndrome
Slide 14
Comparison of opioid analgesics by 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: - does not involve the gastrointestinal tract - duration of action - elimination 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 a fentanyl depot during the first 17-24 hours Achieving maximum analgesic effect after 24 hours FENTANYL TRANSDERMAL THERAPEUTIC SYSTEM TTC area: 10, 20, 30 and 40 cm Fentanyl release per hour: 25, 50, 75 and 100 mcg
Slide 17
SINGLE APPLICATION OF 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 mcg/h
Slide 18
Ascending signal Descending signal Pain sensation Spinal cord Peripheral nociceptors Pathological fracture of the vertebral body in metastases of breast cancer Neuropathic pain occurs in 30-60% of patients with advanced cancer Nerve damage (compression) + osteoporosis
Slide 19
Clinic of neurogenic pain Symptoms described by the patient: - prolonged, burning pain, shooting, piercing pain - pain similar to an electrical discharge - paresthesia Symptoms determined by the doctor: - hyperalgesia - allodynia - dysesthesia - hyperpathia
Slide 20
Drugs used (for neurogenic pain) Anticonvulsants Muscle relaxants Antidepressants Neuroleptics Antiarrhythmics Local anesthetics Non-pharmacological agents (transcutaneous electrical neurostimulation, physiotherapy, relaxation, biofeedback methods, etc.). Adjuvant therapy (Three-step pain control regimen, WHO, 1986, 1992, 1996) Drug of choice for neuropathic pain: Lyrica (pregabalin)
Slide 21
Pathogenetic (targeted) agents for the treatment of neuropathic pain syndrome Pregabalin (Lyrica) Gabapentin Oxcarbazepine Carbamazepine Amitriptyline Lamotrigine Local anesthetics (lidocaine patch)
Slide 22
Action of Lyrica (pregabalin) Kavoussi R. Eur Neuropsychopharmacol. 2006;16 Suppl 2:S128-133. Danilov A.B., Davydov O.S. Neuropathic pain. 2007. – pp. 10-12. Pregabalin regulates the functioning of overly excitable neurons: Target - a2-d subunit of voltage-gated calcium channels2 Reduces excessive release of excitatory mediators2 This mechanism of action explains its analgesic, anticonvulsant and anxiolytic activity1,2 Pregabalin prevents excess release of excitatory mediators1
CHRONIC HEPATITIS IS A GROUP OF LIVER DISEASES CAUSED BY VARIOUS CAUSES, CHARACTERIZED BY DIFFERENT DEGREES OF SEVERITY OF HEPATIC CELL NECROSIS AND INFLAMMATION AND PROCEEDING WITHOUT IMPROVEMENT FOR AT LEAST 6 MES. CHRONIC HEPATITIS IS A GROUP OF LIVER DISEASES CAUSED BY VARIOUS CAUSES, CHARACTERIZED BY DIFFERENT DEGREES OF SEVERITY OF HEPATIC CELL NECROSIS AND INFLAMMATION AND PROCEEDING WITHOUT IMPROVEMENT FOR AT LEAST 6 MES.
ETIOLOGY VIRUSES A, B, C, E, E VIRUSES A, B, C, E, E ALCOHOL ALCOHOL TOXIC SUBSTANCES TOXIC SUBSTANCES DISEASES OF THE DIGESTIVE ORGANS DISEASES OF THE DIGESTIVE ORGANS VARIOUS MEDICINES – ANTI-TUBERCULOSIS DRUGS, ANTIBIOTICS FOR LONG-TERM THERAPY VARIOUS MEDICINES – ANTI-TUBERCULOSIS DRUGS, ANTIBIOTICS FOR LONG-TERM THERAPY
Hepatotropic toxic substances - directly damage hepatocytes to the point of necrobiosis, then a secondary inflammatory reaction develops in the liver mesenchyme. Hepatotropic toxic substances - directly damage hepatocytes to the point of necrobiosis, then a secondary inflammatory reaction develops in the liver mesenchyme. Toxic-allergic factors - under the influence of these factors, the sensitivity of the liver to certain substances increases. Toxic-allergic factors - under the influence of these factors, the sensitivity of the liver to certain substances increases.
The CLINIC depends on the form of the disease and the degree of activity of the process. Chronic hepatitis - occurs more often in middle age, among adult men. The disease is usually caused by a virus and the virus and alcohol together. There are few clinical signs. Chronic hepatitis - occurs more often in middle age, among adult men. The disease is usually caused by a virus and the virus and alcohol together. There are few clinical signs.
1. Pain syndrome is expressed in the appearance of dull pain and heaviness in the right hypochondrium 1. Pain syndrome is expressed in the appearance of dull pain and heaviness in the right hypochondrium 2. Asthenovegetative syndrome - fatigue, weakness, decreased performance, sleep disturbance, emotional instability and rapid weight loss body 2. Asthenovegetative syndrome - fatigue, weakness, decreased performance, sleep disturbance, emotional instability and rapid loss of body weight 3. Dyspeptic syndrome - anorexia, loss of appetite, nausea, feeling of bitterness in the mouth, constipation, sometimes alternating with diarrhea 3. Dyspeptic syndrome – anorexia, loss of appetite, nausea, feeling of bitterness in the mouth, constipation, sometimes alternating with diarrhea 4. Liver failure syndrome – bleeding, jaundice, ascites, encephalopathy 4. Liver failure syndrome – bleeding, jaundice, ascites, encephalopathy
5. Cholestasis syndrome - skin itching, increased levels of direct bilirubin, alkaline phosphatase and glutamyl transpeptidase 5. Cholestasis syndrome - skin itching, increased levels of direct bilirubin, alkaline phosphatase and glutamyl transpeptidase 6. Minor "liver" signs - spider veins, palmar erythema, gynecomastia 6 Small "liver" signs - spider veins, palmar erythema, gynecomastia 7. Jaundice - often icteric sclera 7. Jaundice - often icteric sclera
In the “reactive” form of chronic hepatitis, interstitial metabolism in the liver is disrupted due to a lack of proteins, vitamins and dysproteinemia. In the “reactive” form of chronic hepatitis, interstitial metabolism in the liver is disrupted due to a lack of proteins, vitamins and dysproteinemia. The basis of the pathogenesis of cholestatic hepatitis is violation of primary bile formation, stagnation of bile. The basis of the pathogenesis of cholestatic hepatitis is a violation of primary bile formation, stagnation of bile
CLASSIFICATION OF CHRONIC HEPATITIS S.D. PODYMOVA, 1983 WITH CHANGES BY THE CENTER OF GASTROENTEROLOGY OF THE REPUBLIC, 2003 BY ETIOLOGY VIRUSES A, B, C, D, E VIRUSES A, B, C, E, E ALCOHOL ALCOHOL TOXIC SUBSTANCES TOXIC SUBSTANCES DISEASES OF ORGANS P DIGESTION DISEASES OF THE DIGESTIVE ORGANS VARIOUS MEDICINES – ANTI-TUBERCULOSIS DRUGS, ANTIBIOTICS FOR LONG-TERM THERAPY VARIOUS MEDICINES – ANTI-TUBERCULOSIS DRUGS, ANTIBIOTICS FOR LONG-TERM THERAPY
CLINICAL FORMS: PERSISTENT HEPATITIS – HEPATITIS WITH MINIMUM ACTIVITY PERSISTENT HEPATITIS – HEPATITIS WITH MINIMUM ACTIVITY ACTIVE HEPATITIS ACTIVE HEPATITIS AUTOIMMUNE (LUPOID) HEPATITIS AUTOIMMUNE (LUPO) IDNY) HEPATITIS CHOLESTATIC HEPATITIS CHOLESTATIC HEPATITIS
DIAGNOSTICS HISTORY ANAMNESIS CLINICAL FORMS CLINICAL FORMS LABORATORY INSTRUMENTAL STUDIES (increased ESR, leuko- and thrombocytopenia, hypergammaglobulinemia, increased ALT and AST, bilirubin, dysproteinemia) LABORATORY INSTRUMENTAL STUDIES (increased decreased ESR, leuko- and thrombocytopenia, hypergammaglobulinemia, increased ALT and AST , bilirubin, dysproteinemia) RESULTS OF HISTOLOGICAL STUDY OF LIVER BIOPSTATE RESULTS OF HISTOLOGICAL STUDY OF LIVER BIOPSTATE
TREATMENT OF CHRONIC HEPATITIS DURING THE ACHIEVEMENT STAGE HOSPITALIZATION AT THE ACHIEVEMENT STAGE HOSPITALIZATION DIET TABLE 5 – FRIED, SPICY FOOD IS EXCLUDED. DIET TABLE 5 – FRIED, SPICY FOOD IS EXCLUDED. Antispasmodics - NOSHPA, PLATIFILLINE. Antispasmodics - NOSHPA, PLATIFILLINE. HEPATOPROTECTORS-ESSENTIALE, CARSIL, VITAMINS HEPATOPROTECTORS-ESSENTIALE, CARSIL, VITAMINS
The prognosis depends on the stage of the disease, histological signs of process activity, and the type of necrosis. Complete recovery is insignificant. The prognosis depends on the stage of the disease, histological signs of process activity, and the type of necrosis. Complete recovery is insignificant. In 10-25% of patients there is spontaneous remission In 10-25% of patients there is spontaneous remission In 30-50% of patients there is a transition to cirrhosis of the liver In 30-50% of patients there is a transition to cirrhosis of the liver Hepatocellular carcinoma Hepatocellular carcinoma Malignancy Malignancy
Baseline tests
Clinical anatomy and physiology of the pancreas
Innervation and blood supply of the pancreas
Exocrine function of the pancreas.
Secretion phases
Humoral and nervous regulation of the pancreas
Hormonal function of the pancreas
Definition
Epidemiology
Etiology
Pathogenesis
Classification of chronic pancreatitis
Classification of CP by severity
Imaging methods in the diagnosis of chronic pancreatitis:
Complications
Treatment
Final level tests
Clinical anatomy and physiology of the pancreas
The pancreas (P) is a gland of the digestive system,producing pancreatic juice and simultaneously possessing
endocrine function. Located in the upper half of the abdomen, in
retroperitoneal space at the level of the I-II lumbar vertebrae,
behind the back wall of the stomach. Has the shape of a flattened cord, in
which distinguishes the head, body, and tail. The length of the pancreas 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 pancreas parenchyma (exocrine
part) secretes enzymes necessary for digestion. They
enter the pancreatic duct, which often merges at the end
parts with the common bile duct and opening into the descending
section of the duodenum at the apex of the papilla of Vater
(major duodenal papilla). Vater's papilla
has a sphincter of the hepatic-pancreatic ampulla (sphincter of Oddi),
regulating the flow of pancreatic juice and bile into
duodenum
gut.
Smaller
Part
(endocrine)
grouped in the form of tiny islands (islets of Langerhans)
and is embedded in the parenchyma of the exocrine part of the gland. Islets
Langerhans cells are formed by groups of secretory cells (insulocytes). Highlight
four
cell type: α-cells,
producing
glucagon, β-cells,
producing
insulin,
γ cells,
producing
somatostatin;
rr cells producing
not pancreatic
polypeptide.
Much bigger
pancreatic
islets is located in
caudal part of the pancreas.
Innervation and blood supply of the pancreas
Innervates the pancreatic nerveswalking
from
hepatic,
splenic, celiac and
superior mesenteric plexus
and branches of the vagus nerve.
IN
their
compound
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
V
portal vein. Lymphatic drainage
carried out
V
regional lymphatic
nodes.
Exocrine function of the pancreas.
Exocrinefunction
pancreas
is
V
production
cells
exocrine part of the pancreatic gland
juice containing enzymes necessary
for the digestion of proteins (proteases), fats
(lipases)
And
carbohydrates
(glycosidases).
Basic
from
them
(trypsinogen,
chymotrypsinogen)
secreted
V
inactive form and are activated only in
duodenum, turning
under the influence of enterokinase into trypsin and
chymotrypsin. Along with enzymes
pancreatic juice supplies water,
electrolytes and especially hydrocarbonates
and a large amount of protein. Hydrocarbonate
makes pancreatic juice alkaline
reaction,
necessary
For
enzymatic breakdown of nutrients.
Branch
pancreatic
juice
carried out due to the pressure difference in
proximal and distal sections
duct
pancreas,
A
Also
And
V
duodenum and occurs
periodically, intensifying when exposed to
conditioned reflex (the sight and smell of food) and
unconditionally reflexive
irritants
(chewing and swallowing).
Secretion phases
Distinguish3
phases
secretion
pancreatic juice:
- complex reflex,
happening
under
the influence of the mentioned
above irritants;
-gastric, which
associated with stretching
stomach
at
filling it with food;
-intestinal, having
humoral nature.
Humoral and nervous regulation of the pancreas
Humoralregulation
carried out
V
mostly
intestinal
polypeptide
hormones
secretin
And
pancreozymin. They stand out
special hormone-producing
cells
mucous membrane
shell
duodenum with
entering it from the stomach
hydrochloric acid, as well as products
partial digestion of protein. On
pancreatic secretion is also affected
pituitary and thyroid hormones
glands, adrenal glands and some
other.
Nervous
center,
regulating
secretion
pancreatic juice, located in
medulla oblongata.
Hormonal function of the pancreas
Hormonalfunction
carried out by islets
Langerhans,
which
release hormones (insulin
and glucagon), regulating
carbohydrate metabolism and
somatostatin
And
pancreatic
polypeptide,
being
hormonal
regulators
some
digestive functions
systems. In case of defeat
islets of Langerhans in
first of all it is violated
carbohydrate
exchange
develops
sugar
diabetes.
Definition
Chronic pancreatitis (CP)- long-term inflammatory
disease
pancreas
glands,
manifesting
irreversible
morphological
changes,
which
cause pain and/or persistent
decreased function. For CP
morphological
changes
pancreas
glands
persist after termination
impact
etiological
factor a.
Epidemiology
Prevalencechronic
pancreatitis according to
autopsies range from
0.01 to 5.4%, on average
0,3-0,4%.
Frequency
identifying
chronic
pancreatitis is
3.5-4 per 100,000
population
V
year.
Disease
usually
starts on average
age (35-50 years).
Etiology
The most common cause of the disease is alcohol consumption(up to 90% of adult patients); people usually get sick
taking 150-200 ml of pure alcohol per day on average
for 10 years or more, however, the timing of the onset of pancreatitis in
may vary significantly between different people. Besides,
Possible hereditary pancreatitis - a disease inherited
according to the autosomal dominant type with a penetrance of 80%.
Hereditary pancreatitis is associated with a mutation in the gene encoding
synthesis of trypsin, which causes disruption of the defense mechanism against
intracellular activation of trypsin. Pancreatitis occurs in 3%
patients with hyperparathyroidism, with duct obstruction
pancreas (PG) (stenosis, stones, cancer),
congenital anomalies: ring-shaped pancreas, bifurcated pancreas
(pancreas divisum), with diverticula of the duodenum.
Rarely, chronic pancreatitis occurs due to stenosis
duct that arose during acute, in particular biliary,
pancreatitis.
Pathogenesis
Several roles play a role in the pathogenesis of chronic pancreatitis.factors. One of the main ones is obstruction of the main
pancreatic duct with stones, inflammatory stenosis
or
tumors.
At
alcoholic
pancreatitis
damage
pancreas is associated with an increase in protein content in
pancreatic secretion, which leads to the appearance of protein
plugs and obstruction of small gland ducts. Another factor
involved in the pathogenesis of alcoholic pancreatitis is
change
tone
sphincter
Oddy:
his
spasm
causes
intraductal hypertension, and relaxation promotes reflux
duodenal
content
And
intraductal
activation
pancreatic enzymes. Calcification
pancreas
glands
arises
How
at
alcoholic,
So
And
at
non-alcoholic pancreatitis more often
Total
after
traumatic
damage due to hypercalcemia,
tumors
insular
cells.
Plays a significant role in this
pancreatic stone protein
glands,
inhibitory
precipitation
oversaturated
solution
carbonate
calcium,
quantity
this
squirrel
V
pancreatic
secret
deterministic
genetically.
Observed
some
phases
calcification
pancreas
glands: growing, stable
phase that comes through
several years and a decrease in degree
calcification (observed in 30%
sick),
despite
on
progressive
decline
exocrine function of the organ. Destruction
exocrine
parts
pancreas
glands
causes
progressive decrease in secretion
bicarbonates and enzymes, however
clinical manifestations of the disorder
food digestion develops
only with destruction of more than 90%
organ parenchyma. First of all
arise
manifestations
lipase deficiency, which
manifested by malabsorption
fats, fat-soluble vitamins
A, D, E and K, which does not appear often
bone damage, disorders
coagulation
blood.
At
HP
due to
deficit
proteases
violated
split
communications
Vitamin B12 is an R protein and is reduced
secretion of cofactors that determine
absorption of vitamin B12, however
clinical
symptoms
this
are rarely observed. In 10-30% of patients with CP
diabetes mellitus develops,
usually in later stages
diseases, much more often
observed
violation
glucose tolerance. For
it is typical for such patients
development of hypoglycemic
reactions
on
insulin,
malnutrition or
drinking alcohol. Ketoacidosis
develops
rarely,
What
associated with simultaneous
decrease
products
insulin and glucagon.
Table 1. Etiopathogenesis of chronic pancreatitis (according to P. Layer and U. Melle 2005)
AlcoholicMutations in SPINK1 (serine protease inhibitor kazal type1), trypsinogen gene or CFTR (cystic fibrosis
transmembrane regulator) genes.
Caused by smoking
Hereditary
Mutation of the trypsinogen gene.
Autoimmune
Metabolic/nutritional.
Hypercalcemia
Hyperparathyroidism
Acquired or hereditary hypertriglyceridemia
Tropical (SPINK1 mutations)
Tropical calculous pancreatitis
Fibrous-calculous pancreatogenic diabetes
Idiopathic
Early onset (SPINK1 mutations)
Late start
Obstructive.
Mild obstruction of the gastrointestinal tract
Traumatic stricture
Stricture after necrosis
Sphincter of Oddi stenosis
Sphincter of Oddi dysfunction
Stones
Duodenal obstruction (diverculum, duodenal wall cysts)
Malignant stricture of the pancreatic duct.
Pancreatic, ampullary and duodenal calcinoma
Classification of chronic pancreatitis
Currently, the classification of chronic pancreatitis proposed by Ivashkin is usedV.T., Khazanov A.I. et al. (1990), based on what was 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 according to the nature of the clinical course
Rarely recurrent
Often recurrent
With constantly present symptoms
3. Variants of chronic pancreatitis according to morphological characteristics
Interstitial-edematous
Parenchymatous
Fibrous-sclerotic (indurative)
Hyperplastic (pseudotumorous)
Cystic
4. Variants of chronic pancreatitis according to clinical manifestations
Painful
Hyposecretory
Asthenoneurotic
Latent
Combined
The most difficult section of the classification is the division of CP according to morphological characteristics. The authors based these principles on the given
Interstitial-edematous CP
onheight of exacerbation (according to ultrasound data
and CT) is characterized by moderate
increase
sizes
PJ.
Due to swelling of the gland itself
And
parenchymal
fiber
contours
pancreas
are visualized
unclear, its structure seems
heterogeneous, there are areas
both high and low
density; heterogeneous
echogenicity. As it subsides
exacerbations, the size of the pancreas becomes
normal, contours clear. IN
difference from acute pancreatitis
part of the morphological changes
turns out to be stable (mostly
or to a lesser extent are preserved
areas of gland compaction). U
most patients with severe
no changes in the duct system
discovered.
Parenchymal variant of CP
For parenchymal variantHP
characteristic
significant
duration
diseases,
alternating periods of exacerbation and
remission. Pain during exacerbation
less pronounced, amylase test
turns out to be positive less often and
the level of increase is less. More
how
at
half
sick
are fixed
symptoms
exocrine
pancreatic failure: steatorrhea,
polyfecality, tendency to diarrhea,
which
relatively
easily
docked
enzymatic
drugs. According to ultrasound and CT data
dimensions and contours of the pancreas exist
not changed at all, stable
uniform compaction is noted
glands. Changes in the ducts
majority
sick
Not
is revealed.
Fibrous-sclerotic variant of CP
-long history - more than 15years. Almost all patients
fixed
exocrine
pancreatic failure, intense pain,
not inferior to drug therapy.
The clearly defined line between
exacerbation and remission. Amylase
the test turns out to be true in half the cases
negative. Complications are common and
character
their
depends
from
preferential localization of the process
(in the head - violation of the passage of bile, in
tail-breaking
cross-country ability
splenic vein and subhepatic vein
form of portal hypertension). By
data
Ultrasound
And
CT dimensions
pancreas
glands
reduced,
parenchyma of increased echogenicity,
significantly compacted, clear contours,
uneven,
often
are revealed
calcification. In some patients, the ductal system of the gland is dilated.
Hyperplastic variant of CP
-occurs approximately5%
sick.
Disease
lasts a long time (usually
more than 10 years). The pains are
expressed
character
And
permanent
How
as a rule,
fixed
failure
exocrine function of the pancreas.
Sometimes
pancreas
Maybe
palpable; amylase test
only 50% are positive
sick. According to ultrasound and CT data,
The pancreas or its individual parts sharply
increased.
IN
plan
differential diagnosis with
pancreatic tumor
it is advisable to conduct a test
with Lasix, as well as repeated
blood serum test for
tumor markers.
Cystic variant of CP
- occurs 2 timesmore often than hyperplastic. He stands out in
a separate option, as it is characterized
a peculiar clinical picture - pain
moderate but almost constant, amylase test,
usually positive and persists
long time. According to ultrasound and CT scan of the pancreas
enlarged, there are liquid formations, areas
fibrosis and calcification, the ducts are usually
expanded. Exacerbations are frequent and do not always occur
"apparent" reason.
Reactive pancreatitis is a reaction of the pancreas
glands for acute pathology or exacerbation
chronic pathology of organs, functional,
morphologically
related
With
pancreas
gland. Reactive pancreatitis ends with
eliminating the exacerbation of the underlying disease, but
its identification requires therapeutic 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 was made
can not.
Classification of CP by severity
Mild course of the disease. Rare (1-2 times a year) and short-livedexacerbations, quickly relieved pain syndrome. The functions of the pancreas are not
violated.
Outside
exacerbation
well-being
sick
quite
satisfactory. There is no decrease in body weight. Indicators
coprograms are within normal limits.
Moderate weight. Exacerbations 3-4 times a year with a typical long-term
pain syndrome, with the phenomenon of pancreatic hyperfermentemia,
detected by laboratory research methods. Violations
exocrine and endocrine functions of the pancreas
moderate (change in the character of feces, steatorrhea, creatorrhea according to data
coprograms, latent diabetes mellitus), with instrumental
examination - ultrasound and radioisotope signs of damage
pancreas.
Heavy current. Continuously relapsing course (frequent
prolonged exacerbations), persistent pain syndrome, severe
dyspeptic disorders, “pancreatic diarrhea”, severe
disturbance of general digestion, profound changes in exocrine
pancreatic functions, development of pancreatic diabetes mellitus, pancreatic cysts.
Progressive wasting, polyhypovitaminosis, extrapancreatic
exacerbations (pancreatogenic effusion pleurisy, pancreatogenic
nephropathy, secondary duodenal ulcers).
Clinical picture:
Pain in the epigastric region after eating, radiating toback, which may last for many hours or
several days.
Nausea, vomiting.
Loss of body weight (in 30-52% of patients).
Jaundice (in 16-33% of patients). Edema and development of fibrosis of the pancreas can
cause compression of the bile ducts and surrounding vessels.
Transient jaundice occurs due to swelling of the pancreas during exacerbations
chronic pancreatitis, constant - associated with obstruction of the general
bile duct due to fibrosis of the head of the pancreas. With lighter
obstruction, only the level of alkaline phosphatase increases.
During an attack of chronic pancreatitis, fatty
necrosis, the subcutaneous tissue of the legs is more often affected, which manifests itself
painful nodules that can be mistaken for nodular
erythema.
Inflammation and fibrosis of peripancreatic tissue can lead to
compression and thrombosis of the splenic, superior mesenteric and portal veins,
however, the full picture of portal hypertension is rarely observed.
Formation of pseudocysts due to ruptures of the pancreatic ducts, 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 neighboring organs.
Exocrine insufficiency syndrome
With a long course of the disease, asdestruction of the pancreas parenchyma intensity of pain
seizures
becomes
less
(however
Continued alcohol consumption may cause
persistence of pain), and with a decrease in volume
functioning parenchyma up to 10% of normal
signs of malabsorption appear - polyfecalia,
fatty stools, weight loss. In patients with
alcoholic pancreatitis signs of malabsorption
appear on average 10 years after appearance
first clinical symptoms.
Diagnosis is made based on characteristic
pain syndrome, signs of insufficiency
exocrine function of the pancreas in a patient,
regularly drinking alcohol. Unlike
acute pancreatitis, rarely in chronic
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 Persistently elevated
the level of amylase in the blood allows you to make
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
extrapancreatic sources of hyperamylasemia.
Table 2. Extrapancreatic sources of hyperamylasemia and hyperamylasuria (according to W. V. Salt II, S. Schtnkor):
Kidney failureDiseases of the salivary glands:
parotitis
calculus
radiation sialadenitis
Complications of maxillofacial surgery
Tumor hyperamylasemia:
lung cancer
esophageal carcinoma
ovarian cancer
Macroamylasemia
Burns
Diabetic ketoacidosis
Pregnancy
Kidney transplant
Brain injury
Drug treatment:
morphine
Diseases of the abdominal organs:
diseases of the biliary tract (cholecystitis, choledocholithiasis)
complications of peptic ulcer - perforation or
penetration of ulcers
intestinal obstruction or infarction
ectopic pregnancy
peritonitis
aortic aneurysm
postoperative hyperamylasemia
Imaging methods in the diagnosis of chronic pancreatitis:
X-ray of the areaPJ.
Transabdominal ultrasound
(extension
ducts,
pseudocysts,
calcification, expansion
common bile duct,
gate,
splenic
veins, ascites).
Endoscopic ultrasound.
ERCP
(change
structures
ducts,
pseudocysts).
CT scan
(With
intravenous
contrasting)
Scintigraphy with introduction
granulocytes,
tagged
99mТс or 111Iп. Plain radiography in 30-40% of cases
reveals
calcification
pancreas
glands or intraductal stones, especially
when examined in oblique projection. This
removes
necessity
further
examinations to confirm the diagnosis of CP.
Ultrasound examination (ultrasound) allows
assess the size of the organ, expansion and
irregularities in the contour of the ducts, pseudocysts.
Endoscopic
retrograde
Cholangiopancreatography (ERCP) allows
identify the majority of patients with CP. This
research makes it possible to discover
changes in the main pancreatic duct and
its branches (irregular expansion of the ducts
- "chain of lakes"). Computed tomography
(CT) and angiography are usually performed for
preparation for upcoming surgery
intervention. Areas of pancreatic necrosis
glands can be detected using
use of contrast in CT
(no accumulation of contrast agent),
and also using a new technique -
scintigraphy
pancreas
glands
With
injection of a suspension of labeled granulocytes
(accumulation of radioactivity in the focus of necrosis). Scatological research
is
main
method
assessments
exocrine
pancreatic functions.
With severe pancreatic
insufficiency of stool
acquire
grey
shade,
foul odor and greasy appearance.
The total number increases
feces (normal weight
is 50-225 g per day).
Increased
content
neutral fat in feces -
steatorrhea is an indicator
expressed
exocrine
Research should be carried out
against the background of taking sufficient
amount of fat by the patient (100 g
per day for 2-3 days before
analysis), most characteristic
detection of large drops
(diameter more than 8 microns).
Functional tests can be divided into three groups:
direct tests of pancreatic secretion. Conducting a collectionand examination of pancreatic or duodenal juice
contents after stimulation of secretion
pancreas
exogenous
hormones
or
hormone-like peptides (secretincholecystokinin test);
indirect
tests
study.
duodenal contents after food
stimulation (Lund test);
oral tests - performed without
cannulation of the pancreatic duct or insertion
probe (N-benzoyl-L-tyrosyl-paraaminobenzoic acid test - BTPAB; fluorescein dilaurate or
pancreatolauryl test; respiratory
tests
With
substrate,
tagged
radioisotopes). Secretin-pancreozymin test
Secretin-pancreozymin test
is
"golden
standard"
diagnostics
violations
exocrine
functions
pancreas. In the received
secretion determine the concentration
bicarbonates and enzymes: amylase,
trypsin, chymotrypsin and lipase.
The most important ones are:
indicators,
How
maximum
bicarbonate concentration, flow rate
pancreatic juice (duodenal
content),
maximum
concentration and flow rate of enzymes. At
CP usually shows a decrease
concentrations
bicarbonates
(<90
meq/l) and enzymes with normal
volume
aspirate
(>2
ml/kg).
Reduction in pancreatic volume
secretion
at
normal
concentrations
bicarbonates
And
enzymes helps to suspect cancer
pancreas.
Lund test
When performing the Lund test, secretion stimulation is performed withusing a liquid food mixture containing 6% fat, 5% protein and
15% carbohydrates. This method is technically easier to carry out,
however, it does not allow assessing the secretion of bicarbonates, and, in addition,
its results depend on the condition of the small intestine as a place
production of endogenous stimulants. The Lund test has a lower
sensitivity and specificity compared with the secretin pancreozymine test, especially in mild cases
pancreatic insufficiency.
Method for determining pancreatic enzymes
In recent years, more and moreapplication
finds
method
definitions
pancreatic
enzymes (trypsin, chymotrypsin,
elastase, lipase) in feces, before
Total
thanks to
his
non-invasiveness.
Largest
benefits has definition
elastase in feces by enzyme immunoassay
method.
Sensitivity
And
specificity of the elastase test in
sick
With
exocrine
pancreatic insufficiency
severe
And
average
degrees
are close to those of the secretin pancreozyme test. For mild
degrees
exocrine
sensitivity deficiency
method is 63%.
Figure 2
*recommendations of the European Multicenter Study Group on Chronic Pancreatitis 2005Table 3. DIAGNOSIS OF CHRONIC PANCREATITIS ACCORDING TO THE SCORE SYSTEM (according to P. Layer and U. Melle 2005)
PARAMETERS ASSESSEDSCORE
Y
Pancreatic calcification
4
Characteristic histological changes
4
Characteristic changes on ultrasound or ERCP
(see Cambridge classification)
3
Exocrine pancreatic insufficiency
2
Attacks of pancreatitis and/or chronic abdominal pain
2
Diabetes
1
Table 4. CAMBRIDGE CLASSIFICATION OF STRUCTURAL CHANGES IN THE PANCREAS IN CHRONIC PANCREATITIS
ChangesERCP
Ultrasound or CT
Main pancreatic duct Normal size, clear contours of the pancreas.
Normal pancreas
(GPP) and side branches are not
GPP = . The parenchyma of the pancreas is homogeneous
changed
One of the following signs:
Questionable changes
GPP is not changed, less than 3
GPP = 2-. The size of the pancreas is within 1-2 norms.
altered lateral branches
Heterogeneous pancreatic parenchyma
Soft changes
Moderate changes
Significant changes
GPP not changed, more than 3
altered lateral branches
Changes in GPP and more than 3
lateral branches
Two or more signs: GLP = 2-4
mm. Slight increase in size
Pancreas Heterogeneity of the parenchyma
Blurred contours of the pancreas.
Small cysts (less.).
Uneven GPP. Acute focal
necrosis. Increased echogenicity of the wall
duct. Irregularity of the contours of the pancreas.
All of the above + one or more of the following:
Cysts are larger in diameter
Intraductal filling defects
Stones/pancreatic calcification
GLP obstruction or stricture
Pronounced dilatation and unevenness of the gastrointestinal tract
Invasion into neighboring organs
Complications
Most commoncholestasis,
infectious
complications
(inflammatory
infiltrates,
purulent
cholangitis,
septic
state).
Possible
subhepatic
form
portal
hypertension,
erosive esophagitis, syndrome
Mallory-Weiss,
gastroduodenal ulcers (they
conditioned
significant
decrease
products
bicarbonates of the pancreas), chronic
obstruction
duodenum, cancer
pancreas
And
abdominal
ischemic syndrome.
Examples of diagnosis formulation
Main Ds: Chronic pancreatitis,biliary dependent, rarely relapsing
course, exacerbation phase.
Concomitant Ds: Gallstone disease,
chronic calculous cholecystitis in Art.
remission.
Main Ds: Chronic pancreatitis,
alcohol etiology, often
recurrent course, exacerbation phase.
Complication: Portal hypertension.
Secondary diabetes mellitus, mild course,
compensation.
Treatment
includes waiverfrom
use
alcohol,
compliance
diets
With
low
fat content (up to
50-75 g/day) and frequent
reception
small
quantities
food,
cupping
pain,
enzymatic
replacement therapy,
fight against vitamin
insufficiency,
treatment
endocrine
violations.
Treatment of an attack of chronic pancreatitis
similar to treatmentacute pancreatitis. Mandatory components of treatment
are intravenous administration of electrolyte solutions and
colloids, fasting diet and analgesia (eg meperidine)
Administration of fresh frozen plasma or albumin is recommended.
Diuretics are not indicated for most patients: oliguria
resolved when hypovolemia disappears and normalization
renal perfusion. To relieve vomiting and relieve paresis
gastrointestinal
tract
And
decrease
stimulation
pancreas, aspiration can be used
stomach contents through a nasogastric tube. Coagulopathy,
occurring with pancreatitis, usually requires the use of heparin,
fresh frozen plasma
Digestive enzyme preparations can be used to
treatment as at the height of the disease in order to suppress
pancreatic secretion, and during the recovery period with
restoration of oral food intake.
Long-term therapy for CP can be divided into two main ones:
parts in accordance with leading clinical syndromes.
Relief of chronic pain
in patients with pancreatitis - extremely difficulttask. First of all, you need to be sure that there is no
patient complications that can be corrected by surgery
by (eg pseudocysts, intraductal obstruction or compression
neighboring organs).
It is of fundamental importance to stop the patient from drinking alcohol, which
significantly increases the survival rate of patients with severe pancreatitis.
Non-narcotic drugs shown
analgesics: paracetamol, tramadol.
Modern research shows that only
high doses of analgesic drugs, for example, tramadol is necessary
prescribe 800 mg/day or more. In Western countries, gastroenterologists
narcotic drugs are often prescribed, which creates a developmental problem
addiction in 10-30% of patients. It is of great importance to simultaneously
prescribing auxiliary medications such as antidepressants,
which can have a direct analgesic effect, contribute to
relief of concomitant depression, and also potentiate the effect
analgesics (amitriptyline orally 75–150 mg per day). Antispasmodics and
anticholinergics normalize the flow of bile and pancreatic juice (which
reduces intrapancreatic pressure) and are necessary
component of therapy (duspatalin 1 tablet 3 times or 1 capsule 2 times,
papaverine hydrochloride IV or IM 2 ml of 2% solution 2 – 4 times a day,
hyoscine hydrobromide IM 20 mg 1 – 2 times a day or platyphylline IV or
IM 4 mg 1 – 2 times a day).
Often non-narcotic analgesics are ineffective, and the question arises about
prescribing narcotic drugs (promedol). Large doses may relieve pain
pancreatic
enzymes.
Hit
pancreatic enzymes (formerly
total trypsin) into the duodenum
by a negative feedback mechanism
causes a decrease in pancreatic secretion,
decrease in intraductal pressure and
reduces pain. Traditionally for this purpose
used powder or tablets
pancreatin preparations. However, the latest
works of domestic and foreign authors
show that the administration of pancreatin in
capsules more effectively (in the same doses) than
in tablets.
Creation of functional rest of the pancreas
achieved by maximally complete blockade
gastric secretion, which
provides
decreased synthesis of natural stimulants
its activity – cholecystokinin and secretin. WITH
inhibitors are used for this purpose
proton pump: omeprazole or rabeprazole
or esomeprazole 20 mg 2 times or lansoprazole
30 mg once daily or H2 blockers –
histamine receptors (famotidine 20 mg 2 times
per day intravenously).
Effect of a potent inhibitor on pain
pancreatic secretion of octreotide was
studied
V
several
clinical
research. It is shown that compared to
placebo octreotide significantly reduces pain and
need for analgesics. There is evidence that
the drug may reduce the frequency of
common complication of chronic
pancreatitis – formation of pseudocysts. If pain is resistant to therapy,
at
expansion
main
duct more than 8 mm in 70-80%
sick
relief
Maybe
bring
lateral
Pancreatojejunostomy.
If
pancreatic
duct
Not
expanded, showing
distal
pancreatectomy
(at
preferential
damage to the tail of the gland) or
Whipple operation (with
mainly affects the head
glands).
An alternative
surgery is percutaneous
denervation
sunny
plexuses by introducing alcohol,
however, the effect of this procedure
only a few are preserved
months. Very promising
is
endoscopic
treatment
under
control
endoscopic
Ultrasound
(drainage
pseudocyst,
neurolysis of the solar plexus).
Indications for replacement therapy of exocrine pancreatic insufficiency are exclusively clinical indicators:
The choice of drug for replacement therapy shouldbe based on the following indicators:
high lipase content in the preparation -
the dosage should be convenient enough for
reception: up to 30,000 units. lipase per meal
(since with exocrine pancreatic
insufficiency
lipolytic
activity
decreases first);
the presence of a shell that protects enzymes from
digestion by gastric juice (main
components of enzyme preparations - lipase and
trypsin - quickly lose activity in an acidic environment
- lipase at pH less than 4; trypsin at pH less than 3,
before the drug enters the duodenum
up to 92% of lipase can be destroyed in the intestine);
small size granules or microtablets,
filling capsules (along with food
Evacuation of the drug from the stomach occurs only in
if the particle size does not exceed 2
mm);
rapid release of enzymes in the upper
parts of the small intestine. The ability of the drug to be activated only in an alkaline environment is very
an important property that dramatically increases the efficiency of enzymes.
Thus, when using a drug that has an enteric
membrane, fat absorption increases by an average of 20%
compared to the same dose of a conventional drug. However, with CP
there is a significant decrease in bicarbonate production, which
leads to disruption of alkalization in the duodenum.
This creates several problems. The first concerns activation disorder
particles of an enzyme preparation coated with enteric
shell. The second problem is that in an acidic environment
Precipitation of bile salts and disruption of emulsification occurs
fat, which makes it difficult to digest by lipase.
Therefore, the effectiveness of enzyme therapy can be increased
simultaneous administration of antacids 30 minutes before and 1 hour after
food or antisecretory drugs (proton pump inhibitors
or H2-histamine receptor blockers intravenously), but
It must be remembered that antacids containing calcium or magnesium
weaken the effect of enzyme preparations. Significant reduction
the quality of life of a patient with pancreatitis is associated with such a problem as
persistent bloating. Often the bloating does not stop even with
carrying out replacement therapy with high doses of enzymes. IN
In this case, it is necessary to add adsorbents to the therapy
(simethicone,
dimethicone)
or
use
combined
enzyme preparations containing adsorbents
(pancreoflat). When performing an enzymatic
therapy
pancreatitis
necessary
avoid
drugs,
containing
bile acid components
in its composition, because
bile acids cause
gain
secretion
pancreas, which
usually undesirable when
exacerbation of pancreatitis; A,
except
Togo,
high
bile acid content
V
intestines,
which
created with intense
enzymatic
therapy, therapy
causes
hologenic
diarrhea. A single dose of enzymes that
recommended
For
treatment
exocrine pancreatic
insufficiency, must contain
at least 20,000-40,000 units. lipases.
Typically the patient should take
2-4 capsules of the drug for main
meals and 1-2 capsules at
small amounts
food. With clinically significant
pancreatic
insufficiency
usually fails completely
eliminate
steatorrhea
even
With
using high doses of drugs,
therefore the adequacy criteria
selected dose of digestive
enzymes are: increase
body weight, normalization of stool
(less than 3 times a day), decreased
bloating. For severe
steatorrhea is additionally prescribed
fat-soluble vitamins (A, D,
E, K), as well as B vitamins. Treatment of endocrine
violations
at
HP
similarly
treatment
diabetes mellitus of another
origin,
however,
given the inclination to
hypoglycemia
And
caloric
failure
these
sick,
limitation
carbohydrates
V
food
undesirable. Moreover,
should
observe
caution
at
purpose
insulin,
because the accompanying
defeat
liver
And
ongoing
use
alcohol
increase the risk of developing
hypoglycemia.
If conservative therapy for CP, especially its biliary-dependent form, is insufficiently effective, endoscopic treatment is indicated:
Surgical interventions are also possible, the indications for which are:are:
pain syndrome that cannot be relieved by other means;
increasing dilatation and deformation of the head of the pancreas;
stricture or obstruction of the bile ducts with the development of mechanical
jaundice;
cysts;
the appearance of a pancreatic fistula with the development of ascites or pleural effusion;
intrapancreatic abscess;
calculosis;
compression of surrounding tissues;
segmental portal hypertension;
suspicion of developing pancreatic cancer. Usually performed straight
(pancreatoduodenal,
subtotal
or
distal resection of the pancreas;
overlay
cystovirsungoenteroanasto
mosa)
or
sanitizing
gallstone interventions
bladder and ducts, as well as
DPK
And
stomach.
By
indications
can
drainage be performed
intervention on Vaterov
papilla
DPK
(sphincterotomy,
virsungotomy)
And
drainage
cyst
under
ultrasound control.
