TABLE OF CONTENTS
Thematic plan of the practical lessons:
Theme 1 «Pathophysiology of digestion, insufficiency of digestion in oral cavity»
Theme 2 «Insufficiency of digestion»
Theme 3 «Pathology of liver. Hepatic failure»
Theme 4 «Kidneys pathology»
Theme 5 «Kidneys insufficiency. Urograms analyses»
Theme 6 Practical training «Pathophysiology of digestive system, liver and kidney»
THEME: PATHOPHYSIOLOGY OF DIGESTION. INSSUFICIENCY OF DIGESTION IN ORAL CAVITY.
Actuality of theme.
A function of the digestive system is providing of an organism by the nutritives, water, which are needed for supporting of organism vital functions and providing of it by energy and plastic materials. There is close communication between the different parts of the digestive system. Violation of one link function can cause substantial changes in all digestive system. Consequences of digestion insufficiency can be serious enough: metabolic disturbance, intoxication, exhaustion and other.
The study of reasons, mechanisms of development of violations which arise up at pathology of digestive system matters very much for a future doctor.
General purpose of the lesson.
To learn the reasons and mechanisms of stomach, intestine and pancreas functions violations.
For this it is necessary to know (the concrete purposes):
➢ To identify typical pathological conditions in the digestive system: lack of digestion (maldigestia) and malabsorption;
➢ To use different principles of classification the most typical forms of diseases of the digestive tract;
➢ To evaluate the significance of experimental modeling of various forms of pathology of the alimentary canal for determining of the causes and mechanisms of their development;
To use the knowledge about the role of nervous and humoral regulation of various departments of the alimentary canal
For realization of purposes of lesson it is necessary to have the base knowledges-skills:
1. Features of digestive channel (department of histology)
2. Functions of stomach, intestine and pancreas (department of physiology)
Checking of the primary level of knowleges.
Give the answer on the next questions:
1. Definition of “digestion insufficiency”.
2. Give the classification of the digestion insufficiency.
3. What disorders of saliva secretion do you know?
4. Characterise the reasons and mechanisms of hypersalivation development.
5. Characterise the reasons and mechanisms of hyposalivation development.
Theoretical questions at the base of which the execution of purpose types of activity is possible.
1. Causes and mechanisms of digestive disorders in the oral cavity.
2. Etiology, pathogenesis, experimental models of dental caries and periodontal disease.
3. Causes, mechanisms and consequences of salivation violations.
4. Violation of esophageal motive function. Etiology and pathogenesis of heartburn.
5. General concept about lack of digestion, principles of classification.
6. Reasons of digestion failure (maldigestia).
7. Role of nutritional and infectious agents, nervous disorders and humoral regulation of the digestive system functioning.
8. Connection of digestive disorders with metabolic and energy disorders in the organism.
9. Disorders of appetite. Anorexia.
Literature.
1. Handbook of general and Clinical Pathophysiology/ Edited by prof.A.V.Kubyshkin, CSMU, 2005.
2. Pathophysiology/ Edited by prof. Zaporozan, OSMU, 2005
Topics for reports:
1. Violation of occlusion in children and their impact on the function of digestion.
2. Sìalolìtìasis, causes and mechanisms of development.
Tests from open base:
1.A 40 year old man who took part in disaster-management at a nuclear power plant fell sick with paradontitis. What etiological agent is the most important for the development of this pathology?
A Emotional stress
B Iron deficit
C Malnutrition
D Increased load of dentoalveolar apparatus
E Streptococcus
2.A patient with inflammation of trigeminal nerve has been having progressive paradontitis for some years. What factor is the most important for parodontitis development?
A Neurodistrophic disorders
B Low activity of leukocytic elastase
C Poor formation of immunoglobulins
D Increased tone of vagus nerve
E Low activity of kallikrein-kinin system
3.In routine examination of the children in a Trans-Carpathian village, many of them displayed multiple caries. Lack of what mineral in food can be linked to the development of caries?
A. Fluoride
B. Iodine
C. Molybdenum
D. Iron
E. Cobalt
4.A patient with inflammation of the trigeminal nerve, has developed in recent years. What is the main factor in the parodontosis development?
A. Neurodystrophic malfunction of parodentium
B. Reduced activity of leukocyte elastase
C. Reduced antibodies formation
D. Raised vagus tonus
E. Reduced activity of kallikrein-kinin system
5.Caries was induced in animals. What is the most important compensatory mechanism in the development of this disease?
A. Formation of secondary dentin by odontoblast
B. Enamel Neoplasm
C. Hypotrophy of salivary glands
D. Inhibition of phagocytosis
E. Over-activity of parathyroid
6.A patients from near Carpathians is suffering from the endemic goiter, turned to the doctor with complaints on gum suppuration and loosened teeth. What is the cause of parodontosis in this case?
A. Endocrine malfunction
B. Stress influences
C. Hypersialosis
D. Swallowing malfunction
E. Malnutrition
7.After poisoning by organophosphorus substances the patient has a long-term increase of salivation. What body malfunction can be caused by hypersalivation?
A. Neutralization of gastric juice
B. Strengthening digestion in the stomach
C Hyposmotic dehydration
D. Hyposmotic hyperhydration
E. Inhibition of wall surface etching
Testing according system “Krok-I”
1. A patient with inflammation of the trigeminal nerve, has developed in recent years. What is the main factor in the parodontosis development?
A. * Neurodystrophic malfunction of parodentium
B. Reduced activity of leukocyte elastase
C. Reduced antibodies formation
D. Raised vagus tonus
E. Reduced activity of kallikrein-kinin system
2. In routine examination of the children in a Trans-Carpathian village, many of them displayed multiple caries. Lack of what mineral in food can be linked to the development of caries?
A. * Fluoride
B. Iodine
C. Molybdenum
D. Iron
E. Cobalt
3. A neurological patient has hypersalivation. What can result it?
A. *Increase of n. vagus tonus
B. Increase of sympathetic nerves tonus
C. Pathology of cerebellum
D. Oppressing the sensitiveness of tastes receptors
E. Blockade of n. vagus
THEME 2: PATHOPHYSIOLOGY OF DIGESTION. INSSUFICIENCY OF DIGESTION IN STOMACH.
Actuality of theme.
A function of the digestive system is providing of an organism by the nutritives, water, which are needed for supporting of organism vital functions and providing of it by energy and plastic materials. There is close communication between the different parts of the digestive system. Violation of one link function can cause substantial changes in all digestive system. Consequences of digestion insufficiency can be serious enough: metabolic disturbance, intoxication, exhaustion and other.
The study of reasons, mechanisms of development of violations which arise up at pathology of digestive system matters very much for a future doctor.
General purpose of the lesson.
To learn the reasons and mechanisms of stomach, intestine and pancreas functions violations.
For this it is necessary to know (the concrete purposes):
➢ To analyze stomach ulcer and / or duodenum as a multifactorial disease;
➢ To describe risk factors of gastric ulcer and / or duodenal ulcer;
➢ To use the modern views about the mechanisms of damage and protective possibilities for analysis of digestive tract for analyses of ulcer pathogenesis;
➢ To evaluate the significance of experimental modeling of various forms of pathology of the alimentary canal for determining of the causes and mechanisms of their development;
➢ To use the knowledge about the role of nervous and humoral regulation of various departments of the alimentary canal for the analysis of violations of motive, secretory and reabsorbtion functions;
➢ To identify the indicators of secretory functions and use them to analyze its typical violations;
➢ To analyze the causes and mechanisms of pancreatitis;
➢ To analyze cause-effective relationships, to be able to separate the pathological changes and compensatory-adaptive reactions, local and system changes at the pathogenesis of pancreatic shock;
➢ To analyze the mechanisms of intestinal digestion disorders, development of maldigestia and malabsorption;
➢ To explain the pathogenesis of clinical manifestations of malabsorption syndrome;
➢ To analyze the clinical forms, causes and mechanisms of intestinal obstruction, explain its outcomes and complications.
For realization of purposes of lesson it is necessary to have the base knowledges-skills:
1. Features of digestive channel (department of histology)
2. Functions of stomach, intestine and pancreas (department of physiology)
Checking of the primary level of knowleges.
Give the answer on the next questions:
1. Disorders of digestion in the stomach. Overview of violations of motive and secretory functions of the stomach.
2. Pathological gastric secretion: types, causes and mechanisms of development.
3. Etiology and pathogenesis of gastric ulcer and / or duodenum disease.
4. Role of Helicobacter pylory.
5. Concept about the etiology and pathogenesis of symptomatic ulcers of the stomach and / or duodenum.
6. Disorders of digestion in the intestine, etiology, pathogenesis.
7. Disorders of digestion associated with pancreatic juice failure.
8. Etiology, pathogenesis, complications of acute and chronic pancreatitis. Pathogenesis of pancreatic shock.
9. Intestinal dyskinesia. Causes, mechanisms and manifestations of constipation and diarrhea. Bowel obstruction: types, etiology, pathogenesis.
10. Violation of barrier function of intestine: intestine autointoxication, coli-sepsis, dysbacteriosis.
11. Violation of cavernous and parietal digestion in the intestine.
12. Malabsorption syndrome: definition, manifestations (diarrhea, reduced body weight, protein deficiency, hypovitaminosis), causes and mechanisms of development. Intestinal fermentopathy.
Literature.
1.Handbook of general and Clinical Pathophysiology/ Edited by prof.A.V.Kubyshkin, CSMU, 2005.
2.Pathophysiology/ Edited by prof. Zaporozan, OSMU, 2005
Topics for reports:
1. Zollinger-Ellison syndrome. Reasons, mechanisms of development, value in pathology.
2. Syndrome of malabsorption, its description.
3. Description of dumping syndrome (postgastrectomy syndrome). Mechanisms of basic violations development.
4. Violations of parietal digestion at children. Its value at dyspepsia development.
5. Endocrine function of stomach in pathology.
Tests of an open database (2010)
1.A year after subtotal stomach resection on account of ulcer of lesser curvature the
following blood changes were revealed: anemia, leukocytopenia and thrombocytopenia,
color index - 1,3, megaloblasts and megalocytes. What factor deficiency caused the
development of thos pathology?
A Castle's factor
B Hydrochloride acid
C Mucin
D Pepsin
E Gastrin
2.Typical symptom of cholera is loss of a large quantity of water and sodium ions by an organism What mechanism initiation of diarrhea in this case9
A. Intensified corticotropin synthesis
B. Intensified renin secretion by the cells of renal arterioles
C. Activation of adenylate cyclase of enterocytes
D. Inhibition of vasopressin synthesis in the hypothalamus
E. Aldosterone oxydation in the adrenal cortex
Testing according system “Krok-I”
1. The patient, 52 years, was delivered to clinic with symptoms of acute pancreatitis and the phenomenon of pancreatic shock. What is the basic mechanism of pancreatic shock?
A. * Income of activated protease from gland to blood
B. Stimulation of pancreatic secretion
C. Breach outflow of pancreatic juice
D. Reduced incretion of insulin
E. Reduced blood pressure
2.The patient complains of frequent nausea, which often leads to vomiting. Malfunction of which stomach function is most likely to be suspected in this patient?
A. * Evacuationg
B. Excretory
C. Suction
D. Incretory
E. Secretory
3. Patient, aged 45, diagnosis: gastric ulcer. Examination of secretory function of the stomach revealed that the amount of basal secretion is 100 ml / hr. And basal acid secretion is 60 mmol / liter. Action of which factor contributes to hypersecretion in the stomach?
A. * Gastrin
B. Glucagon
C. Somatostatin
D. Pancreatic polypeptide
E. Beta-Endorphin
4. Patient complains of occasional stool relaxation, connected with intake of food, rich in fats. He also notices reduced coloring of the stool. Laboratory test found normal content of lipids in blood serum. Malfunction of which lipid metabolism occurs in this case?
A. * Absorption
B. Blood transportation
C. Interim metabolism
D. Deposition in adipose tissue
E. Mobilization from adipose tissue
5. A patient, who received prolonged treatment of glucocorticoids, developed ulcers in the stomach. What is the main mechanism in their development?
A. * Increased secretion and acidity of gastric juice
B. Reduced histamine in gastric mucosa
C. Increased tone of sympathetic nervous system
D. Increased production of prostaglandins E1, E2
E. Reduced parasympathetic nervous system tone
6. A 57-year-old patient was admitted to the gastroenterological department with suspicion on Zollinger-Ellison syndrom because of rapid increase of gastrin level in the blood serum. What disorder of the secretory function of the stomach is the most likely?
A Hyperacid hypersecretion
B Hyperacid hyposecretion
C Achylia
D Hypoacid hyposecretion
E Hypoacid hypersecretion
7. A patient has disturbed digestion of proteins, fats and carbohydrates. It is most likely to be caused by reduced secretion of the following digestive juice:
A. Intestinal
B. Pancreatic
C. Gastric
D. Saliva
E. Bile
8. A patient, who received prolonged treatment of glucocorticoids, developed ulcers in the stomach. What is the main mechanism in their development?
A. * Increased secretion and acidity of gastric juice
B. Reduced histamine in gastric mucosa
C. Increased tone of sympathetic nervous system
D. Increased production of prostaglandins E1, E2
E. Reduced parasympathetic nervous system tone
9.A 2-year-old child has got intestinal dysbacteriosis, which results in hemorrhagic syndrome. What is the most likely cause of hemorrhage of the child?
A Vitamin K insufficiency
B Activation of tissue thromboplastin
C PP hypovitaminosis
D Fibrinogen deficiency
E Hypocalcemia
10.A typical symptom of cholera is great loss of water and sodium ions. What mechanism underlies development of diarrhea in this case?
A Activation of adenylate cyclase of enterocytes
B Increased secretion of renin by the cells of renal arterioles
C Aldosterone oxidation in adrenal cortex
D Inhibition of vasopressin synthesis in hypothalamus
E Increased corticotropin synthesis
11.A newborn has signs of dyspepsia after milk feeding. Symptoms of dyspepsia disappear when milk is substituted for glucose solution. The newborn has low activity of the following enzyme:
A Lactase
B Invertase
C Maltase
D Amylase
E Isomaltase
2008 - 2004
1. A patient, 58 years, carried a insult. Later there was the gastric hemorrhage. Patient never suffers on ulcer disease. What from is the leading mechanism of gastric ulcer development?
A.* Increase of glycocorticoid production.
B. Decrease of glycocorticoid production
C. Decrease of local prostaglandin synthesis
D. Damage of mucous barrier.
E. Hypersecretion of gastric juice.
2. Dumping-syndrome is :
A.* Complex of symptoms, which appears after the complete resection of stomach.
B. Complex of symptoms, which appears after the partial resection of stomach
C. Complex of symptoms, which appears after the resection of bottom of stomach
D. Complex of symptoms, which appears for some patients with ulcer disease
E. Complex of symptoms, which appears after the considerable resection of colon
3. Sick L., complains about a belch, heartburn, frequent constipations. At titruvanni of gastric juice got such information: general acidity - 88 mmol/L, general HCl - 83 mmol/L, free HCl - 50 mmol/L, linked HCl - 33 mmol/L, acid phosphates and organic acids - 5 mmol/L. Estimate the state of acidity of stomach:
A. *Hyperacidic state
B. Gipoacidic state
C. Axilia
D. Norma
E. Hypochlorgydria
4. Sick, 66 years, suffers on reumatoid arthritis over 10 years. Acetylsalitcyl acid and prednisolon adopted in connection with sharpening. Complains about a stomach-ache, belch, nausea, feeling of overfill in epigastrii, flatulence. At gastroscopia found out erosion (0.5 sm x 0.5 sm) of mucus membranes of stomach. What reason of forming of defect of mucous membrane of stomach:
A.* Protracted reception of aspirin and hormones
B. Immune defeat of stomach mucous
C. Development of dysbacteriosis
D. Age-old changes of mucous
E. Protracted hypertonus of stomach musculature
5. A new-born child has diarrhea, signs of intoxication, dehydration of organism appeared on 5-6 days. Indicated phenomena are disappeared after passing to the artificial soul-milk mixtures. A conclusion is done about inheredity insufficiency of galaktosa. What process did develop in a child?
A. *Disorder of membranous digestion
B. Disorder of cavity digestion
C. Disorder of intestine excretory function
D. Disorder of pancreas secretory function
E. Disorder of stomach secretory function
6. For a patient with stomach ulcer disease at an inspection a presence in stomach mucous of stomach of Helicobacter of pylori is discovered. What role of Helicobacter of pylori in development of ulcer disease?
A. *Damage of mucous barrier
B. Causes a hypersecretion
C. Damages of stomach wall blood supply.
D. Inhibition of prostaglandin synthesis
E. Brakes development of ulcer.
7. Ulcers of stomach were found out in a patient, who was treated with glucocorticoids for a long time. What is the main mechanism of ulcer development in this case?
A. *Increase in secretion and acidity of gastric juice
B. Decrease in histamine concentration in stomach wall
C. Increased tonus of sympathetic nervous system
D. Increased production of prostaglandins E
E. Decreased tonus of parasympathetic nervous system
8. Malabsorption syndrome is:
A. Syndrome of membraous maldigestion
B. Syndrome of gastric malabsorption
C. Syndrome of malabsorption in small intestine
D. * Syndrome of intestinal malabsorption
E. Malabsorption of proteins
9. A woman, 50 years, complain about pain in epigastrial area, which calm down after adopting a meal. At an inspection ulcer disease of stomach is diagnosed. What is main factor in development of this pathology?
A. HCl acid and pepsin
B. Bilious acids
C. *Heliсobaсter pylori
D. Decrease of mucous secretion
E. Increase of Е2, Е2b prostaglandin synthesis
10. At an inspection in a diagnostic center patient with ulcer disease of bulbus duodenum found out the presence of Heliсobaсter pylori. Indexes: free acidity - 50 mmol/L, common acidity - 70 mmol/L. What mechanism is main in the origin of this disease?
A. *Stimulation of gastrin and histamin secretions
B. Insufficient secretion of mucus
C. Decrease of Е2, Е2b prostaglandin synthesis
D. Rapid emptying of stomach
E. Decrease of bicarbonate secretion
11. A woman, 45 years, complain about unbearableness of some products (eggs, fish, crabs), dyspeptic phenomenon. At an inspection found out the deficit of iron, dysbacteriosis. In what state acid making function of stomach in patients?
A. Hypersecretion
B. Hyperacidity
C. *Аhilia
D. Normal acidity
E. Normal secretion
12. Patient B. for a long time adopted salicylats, indometacin for treatment of rheumatism. Lately pains appeared in epigastrial area and dyspeptic disorders. During fibrogastroscopif the ulcer of small curvature of stomach is found. What mechanism of ulcer development in this case?
A. Braking of prostaglandin synthesis
B. Decrease of mucin production
C. Increase of stomach secretory activity
D. *Increase of HCl secretions
E. Strengthening of stomach motoric function
13. Patient suffer Zolingera-Elisona syndrome, hypergastrinemia is found out. What state of stomach secretory function is most credible in this case?
A. Organic axilia
B. Functional axilia
C. Hyposecretion
D. Hypoacidity
E. *Hypersecretion
14. At an inspection in gastroenterology for a patient hyperchloremia is discovered. Such violation of stomach secretory function is characteristic?
A. Cancer of stomach
B. *Ulcer disease of duodenum
C. Atrophy gastritis
D. В-12-deficiency anemia
E. Iron –deficiency anemia
15. Patient complain about the decrease of appetite, belch rotten, frequent diarrhea, flatulence. General acidity of gastric juice is 10 units. What disease is most credible in patients?
A. Hyperacidic gastritis
B. Ulcer disease of stomach
C. Ulcer disease of duodenum
D. *Hypoacidic gastritis
E. Anacidic gastritis
16. Patient suffers from duodenum ulcer disease. Violations of what stomach function have a pathogenetic value in the origin of this disease?
A. Motoric
B. *Secretory
C. Reservoir
D. Evacuatory
E. Escritoire
17. To the patient suffers from duodenum ulcer disease the operation of vagotomia was done. What pathogenetic mechanism of this method?
A. *Increased of gastrin secretion
B. Reduced synthesis of prostaglandins
C. Reduced mucus secretion
D. Reduced bicarbonates secretion
E. Broken mucus membranes microcirculation
18. A man, 28 years, complain about pain in epigastrial area, dyspeptic disorders. At gastroscopia found out the numerous ulcer defects of stomach mucus membranes. Zolingera-Elisona syndrome is diagnosed. What pathogenetic mechanism takes leading part in the origin of this pathology?
A. Hypersecretion of pepsinogen
B. Decrease of protective factors action in mucus membranes of stomach
C. *Hypersecretion of gastrin
D. Reflux in stomach duodenal maintenance
E. Increase of stomach motoric
19. A woman, 47 years, long time suffers on functional disorders of nervous system. Development of what disease can be pathogenetic related to the neurosis?
A. Disease of Itsenko-Cushing
B. Chronic glomerulonefritis
C. *Ulcer disease of stomach
D. Pancreatitis
E. Hepatitis
20. A patient complain about «hungry» pains in epigastrial area, feeling of discomfort after adopting rough, rich, spicy food. At an inspection the defect of stomach mucus membranes is set, the protracted uncontrolled application of glycocortikoids is marked in anamnesis. The leading link of pathogenesis was in this case:
A. Surplus of histamin
B. Lack of prostaglandin
C. *Increase n.vagus tonus
D. Surplus of prostaglandin
E. Lack of histamin
21. As a result of gastric juice analyses is set: general acidity - 28 mmol/L, free HCl acid - 1,5 mmol/L, maintenance of gastromucoprotein is reduced. Lack of what vitamin is observed in organism?
A. *Cyancobalamine
B. Folic acid
C. Pantotenic acid
D. Nicothinamid
E. Bioflavonoid
22. Duodenum was removed for a patient. It is caused the decrease of gastrointestinal hormones secretion:
A. Histamin
B. Cholecystokin and secretin
C. *Gastrin and histamin
D. Neurotenzin
E. Gastrin
23. 150 ml of meat broth were introduced into the stomach cavity of experimental dog to a probe the content of what substance will increase quickly in the animal’s blood?
A. Insulin
B. Vasointestinal peptide
C. Neurotensin
D. Somatostatin
E. *Gastrin
24. Patient month ago carried pneumonia with the expressed respiratory insufficiency. Therapy with cefazolin was conducted. Сomplaine about the speed-up (to 6 times for days) selection of the liquid emptying with a specific smell, stomach-ache, feeling of gurchannya. Specify possible reason of diarrhea development:
A. *Development of dysbacterios
B. Toxic influence of antibiotics on intestine mucous
C. Formation of antigen-antibody complexes
D. Violation of the peristaltic reflex regulation
E. Hypoxic damage of mucus membranes
25. On laboratory examination increased amount of diastase in the urine and also a large amount of undigested fat in stool were revealed in a patient female with complain of circular character pain in epigastric area. What form of gastrointestinal tract pathology are described signs typical for?
A. Inflammation of large intestine.
B. Acute appendicitis.
C. Infectious gastritis.
D. Ulcer disease of the stomach
E. *Acute pancreatitis
26. A 8-month child suffers from diarrea, vzduttya stomach, hypotropia, abundant stinking emptying. Symptoms began to show up and grow after introduction to the ration of flour wares feed. Emptying is abundant, foamy, whitishness with a putrid smell, pH - 6. What pathology can be assumed?
A. Pankreatit
B. *Celiacia
C. Malabsorbtion syndrome
D. Hypoacidic gastritis
E. Enterocolitis
27. A new-born child after feeding with milk had dyspepsia, vomit. At feeding with solution of glucose these phenomena disappeared. Insufficient activity of what enzyme which takes part in overcooking of carbohydrates does result in the noted disorders?
A. *Lactase
B. Amilaze
C. Maltaze
D. Saccaraze
E. Isomaltaze
28. Man, 58 years, has clinical picture of sharp pancreatitis. Appearance of what matter in urine can confirm diagnosis?
A. *Diastase
B. Albumen
C. Remaining nitrogen
D. Urea
E. Urinary acid
29. Man 20 years, complaints about sudden strong diarrhea, tenesms, flatulence. All these symptoms arose up after he drink milk. The deficit of what ferment could cause these dyspeptic disorders?
A. * Lactase.
B. Lipase.
C. HCl
D. Tripsin.
E. Bile
30. A patient with the Zollinger-Ellison syndrome [tumour of pancreas] have multiplying secretion of gastric juice, increase of digestive system peristaltic, diarrhea and peptic ulcers. What matters, secretated by the tumour that, does cause the complex of symptoms?
A. *Gastrin
B. Vasoactive intestinal peptid
C. Pepsinogen [pepsins].
D. Tripsinogen [tripsini]
E. Secretin
31. Intrastomach pH metria is done for patient with chronic gastritis. The decrease of gastric juice acidity is set by. The function of what cells is reduced?
A. Endocrinocytes
B. Main eksocrinocytes
C. *Parietal eksocrinocytes
D. Neck cell
E. Additional cell
32. At FGDS for a patient found out in antral part a chronic peptic ulcer associated with Helicobacter pylori. The frequent receives is related with secretion disorder of:
A. *Mucous
B. Pepsin
C. НСl
D. Lipaze
E. Gastrin
Practical work: "CHANGES OF THE GASTRIC ACIDITY AT DISEASES OF STOMACH "
Object of work: determine total, free and combined acid and lactic acid in the gastric juice at hypo-and hyperacidic states.
EXPERIMENT № 1. Determination of gastric juice acidity at hyper-and hypoacidic states (Michaels’s method).
Pour 5ml of gastric juice into the glass, add 2 drops of indicator (dimethylamidoazobenzol and phenolphthalein). Titrate by 0.1 N solution of caustic soda.
Note the initial level of alkali in the burette, the level of the first titration to the color of salmon, while the second - to steady yellow, with the third - to pink.
Gastric juice
before titration 1 2 3
[pic]
Total acidity is determined by the number of 0.1 N NaOH, which was used for the neutralization of 100ml of gastric juice.
Total acidity is calculated by multiplying the number of alkali, which was used for the titration to pink (third titration), at 20.
Free hydrochloric acid is calculated by multiplying the number of alkali, which was used for the first titration (salmon color), at 20.
For calculation of combined acidity deduct the number of alkali, which was used for the first titration from average number of alkali, which was used for the second and third titration and multiply the difference at 20.
I titration - ________ml 0.1 N NaOH
_______ml 0.1 N NaOH x 20 = _______ TU (titration units) - free acid.
II titration - ________ml 0.1 N NaOH
III titration - _______ml 0.1 N NaOH
_______ml 0.1 N NaOH x 20 = __________ TU - total acid.
( + ) - _________ X 20 = ________ TU - combined acid.
2
Conclusion:_____________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
EXPERIMENT № 2. Determination of lactic acid in the gastric juice.
Pour 2ml reagent for lactic acid into the glass. Add the gastric juice drop by drop. If the lactic acid is present at the gastric juice the reagent changes color to yellow.
[pic]
Conclusion:______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
Types of gastric secretions
Norm
[pic]
Вraking type
[pic]
Іnert type
[pic]
Аstenic type
[pic]
Excitement type
[pic]
Situation tasks
1. Sick 45 years, complains on nausea, eructation with unpleasant smell, periodical vomiting, flatulence. Objectively: reduction of body weight, dry skin and mucous membranes. Detected: basal secretion of HCl-15 mmol/l, the maximal-50 mmol\l.
1. What violation of the secretory function in a patient
________________________________________________________________________
2. Specify the mechanisms of development of the symptoms.
_________________________________________________________________________________________________________________________________________________________________________________________________________________________________
3. Name the main principles of the patogenetical treatment of this violation.
_________________________________________________________________________________________________________________________________________________________________________________________________________________________________
2. Patient, 42 years, complaints about pain in the epigastrium, vomiting dark-red by color. In anamnesis a ulcer disease of stomach. Analysis of blood: erythrosytes – 2.8×1012/l, leukocytes – 8×109/l, hemoglobin 90 g/l.
1. Select the most possible complication that arose in the patient? Relevance.
________________________________________________________________________________________________________________________________________________________________________________________________________________________________
2.Name the complication of ulcers disease.
________________________________________________________________________________________________________________________________________________________________________________________________________________________________
3. Name the main principles of the patogenetical treatment of this violation.
________________________________________________________________________________________________________________________________________________________________________________________________________________________________
3. Patient complains at the "hungry" pain in the epigastria area, pyrosis, and feeling of discomfort after taking oily, spicy food. During the examination revealed an ulcer of the stomach, in anamnesis noted continuous using of glucocorticoids without prescription.
1. What is the cause of ulcers in this patient
________________________________________________________________________________________________________________________________________________________________________________________________________________________________
2. Specify mechanisms for the development of ulcers disease.
________________________________________________________________________________________________________________________________________________________________________________________________________________________________
4. Patient complains of pain in the epigastrial area, eructatio, pyrosis, frequent constipation. Detected: basal secretion of HCl-80 mmol/l, the maximal-130 mmol/l.
1. What violation of the secretory function in this patient?
________________________________________________________________________________________________________________________________________________________________________________________________________________________________
2.Specify the mechanisms of development of the symptoms in this condition
_______________________________________________________________________________________________________________________________________________________________________________________________________________________________
3. Name the main principles of the patogenetical treatment of this violation.
________________________________________________________________________________________________________________________________________________________________________________________________________________________________
5. Sick, 66 years old, 10 years he suffers from rheumatoid arthritis. During durable time he use aspirin and prednisolon. Complains on the pain in his stomach, pyrosis, nausea, flatulence. During FGDS an ulcer (1 cm x 1 cm) the mucous membrane of the stomach was found.
1. What is the cause of ulcers in this patient?
________________________________________________________________________________________________________________________________________________________________________________________________________________________________
2. Name the main principles of the patogenetical treatment of this violation Назвіть основні причини виникнення виразкової хвороби шлунка.
________________________________________________________________________________________________________________________________________________________________________________________________________
THEME: «PATHOLOGY OF LIVER».
Actuality of theme.
The pathology of liver and biliary ways is the topical problem of modern medicine, that it is related to the high level of morbidity and death from this pathology.
Various etiologic factors (hepatotropic viruses, bacteria, protozoan, helmints, alcohol, enormous medications, toxic substanses and great number of other reasons) are able to entail the acute or chronic damage of liver which can be completed by hepatic insufficiency development.
Because of said higher, knowledge of reasons and mechanisms of this pathology development will promote in subsequent activity of choice of rational approaches to treatment of every concrete.
General purpose of the lesson.
To learn the reasons and mechanisms of development of different jaundices. To learn reasons of origin of hepatic insufficiency different types, violation of liver functions.
For this it is necessary to know (the concrete purposes):
➢ To describe the concept, evaluate the criteria and use them for the classification of hepatic failure, hepatic coma, jaundice, portal hypertension;
➢ To analyze various options for liver failure causes and mechanisms of the origin, nature of occurrence, severity;
➢ To describe the etiological factors and the mechanisms of liver failure development, jaundice, portal hypertension;
➢ To explain the metabolic (protein, lipid, carbohydrate, xenobiotics metabolism) and hormonal disorders in the organism at liver failure;
➢ To use the modern achievements of neurophysiology for explanation of the pathogenesis of encephalopathy and coma at hepatic failure;
➢ To explain the mechanisms of jaundices;
➢ To analyze the causes, mechanisms of development of the most important clinical syndromes at various types jaundices;
➢ To analyze pathogenesis of portal hypertension, to explain the mechanisms of its main clinical manifestations.
For realization of purposes of lesson it is necessary to have the base knowledges-skills:
1. To explain the structure of liver and biliary ways (department of normal anatomy).
2. To name the basic functions of liver (department of normal physiology).
3. To name composition of bile and its role in the process of digestion (department of normal physiology).
The checking of primary level of knowledges.
Give the answers to the following questions:
1. Definition of conception «jaundice».
2. Classification of jaundices by pathogenesis.
3. Reasons, mechanisms of hemolitic jaundice development.
4. Reasons, mechanisms of hepatocellular jaundice development.
5. Reasons, mechanisms of mechanic jaundice development.
6. Mechanisms of pigmental metabolism violation at a hemolitic jaundice.
7. Mechanisms of pigmental metabolism violation at a hepatocellular jaundice.
8. Mechanisms of pigmental metabolism violation at a mechanic jaundice.
9. Reasons and mechanisms of cholemic syndrome development.
10. Reasons and mechanisms of acholic syndrome development.
11. Definition of conception «hepatic insufficiency».
12. Classification of hepatic insufficiency by pathogenesis, disease course, expression of clinical manifestations.
13. Reasons and mechanisms of hepato-vascular insufficiency development.
14. Reasons and mechanisms of hepato-cellular insufficiency development.
15. Reasons and mechanisms of cholestatic insufficiency development.
16. Basic clinical manifestations of hepatic insufficiency and mechanisms of their development.
17. Hepatic comma, definition of concept. Reasons and mechanisms of its development.
18. Conception about portal hypertension. Reasons and mechanisms of its development.
Topics for reports:
1. Violation of antitoxic function of liver.
2. Surgical methods of hepatic insufficiency treatment.
3. Modern instrumental methods of liver research.
4. Role of cerebrotoxic substances in hepatic comma development
Differentiate diagnostic of the different kind of jaundice
|Indexes |Hemolytic jaundice |Hepatocellular jaundice |Mechanic jaundice |
|Unconjugated bilirubin of |↑ |↑ |N |
|blood | | | |
|Conjugated bilirubin of |N |↑ |↑ |
|blood | | | |
|Bile acids |- |+ |+ |
|Stercoboloi in the feces |↑ |+ (1ст.); - (3ст) |- |
|Urobilin |+ |+ (1ст.); - (3ст) |- |
|Bilirubinyuria |- |+ |+ |
|Cholalyria |- |+ |+ |
|Colour of urine |yellow |dark colour |dark colour |
|Colour of feces |hypercholic |hypo-, acholic |acholic |
|Cholemic syndrome |- |+ |+ |
|Acholic syndrome |- |+ |+ |
Theoretical questions at the base of which the execution of purpose types of activity is possible.
1. Liver insufficiency: definition, classification.
2. Etiology, pathogenesis, experimental models of liver failure.
3. Typical disorders of carbohydrate, protein, lipid, water-electrolyte metabolism, metabolism of microelements, vitamins and hormones, disorders of functional systems of the organism at failure.
4. Inssuficiency of antitoxic liver function, mechanisms of manifestations.
5. Types, causes, pathogenesis of hepatic coma. Role of cerebrotoxic substances.
6. Lack of excretory liver function, main manifestations.
7. Definition, criteria, types of jaundice, their causes and mechanismsof development.
8. Comparison of pigmentary disorders at hemolytic, parenchimatous and mechanical jaundice; cholemic syndrome and hypo-, acholia.
9. Gallstone disease.
10. Portal hypertension syndrome: etiology, pathogenesis, manifestations.
11. Mechanisms of ascites, hepatolienal and hepatorenal syndromes.
Literature.
1. Handbook of general and Clinical Pathophysiology/ Edited by prof.A.V.Kubyshkin, CSMU, 2005.
2. Pathophysiology/ Edited by prof.Zaporozan, OSMU, 2005
Tests of an open database (2010)
1.A patient ill with jaundice has increased content of conjugated bilirubin and bile acids in blood, no stercobilinogen in urine. What jaundice are these symptomps typical for?
A Obstructive
B Hepatic
C Hepatocellular
D Hemolytic
E Cythemolytic
2.A 16 year old boy after an illness has diminished function of protein synthesis in liver as a result of vitamin K deficiency. It will cause disturbance of:
A Blood coagulation
B Erythrocyte sedimentation rate
C Anticoagulant generation
D Erythropoietin secretion
E Osmotic blood pressure
3.After consumption of rich food a patient has nausea and heartburn, steatorrhea. This condition might be caused by:
A Bile acid deficiency
B Increased lipase secretion
C Disturbed tripsin synthesis
D Amylase deficiency
E Disturbed phospholipase synthesis
4.A patient complains of frequent diarrheas, especially after consumption of fattening food, and of body weight loss. Laboratory examination revealed steatorrhea; hypocholic feces. What can be the cause of this condition?
A Obturation of biliary tracts
B Mucous membrane inflammation of small intestine
C Lack of pancreatic lipase
D Lack of pancreatic phospholipase
E Unbalanced diet
5.In patients with the biliary tract obstruction the blood coagulation is inhibited; the patients have frequent hemorrhages caused by the subnormal assimilation of the following vitamin:
A K
B A
C D
D E
E C
6.Examination of a patient suffering from chronic hepatitis revealed a significant decrease in the synthesis and secretion of bile acids. What process will be mainly disturbed in the patient’s bowels?
A Fat emulsification
B Protein digestion
C Carbohydrate digestion
D Glycerin absorption
E Amino acid absorption
7.A patient has yellow skin color, dark urine, dark-yellow feces. What substance will have strengthened concentration in the blood serum?
A Unconjugated bilirubin
B Conjugated bilirubin
C Mesobilirubin
D Verdoglobin
E Biliverdin
8.A 46 year old woman suffering from cholelithiasis developed jaundice. Her urine became dark-yellow and feces became colorless. Blood serum will have the highest concentration of the following substance:
A Conjugated bilirubin
B Unconjugated bilirubin
C Biliverdin
D Mesobilirubin
E Urobilinogen
9.A patient ill with jaundice has increased content of conjugated bilirubin and bile acids in blood, no stercobilinogen in urine. What jaundice are these symptomps typical for?
A Obstructive
B Hepatic
C Hepatocellular
D Hemolytic
E Cythemolytic
Testing according system “Krok-I”
1.A patient who has been treated for viral hepatitis B developed symptoms of hepatic insufficiency. What changes indicating disorder in protein metabolism are likely to be observed in this case?
A. Absolute hyperalbuminemia
B. Absolute hypoalbuminemia
C. Protein rate in blood will stay unchanged
D. Absolute hyperglobulinemia
2. Absolute hyperfibrinogenemia Blood analysis of a patient suffering from jaundice revealed increase of total bilirubin by its indirect fraction. Urine and feces have intense coloring. What is the most probable mechanism of these abnormalities?
A. Impaired transformation of urobilinogen in the liver
B. Damage of liver parenchyma
C. Obstraction of bile outflow from liver
D. Increased hemolysis of erythrocytes
E. Impaired generation of direct bilirubin
3.A female patient suffering from chronic hepatitis complains about an increased susceptibility to barbiturates, which previously induced no symptoms of intoxication. This may be explained through the following liver dysfunction:
A. Metabolic
B. Hemopoietic
C. Hemodynamic
D. Cholepoietic
E. Phagocytal
4.A 43 year old female patient was admitted to the hospital with compaints op in the right subcostal area, skin itch. Examination revealed hypalgesia and hematolysis, skin icteritiousness, bradycardia, hypotonia. What is the most probable cause of these symptoms?
A. Diabetes mellitus
B. Hepatocellular jaundice
C. Parenchymatous jaundice
D. Cholemia
E. Intensification of erythrocyte haemolysis
5. A patient with apparent icteritiousness of skin, sclera and mucous membranes was admitted to the hospital. The patient’s urine was of brown by color, analysis revealed presence of direct bilirubin. Feces had low concentration of bile pigments. What type of jaundice is it?
A. Obturative
B. Absorbtion
C. Parenchymatous
D. Conjugated
E. Haemolytic
6. A patient `consulted a doctor about acute pain in the right subcostal area. During examination the doctor noticed yellowed sclera of the patient. Laboratory analyses revealed high activity of alanine-aminotransferase and negative reaction to stercobilin in feces. What disease are these symptoms typical for?
A. Hepatitis
B. Chronic colitis
C. Chronic gastritis
D. Haemolytic jaundice
E. Cholelithiasis
7.Examination of a patient revealed that dental hypoplasia was caused by hypovitaminosis of vitamins A and D. These vitamins were administered per os but they didn't have any medicinal effect. What is the probable cause of disturbed vitamin assimilation9
A.Achlorhydria
B.Bile acid deficiency
С Hypochlorhydria
D. Hyperchlorhydria
E. Achylia
8.Hepatic dysfunctions accompanied by insufficient inflow of bile to the bowels result in coagulation failure. This phenomenon can be explained by:
A.Iron deficiency
B.Vitamin К deficiency
C.Erythropenia
D.Leukopenia
E.Thrombocytopenia
9.A patient has disturbed digestion of proteins, fats and carbohydrates. It is most likely to be caused by reduced secretion of the following digestive juice:
A. Intestinal
B. Pancreatic
C. Gastric
D. Saliva
E. Bile
10.Enzymatic jaundices are characterized by dysbalanced activity of UDP-glucuronyl transferase. What compound is accumulated in the blood serum in case of these pathology?
A .Verdoglobin
B. Indirect bilirubin
C. Direct bilirubin
D. Biliverdin
E. Mesobilirubin
11.A patient who has been treated for viral hepatitis B developed symptoms of hepatic insufficiency. What changes indicating disorder in protein metabolism are likely to be observed in this case?
A. Absolute hyperalbuminemia
B. Absolute hypoalbuminemia
C. Protein rate in blood will stay unchanged
D. Absolute hyperglobulinemia
E. -
12.Absolute hyperfibrinogenemia Blood analysis of a patient suffering from jaundice revealed increase of total bilirubin by its indirect fraction. Urine and feces have intense colouring. What is the most probable mechanism of these abnormalities?
A. Impaired transformation of urobilinogen in the liver
B. Damage of liver parenchyma
C. Obstraction of bile outflow from liver
D. Increased haemolysis of erythrocytes
E. Impaired generation of direct bilirubin
13.A female patient suffering from chronic hepatitis complains about an increased susceptibility to barbiturates, which previously induced no symptoms of intoxication. This may be explained through the following liver dysfunction:
A. Metabolic
B. Hemopoietic
C. Hemodynamic
D. Cholepoietic
E. Phagocytic
14.A 43 year old female patient was admitted to the hospital with compaints op in the right subcostal area, skin itch. Examination revealed hypalgesia and hematolysis, skin icteritiousness, bradycardia, hypotonia. What is the most probable cause of these symptoms?
A. Diabetes mellitus
B. Hepatocellular jaundice
C. Parenchymatous jaundice
D. Cholemia
E. Intensification of erythrocyte haemolysis
15.A patient with apparent icteritiousness of skin, sclera and mucous membranes was admitted to the hospital. The patient’s urine was brown by color, analysis revealed presence of direct bilirubin. Feces had low concentration of bile pigments. What type of jaundice is it?
A. Obturative
B. Absorbtion
C. Parenchymatous
D. Conjugated
E. Haemolytic
16. A patient `consulted a doctor about acute pain in the right subcostal area. During examination the doctor noticed yellowed sclera of the patient. Laboratory analyses revealed high activity of alanine-aminotransferase and negative reaction to stercobilin in feces. What disease are these symptoms typical for?
A. Hepatitis
B. Chronic colitis
C. Chronic gastritis
D. Haemolytic jaundice
E. Cholelithiasis
17.Examination of a patient revealed that dental hypoplasia was caused by hypovitaminosis of vitamins A and D. These vitamins were administered perorally but they didn't have any medicinal effect. What is the probable cause of disturbed vitamin assimilation9
A. Achlorhydria
B. Bile acid deficiency
С Hypochlorhydria
D. Hyperchlorhydria
E. Achylia
18.Hepatic dysfunctions accompanied by insufficient inflow of bile to the bowels result in coagulation failure. This phenomenon can be explained by:
A. Iron deficiency
B. Vitamin К deficiency
C. Erythropenia
D. Leukopenia
E. Thrombocytopenia
19.A patient has disturbed digestion of proteins, fats and carbohydrates. It is most likely to be caused by reduced secretion of the following digestive juice:
A. Intestinal
B. Pancreatic
C. Gastric
D. Saliva
E. Bile
20.Enzymatic jaundices are characterized by dysbalanced activity of UDP-glucuronyl transferase. What compound is accumulated in the blood serum in case of these pathologies9
A .Verdoglobin
B. Indirect bilirubin
C. Direct bilirubin
D. Biliverdin
E. Mesobilirubin
21.Patient with chronic hepatitis had his tooth removed. Bleeding that occurred after this failed to stop for 2 hours. Hemostasis system test revealed reduced content of several coagulation factors. Malfunction of which liver function has led to hemostasis breach in this patient?
A. * Protein synthesizing
B. Antitoxic
C. Gastrointestinal
D. Hormonal
E. Security
22.A patient, suffering from bilious - stone illness, due to obtrusion of bile ducts had discolored fat faeces. Absence of which bile component can cause the steatorrhea phenomenon?
A. * Bile acids
B. Cholesterol
C. Bile pigments
D. Fatty acids
E. Alkaline phosphatase
23.A patient, 35 years, developed immune hemolytic anemia. Which blood serum indicated is most likely to grow?
A. * Indirect bilirubin
B. Direct bilirubin
C. Sterkobilinohen
D. Mezobilinohen
E. Protoporphyrin
24.Patient with alcoholic cirrhosis of the liver complaints of general weakness, shortness of breath. Found: lower blood pressure, ascites, enlargement of superficial veins of the anterior abdominal wall, splenomegaly. Which hemodynamic malfunction is observed in the patient?
A. * Portal hypertension syndrome.
B. Insufficiency of the left ventricle of the heart
C. Insufficiency of the right ventricle of the heart
D. Collapse
E. Total heart failure
25. Following mushroom poisoning, the patient displayed yellow coloring of skin and sclera, dark urine. Which pigment causes hemolytic jaundice in patient’s urine?
A. * Stercobilin
B. Monoglyukuronid bilirubin
C. Unconjugated bilirubin
D. Verdoglobin
E. Biliverdin
26.The patient, 25 years, was diagnosed with chronic hepatitis. The patient complains of body weight loss of 10 kg in 2 months. Objectively: the skin is dry, scaly, pale with a yellowish tinge, punctual hemorrhages on the skin, bleeding gums. Malfunction of which liver function is reflected by punctual hemorrhage and bleeding?
A. * Protein-synthesizing
B. Pigment-forming
C. Glikogen-synthesizing
D. Detoxifying
E. Depositing
27. Patient, 48 years, came to the hospital with complaints of weakness, irritability, sleep disturbance. Skin and sclera are yellow. Blood test reveals: direct bilirubin, cholalemia; acholic feces; urine - dark color (bilirubin). What type of jaundice occurs in this case?
A. * Mechanical
B. Hemolytic
C. Parenchymatous
D. Zhilber syndrome
E. Krihlera-Najjar syndrome
28. Patient L., age 55, with acute biliary colic was admitted to the gastroenterological department. Objective: body temperature 38 C, sclera, mucous membranes and skin are icteric, dark urine, light feces. Patient complains of itchy skin. What is the cause of jaundice in this patient?
A. * Obturation of biliary ducts
B. destruction of hepatocytes
C. enhanced breakdown of red blood cells
D. malfunction of lipid metabolism
E. prolonged use of products rich in carotene
29.The patient with jaundice has increased content of direct bilirubin and bile acids in the blood, no sterkobilinogen in urine. What type of jaundice is responsible for these symptoms?
A. * Mechanical
B. Hepatic
C. Parenchymatous
D. Hemolytic
E. Hemolytic
30.Enzymatic jaundices are characterized by dysbalanced activity of UDP-glucuronyl transferase. What compound is accumulated in the blood serum in case of these pathologies9
A .Verdoglobin
B. Indirect bilirubin
С Direct bilirubin
D. Biliverdin
E. Mesobilirubin
31.Examination of a patient revealed that dental hypoplasia was caused by hypovitaminosis of vitamins A and D. These vitamins were administered perorally but they didn't have any medicinal effect. What is the probable cause of disturbed vitamin assimilation9
A. Achlorhydria
B. Bile acid deficiency
С Hypochlorhydria
D. Hyperchlorhydria
E. Achylia
32. Blood analysis of a patient ill with jaundice revealed increase of total bilirubin by its indirect fraction. Urine and feces are intensively stained. What is the most probable mechanism of these abnormalities9
A. Damage of liver parenchyma
B. Increased erythrocyte hemolysis
C. Disturbed conversion of urobilinogen in liver
D. Obstructed bile outflow from the liver
E. Disturbed formation of direct bilirubin
Situation task:
1. Patient K, 48 years, is in a reanimation after poisoning by carbon tetrachloride. The state is grave, patient is unconscious, a pulse is thread, frequency of heart beating - 40’/min, BP - 75/40 mm.Hg. Breathing is periodical (Biot's respiration). In blood: decrease of albumen maintenance (16 g/l), direct bilirubin - 155 micromole /l. In urine is high maintenance of ammonia and bilirubin.
1) Give definition of conception «hepatic insufficiency».
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
2) Give classification of hepatic insufficiency by pathogenesis.
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
3) What type of hepatic insufficiency is developed at a patient?
__________________________________________________________________________________________________
4) Describe the mechanisms of clinical signs development.
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
2. Icteritiousness of skin and mucuses, oppressing of tendons reflexes and pain sensitiveness were founded at a patient who suffers from occurrence of stone in the bile-excreting wais. Urine is of “color of beer”, feces is “acholic”. BP is 90/40 mm.HG, frequency of heart beating - 52‘/min. In blood: increasing of cholesterol, direct bilirubin and bilious acids, in urine - bilious acids, direct bilirubin, sterkobilin is absent.
1) Give definition of conception «hepatic insufficiency».
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
2) Give classification of hepatic insufficiency by pathogenesis.
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
3) What type of hepatic insufficiency is developed at a patient?
__________________________________________________________________________________________________
4) Describe the mechanisms of clinical signs development.
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
3. Patient is suffers from headache, irritability, rapid fatigueability, pain in the right hypochondrium, itching of skin. Objectively: icteritiousness of skin and mucuses, enlargement of liver, during palpation – painful, tenderness, BP - 80/40 mm.Hg, frequency of heart beating - 46‘/min. In the blood: level of direct bilirubin - 34 micromole/l, level of indirect bilirubin - 35,2 micromole/l, in urine - bile acids, direct bilirubin, urobilinogen; sterkobilin in the feces is diminished.
1) Give definition of conception «hepatic insufficiency».
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
2) Give classification of hepatic insufficiency by pathogenesis.
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
3) What type of hepatic insufficiency is developed at a patient?
__________________________________________________________________________________________________
4) Describe the mechanisms of clinical signs development.
__________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
4. Chronic hepatitis was diagnosed at a patient, 25 years. He is suffers from the loss of mass of body on 10 kg during 2 months. Objectively: a skin is dry, peels, pale with a rather yellow tint, petechial hemorrhages on a skin, hemorrhages of gums.
1) Give definition of conception «hepatic insufficiency».
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
2) Give classification of hepatic insufficiency by pathogenesis.
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
3) What type of hepatic insufficiency is developed at a patient?
__________________________________________________________________________________________________
4) Describe the mechanisms of clinical signs development.
__________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
5. Patient N., 46 years, suffers from absence of appetite, nausea, pain in right hypochondrium, which increases at adopting rich food, icteritiousness of sclera, darkening of urine. Intravenous injections were made one months ago. In the blood: multiplying of indirect and direct bilirubin. In urine: direct bilirubin and irobilin are multiplying. Feces - hypocholic.
1) Give definition of conception «hepatic insufficiency».
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
2) Give classification of hepatic insufficiency by pathogenesis.
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
3) What type of hepatic insufficiency is developed at a patient?
__________________________________________________________________________________________________
4) Describe the mechanisms of clinical signs development.
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
6. A patient with an jaundice has an increase of indirect faction of bilirubin in the blood, the promoted level of sterkobilin and urobilin in urine, in the blood smear is microspherocytosis. Feces - hypercholic.
1) Give definition of conception «hepatic insufficiency».
____________________________________________________________________________________________________________________________________________________________________________________________________
2) Give classification of hepatic insufficiency by pathogenesis.
____________________________________________________________________________________________________________________________________________________________________________________________________
3) What type of hepatic insufficiency is developed at a patient?
__________________________________________________________________________________________________
4) Describe the mechanisms of clinical signs development.
________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
Mark the changes at the blood tests. Make a conclusion.
Sign «–» means, that such index is not able to be founded by the methods of laboratory diagnostic or absent at the biomaterial.
|7. |Blood |Urine |Feces |
|Common bilirubin |3,6 mg% |— |— |
|Conjugated bilirubin |2,5 mg% |Present |— |
|Urobilin |Absent |Absent |— |
|Stercobilin |Absent |Absent |«Trace» |
|Bile acids |Absent |Absent |— |
|Activity of ALT |Norm |— |— |
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
|8. |Blood |Urine |Feces |
|Common bilirubin |2,1 mg% |— |— |
|Conjugated bilirubin |0,2 mg% |Absent |— |
|Urobilin |Absent |Absent |— |
|Stercobilin |Increased |Increased |Increased |
|Bile acids |Absent |Absent |— |
|Activity of ALT |Norm |— |— |
____________________________________________________________________________________________________________________________________________________________________________________________________
|9. |Blood |Urine |Feces |
|Common bilirubin |4,4 mg% |— |— |
|Conjugated bilirubin |0,35 mg% |«Trace» |— |
|Urobilin |Present |Present |— |
|Stercobilin |Increased |Increased |Norm |
|Bile acids |Absent |Absent |— |
|Activity of ALT |Increased |— |— |
____________________________________________________________________________________________________________________________________________________________________________________________________
|10. |Blood |Urine |Feces |
|Common bilirubin |3,5 mg% |— |— |
|Conjugated bilirubin |2,1mg% |Present |— |
|Urobilin |Absent |Absent |— |
|Stercobilin |«Trace» |«Trace» |Decreased |
|Bile acids |Present |Increased |— |
|Activity of ALT |Increased |— |— |
____________________________________________________________________________________________________________________________________________________________________________________________________
|11. |Blood |Urine |Feces |
|Common bilirubin |1,8 mg% |— |— |
|Conjugated bilirubin |0,2mg% |Absent |— |
|Urobilin |Absent |Absent |— |
|Stercobilin |Norm |Norm |Norm |
|Bile acids |Absent |Absent |— |
____________________________________________________________________________________________________________________________________________________________________________________________________
|12. |Blood |Urine |Feces |
|Common bilirubin |4,8 mg% |— |— |
|Conjugated bilirubin |0,35mg% |«Trace» |— |
|Urobilin |Absent |Absent |— |
|Stercobilin |Decreased |Decreased |Decreased |
|Bile acids |Present |Present |— |
|Activity of ALT |Increased |— |— |
|Activity of AST |Increased |— |— |
____________________________________________________________________________________________________________________________________________________________________________________________________
|13. |Blood |Urine |Feces |
|Common bilirubin |2,6 mg% |— |— |
|Conjugated bilirubin |0,15mg% |Absent |— |
|Urobilin |Present |Present |— |
|Stercobilin |Increased |Increased |Increased |
|Bile acids |Absent |Absent |— |
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
Practical work: "PATHOLOGY OF LIVER"
Object of work: to show the general toxic effects of bile on the frog’s body, effect on the heart, effects on the rabbit blood coagulation.
EXPERIMENT № 1. Influence of bile at the time of coagulation.
Bring a drop of blood taken from the rabbit ear vein at the paraffined watch glass. Add a drop of physiological solution.
Bring a drop of blood at the other paraffined watch glass. Add a drop of bile diluted by physiological solution in half.
Determine the clotting time in both drops.
Clotting time in the first drop - _______min.
Clotting time in the second drop - ________min.
Conclusion:______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
EXPERIMENT № 2. Toxic effect of bile on the frog’s body.
Inject under the frog skin 1-2ml of bile. Put the frog under the hood and observe the change of the animal general condition. Acute general inhibition develops in 10-15 min. after the bile introduction. For example, if you’ll put a frog on its back, it doesn’t turn to abdomen; if you’ll make the needle stick, the animal reaction poorly to it or no response at all.
Conclusion:______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
EXPERIMENT № 3. Influence of bile acid on the frog’s reflexes speed.
Decapitate a frog. Drop the frog’s arms into the 2% solution of sulfuric or hydrochloric acid and determine the speed of reflexes in drop out of the arms from the acid solution (wash the frog’s arms by water after every immersion in acid).
Inject 2-3ml of bile into the dorsal lymph sac and determine the speed of reflexes in 10-15 min. after the injection. Reflex is slow or absent.
Speed of reflex before the introduction of bile - _______sec;
Speed of reflex after the introduction of bile - _______sec.
Conclusion:______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
EXPERIMENT № 4. Toxic effect of bile on the frog’s heart.
Destroy the frog’s spinal cord. Open the thorax cavity. Free the heart from pericardium, cut the fraenum, take the heart tip by serfin and record initial cardiogram.
Inject 0.2 ml of 20% solution of bile into the heart and record the cardiogram again. Note, bradycardia and reduced the amplitude of heart rate.
Then inject 0.1 ml of undiluted bile into the heart and observe slowing and stopping of cardiac activity.
Conclusion:______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
THEME: «Pathology of kidney functions».
Actuality of theme. Kidney act important part in support of homeostasis, which is characterized by the constancy of liquid volume, its osmotic concentration and ionic composition. Different violations of kidney work can cause proper changes of the noted indexes.
No less important role of kidney is elimination of nitrous metabolism products, foreign matters from the organism. Violation of substances excretion is one of basic manifestations of kidney insufficiency in the case of their direct damage, and also as a result of action of extrarenal factors.
Kidney are not only excretory but also an incretory organ which takes part in the vessels tone and erythropoiesis regulation.
Study of etiology and pathogenesis of kidney pathology is a necessity for practical activity of every doctor. Knowledge of reasons and mechanisms of this pathology development will be the choice of rational ways of every concrete patient treatment.
General purpose of the lesson.
To learn principal reasons and mechanisms of kidney diseases development. To analyze the basic mechanisms of violations at kidney pathology.
For this it is necessary to know (the concrete purposes):
➢ To analyze typical violations of quantitative and qualitative composition of urine;
➢ To describe the causes and mechanisms of glomerular filtration, tubular reabsorption and secretion disorders development;
➢ To understand of renal clearance, be able to calculate and apply it for analyze of different parts of the nephron disorders;
➢ To analyze the mechanisms of pathological proteinuria, explain what kidney disease may be related to the development of its kinds;
➢ To identify acute renal failure, its criteria, to understand the pathophysiological principles of classification;
➢ To analyze the causes and mechanisms of prerenal, renal and postrenal failure;
➢ To be able to explain the mechanism of reduction of glomerular filtration rate at different variants of acute renal failure;
➢ To evaluate the different approaches to experimental modeling of acute diffuse glomerulonephritis in identifying the causes and mechanisms of its development;
➢ To identify nephrotic syndrome according to its clinical and pathophysiological manifestations, explain the etiology of primary and secondary nephrotic syndrome;
➢ To treat acute tubular necrosis as an important cause of acute renal failure;
➢ To identify chronic renal failure, its criteria in terms of kidney function depending on the stage and the clinical manifestations;
➢ To describe the causes and mechanisms of chronic renal failure;
➢ To analyze reactive changes of blood flow in the kidneys when they are damaged;
➢ To explain the metabolic disturbances (metabolism of sodium and water, metabolism of potassium, acid-basic balance, mineral metabolism, metabolism of xenobiotics / drugs) and endocrine changes in kidney function in chronic renal failure;
➢ To evaluate the significance of azotemia retention and other metabolic disorders in the development of multiple organ failure;
➢ To explain the general principles of prevention and treatment of acute and chronic renal failure.
For realization of purposes of lesson it is necessary to have the base knowledges-skills:
1. To explain the anatomic structure of kidney and urinary tracts (department of normal anatomy).
2. To name the basic functions of kidney and explain their mechanisms (department of normal physiology).
3. To name the basic components of urine (department of normal physiology).
The checking of primary level of knowledges.
Give the answers to the following questions:
1. Name the basic quantitative urinary symptoms which arise up at the diseases of kidney.
2. Conception about poly-, oligo-, anuria, mechanisms of their development.
3. Conception about hyper-, hypo-, isosthenuria, mechanisms of their development.
4. Name the basic qualitative urinary symptoms which arise up at the diseases of kidney.
5. Proteinuria, definition. Kinds, mechanisms of development.
6. Glycosuria, definition. Kinds, mechanisms of development.
7. Hematuria, definition. Kinds, mechanisms of development.
8. Conception about leukocyteuria. Reasons and mechanism of development.
9. Cylindruria, definition. Reasons of origin. Types of cylinders, mechanism of their education.
10. Name basic unurinary symptoms which arise up at the diseases of kidney.
11. Mechanism of hypertension development at the diseases of kidney.
12. Mechanism of kidney edema development.
13. Mechanism of anaemia development at the diseases of kidney.
14. Violation of hemostasis at the diseases of kidney. Mechanisms of development.
15. Violation of ABB at the diseases of kidney. Mechanisms of development.
16. Nephritic syndrome, definition of conception. Reasons and mechanisms of development.
17. Basic urinary and unurinary symptoms which arise up at a nephritic syndrome. Mechanism of development.
18. Nephrotic syndrome, definition of conception. Reasons and mechanisms of development.
19. Basic urinary and unurinary symptoms which arise up at a nephrotic syndrome. Mechanism of development.
20. Kidney insufficiency, definition of conception. Kinds. Mechanisms of development.
21. Reasons and mechanisms of acute kidney insufficiency development.
22. Reasons and mechanisms of chronic kidney insufficiency development.
23. Conception about urolithiasis. Reasons, mechanisms of development. Consequences.
Theoretical questions at the base of which the execution of purpose types of activity is possible.
1. Concept about renal insufficiency, principles of classification.
2. Prerenal, renal and postrenal mechanisms of renal processes disorders.
3. Causes and mechanisms of blood circulation disorders in the kidneys.
4. Functional and physical-chemical disturbances of glomerular filtration.
5. Causes and mechanisms of tubular reabsorption and secretion violations. Hereditary tubulopathy.
6. Main indexes of kidneys functions. Using of functional tests for determination of the type of renal dysfunctions.
7. Quantitative and qualitative changes of urine composition.
8. Oliguria, anuria and polyuria. Water, osmotic and hypertensive diuresis. Hypo-and izostenuriya.
9. Abnormal urine components: proteinuria, cylindruria, glucosuria, acidaminuria, hematuria, leukocyteuria. Concept about selective and non-selective proteinuria and its mechanisms.
10. Common manifestations of kidney functions failure.
11. Causes, manifestations and mechanisms of retention azotemia. Pathogenesis of renal edema.
12. Violation of acid-base balance: azotemic renal acidosis, proximal and distal canalicular acidosis.
13. Mechanisms of hypertension, anemia, abnormalities of hemostasis at renal failure.
14. Syndrome of acute and chronic renal insufficiency: criteria, causes and mechanisms of development, clinical manifestations.
15. Pathogenesis of uremic coma. Principles of therapy of renal failure.
16. Concept of extracorporeal and peritoneal hemodialysis, lymphodialysis, lymphosorbtion.
17. Glomerulonephritis: definition, principles of classification.
18. Experimental models and modern understanding of the etiology and pathogenesis of diffuse glomerulonephritis.
19. Nephrotic syndrome, primary and secondary.
20. Causes and mechanisms of kidney stones formation, urolithiasis.
Themes for reports:
1. Diabetes mellitus and pathology of kidney.
2. Glomerulonephritis: basic mechanisms of development. Experimental models.
3. Reasons, mechanisms of development and consequences of pyelonephritis.
4. Pathology of kidney and pregnancy.
Literature.
1. Handbook of general and Clinical Pathophysiology/ Edited by prof.A.V.Kubyshkin, CSMU, 2005.
2. Pathophysiology/ Edited by prof.Zaporozan, OSMU, 2005
Tests of an open database (2010)
1.A 62 y.o. woman complains of frequent pains in the area of her chest and backbone, rib fractures. A doctor assumed myelomatosis (plasmocytoma). What of the following laboratory characteristics will be of the greatest diagnostical importance?
A Paraproteinemia
B Hyperalbuminemia
C Proteinuria
D Hypoglobulinemia
E Hypoproteinemia
2.A 65 year old man suffering from gout complains of kidney pain. Ultrasound examination revealed renal calculi. The most probable cause of calculi formation is the strengthened concentration of the following substance:
A Uric acid
B Cholesterol
C Bilirubin
D Urea
E Cystine
3.A 16 year-old patient got numerous traumas in automobile accident. Now the patient is haning a shock. АP - 80/60 mm Hg. daily urine volume 60-80 ml. What pathogenic mechanism leads to kidneys function violation?
A Decreased hydrostatic pressure in glomerular capillaries
B Increased osmotic pressure in glomerular capillaries
C Increased pressure in Bowman’s capsule
D Increased vasopressin blood concentration
E Trauma of the urinary bladder
4.A patient complains about dyspnea provoked by the physical activity. Clinical examination revealed anaemia and presence of the paraprotein in the zone of gamma-globulins. To confirm the myeloma diagnosis it is necessary to determine the following index in the patient’s urine:
A Bence Jones protein
B Bilirubin
C Haemoglobin
D Ceruloplasmin
E Antitrypsin
5.A patient with primary nephrotic syndrome has the following content of whole protein: 40 g/l. What factor caused hypoproteinemia?
A Proteinuria
B Transition of protein from vessels to tissues
C Reduced protein synthesis in liver
D Increased proteolysis
E Disturbance of intestinal protein absorption
Testing according system “Krok-I”
1.Examination of a patient with chronic renal insufficiency revealed an increase of rest nitrogen concentration in blood - mmole/l. What type of hypernitrogenemia it?
A. Hepatic
B. Combined
C. Residual
D. Retentional
E. Productional
2.Injection of an anaesthetic before the tooth extraction resulted in development of anaphylactic shock accompained by oliguria. What pathogenetic mechanism caused a decrease in diuresis in this case?
A. Increase in hydrostatic pressure in the Bowman´s capsule
B. Decrease in hydrostatic pressure in the renal corpuscle cappillaries
C. Increase in oncotic pressure of blood plasma
D. Increase in vasopressin secretion
E. Damage of glomerular filter
3.A child with renal insufficiency exhibits delayed teeth eruption. This is most likely caused by the abnormal formation of the following substance:
A. α –ketoglutarate
B. Hydroxylysine
C. Glycocyamine
D. 1,25 (OH)2D3
E. Glutamate
4.Poisoning with corrosive sublimate caused acute renal insufficiency. Its progress four stages: 1) initial, 2) oligoanuria, 3) recovery. Name the third stage of acute renal insufficiency:
A. Hemodynamic
B. Ischemic
C. Pathochemical
D. Polyuric
E. Metabolic
5.A 48 year old male patient was admitted to the hospital with acute attack of chronic glomerulonephritis. Examination revealed chronic renal failure. What it the cause of hyperazotemia by chronic renal failure?
A. Disorder of water-electrolytic metabolism
B. Reduction of glomerular filtration
C. Reduction of tubular reabsorption
D. Disorder of protein metabolism
E. Reduction of tubular excreation
6.Analysis of a dentist’s urine obtained at the end of his working day revealed protein concentration at the rate of 0,7g/l/ His morning urine hadn’t such changed. What is this phenomenon called?
A. Extrarenal proteinuria
B. Organic proteinuria
C. Nonselective proteinuria
D. Functional proteinuria
E. Hematuria
7.A patient suffering from chronic renal insufficiency has got osteoporosis. Osteoporosis was caused by abnormal synthesis of the following regulator of mineral metabolism in kidneys:
A. Lysine hydroxylation
B. Cortisol hydroxylation
C. 1,25(OH)2D3 formation
D. Proline hydroxylation
E Glutamate hydroxylation\
8.A 30 y.o. patient who has diagnosed with acute glomerulonephritis has proteinuria. What disturbance is the cause of this phenomenon?
A. Decreased quantity of functioning nephrons
B. Low oncotic pressure of blood plasma
С Increased permeability of renal filter
D. Delayed excretion of products of nitrogen metabolism E. High hydrostatic pressure of in capillaries
9.A patient recently had staphylococcal infection that led to anasarca; laboratory urine revealed massive proteinuria. Results of blood analysis: hypoproteinemia, hyperlipemia What pathology can be suspected9
A. Urolithiasis
B. Chronic renal insufficiency
C. Pyelonephritis
D. Glomerulonephritis
E. Nephrotic syndrome
10. A patient ill with chronic glomerulonephritis has a disturbed incretory function of kidneys. It will result in the deficit of the following blood corpuscles:
A. Thrombocytes
B. Leukocytes
C. Leucocytes and thrombocytes
D. Erythrocytes
E. Erythrocytes and leukocytes
11. A 30 y.o. patient who has diagnosed with acute glomerulonephritis has proteinuria. What disturbance is the cause of this phenomenon9
A. Decreased quantity of functioning nephrons
B. Low oncotic pressure of blood plasma
С Increased permeability of renal filter
D. Delayed excretion of products of nitrogen metabolism
E. High hydrostatic pressure of in capillaries
Situate task:
1. Patient, 25 years, who had frequent tonsillitis suffers from periodic headache, rapid fatigueability, face edema. Arterial hypertension, unmassive proteinuria, microhematuria were founded at. Ultrasonic scanning of kidney: the bilateral damage is with the insignificant increase of kidney parenchyma echogenicity.
1) What disease is most reliable in this case? Give definition of conception.
___________________________________________________________________________
2) Name the reasons of this pathology.
_______________________________________________________________________________________________________________________________________
3) Name the mechanisms of this pathology development
_________________________________________________________________________________________________________________________________________________________________________________________________________
4) Name the urinary symptoms which are arised up at this pathology and mechanism of their development.
__________________________________________________________________________________________________________________________________________
5) Name the unurinary symptoms which are arising up at this pathology and mechanism of their development.
__________________________________________________________________________________________________________________________________________
2. Patient, 45 years, suffers from rapid fatigueability and general edema. In the blood: general albumen – 45g/l, disproteinemia (hypoalbuminemia), cholesterol - 18 millimole/l. In the urine: albumen - 50 ‰, waxy and hyalin cylinders.
1) What disease is most reliable in this case? Give definition of conception.
___________________________________________________________________________
2) Name the reasons of this pathology.
_______________________________________________________________________________________________________________________________________________________________________________________________________________________________
3) Name the mechanisms of this pathology development
__________________________________________________________________________________________________________________________________________________________________________________________________________
4) Name the urinary symptoms which are arises up at this pathology and mechanism of their development.
__________________________________________________________________________________________________________________________________________
5) Name the unurinary symptoms which are arised up at this pathology and mechanism of their development.
__________________________________________________________________________________________________________________________________________
Practical work: "PATHOLOGY OF THE KIDNEYS FUNCTIONS"
Object of work: chemical and microscopic study of urine at glomerules and tubules pathology.
EXPERIMENT № 1. Determination of urine specific gravity.
Urine specific gravity is determined by urometer. Drop the urometer into the cylinder with urine and observe at the scale level of its standing in the lower fluid meniscus. Use the urometers of two types: with the scale of 1000-1025 and 1025-1050.
In the research sample specific gravity is __________.
Conclusion:_____________________________________________________________________________________________________________________________________________________________________________________
EXPERIMENT № 2. Determination of protein in the urine.
a) qualitative determination of protein.
Pour 2 ml filtered urine into the test tube. Add 2-3 drops of 20% sulfosalicylic acid solution, which results the turbidity in the presence of protein. If the turbidity disappears after the heating, it is caused by the presence albumines.
Conclusion:_____________________________________________________________________________________________________________________________________________________________________________________
b) quantitative determination of protein.
Pore 0,5 ml of concentrated nitric acid into the test tube. Cover it gently by pipette with the urine (it is better to drop the urine on the wall of tubes).
The appearance of rings on the border of two liquids in 2-3 min. corresponds to the concentration of protein in urine 0,033 ‰. If the ring will appear earlier, the concentration of protein is higher. Dilute the urine with water at 2, 4, 8, 16 or more times. Cover the nitric acid with diluted urine till the ring appears in 2-3 min.
In the reseach sample protein concentration ______ ‰.
Conclusion:_____________________________________________________________________________________________________________________________________________________________________________________
EXPERIMENT № 3. Qualitative determination of sugar in the urine.
Pour 2 ml filtered urine into the test tube. Add 0.5 ml of 10% solution of alkali and 10% solution CuSO4 drop by drop till formed blue precipitate will dissolve. Heat the tube till the boiling. If the glucose is present in urine, the red precipitate falls.
Conclusion:______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
EXPERIMENT № 4. Investigation of urinary sediment.
Centrifugate the urine. Pour out the upper layer of liquid. Take the drop of sediment from the bottom of tube by the pipette. Place it on the slide, cover with glass covering and investigate first under low magnification, then under high magnification microscope.
[pic]
1. hyaline cylinders 1. epithelial cylinder
2. epithelial cylinders 2. leukocytes
3. granular cylinders 3. pavement epithelium
4. renal epithelium
5. fresh erythrocytes
6. leached erythrocytes
[pic]
1. urates 1. granular cylinder
2. uric acid crystals 2. bloody cylinder
3. oxalate 3. waxed cylinder
4. epithelial cylinder
Conclusion:___________________________________________________________________________________
____________________________________________________________________________________________________________________________________________________________________________________________________
THEME: «Pathology of kidney. Reading of analyses of urine».
Actuality of theme.
Research of urine is a reliable enough and rapid method, which is used in the doctors-practices of all specialities for diagnostics of kidney diseases, and also other organs and systems of human. The study of basic qualitative and quantitative indexes of urine composition can help to make a faithful diagnosis.
Researches of color and organoleptic properties of urine were conducted yet by physicians to our era. Such diseases, as diabetes mellitus and diabetes insipidus were described and diagnosed exactly on the basis of urine research.
Study of qualitative and quantitative indexes of urine in a norm and at pathology is a necessity for practical activity of every future doctor. Knowledge of reasons and mechanisms of basic urinary symptoms development will assist development of logical ideation, choice of rational approaches to treatment of every concrete patient.
General purpose of the lesson.
To read the analyses of urine at different pathology.
For this it is necessary to know (the concrete purposes):
1. To know the mechanisms of proteinuria development.
2. To know the mechanisms of hematuria development.
3. To describe the different forms of cylinders.
4. To explain the changes of urine amount.
5. To explain the changes of specific gravity of urine.
For realization of purposes of lesson it is necessary to have the base knowledges-skills:
1. To explain the anatomic structure of kidney and urinary tract (department of normal anatomy).
2. To name the basic functions of kidney (department of normal physiology).
3. To name the basic components of urine (department of normal physiology).
The checking of primary level of knowledges.
Give the answers to the following questions:
1. Name the indexes of general urine analysis.
2. Name the quantitative urinary indexes.
3. Name the qualitative urinary indexes.
4. What is the color of urine in a norm?
5. What pH of urines is in a norm?
6. Is albumen present in urine in a norm?
7. Is glucose present in urine in a norm?
8. Are red corpuscles present in urine in a norm?
9. Are leucocytes present in urine in a norm?
10. What is specific gravity of urine?
11. Kidney cylinders, kinds, mechanism of their formation.
12. Name basic urinary symptoms which arise up at the prevail damage of glomerules, mechanisms of their development.
13. Name basic unurinary symptoms which arise up at the prevail damage of glomerules, mechanisms of their development.
14. Name basic urinary symptoms which arise up at the prevail damage of tubules, mechanisms of their development.
15. Name basic unurinary symptoms which arise up at the prevail damage of tubule, mechanisms of their development.
General analysis of urine in a norm:
Color straw-coloured
Transparence absolute
pH alkalescent
Albumen absent
Glucose absent
Specific gravity 1,015-1,025
Microscopy of sediment :
· Red corpuscles absent
· Leukocytes 2-3 in eyeshot
· Pavement epithelium 2-3 in eyeshot
Topics for reports:
1. Hemodialysis, its value in treatment of kidney diseases.
2. Transplantation of kidney is a modern method of fight against kidney insufficiency. Problems of kidney transplantation in Ukraine.
3. Modern views about mechanisms of uremia development.
4. Value of hemo- and lymphosorbtion in the treatment of kidney insufficiency.
5. Kidney and arterial hypertension. Modern conceptions about the mechanisms of their development. Principles of pathogenetic therapy.
Literature.
1. Handbook of general and Clinical Pathophysiology/ Edited by prof.A.V.Kubyshkin, CSMU, 2005.
2. Pathophysiology/ Edited by prof.Zaporozan, OSMU, 2005
GENERAL URINE ANALYSIS №1
Color straw-coloured
Reaction acid
Transparence turbid
Specific gravity 1010
Albumen 1,3‰
MICROSCOPY OF SEDIMENT
Pavement epithelium 2-3 in eyeshot
Leucocytes 1-2 in eyeshot
Leached red corpuscles 60-80 in eyeshot
Cylinders:
hyalin 2-3 in eyeshot
grained single in eyeshot
Patient A, 40 years. Rest nitrogen of blood is megascopic. Small edema of face. BP is 180/95 mm Hg. Diuresis - 600 ml.
Conclusion:___________________________________________________________________________________
__________________________________________________________________________________________________
GENERAL URINE ANALYSIS №2
Color yellow
Reaction acid
Transparense turbid
Specific gravity 1015
Albumen 10,6 ‰
MICROSCOPY OF SEDIMENT
Pavement epithelium 3-4 in eyeshot
Leukocytes 6-10 in eyeshot
Leached red corpuscles single in eyeshot
Cylinders:
hyalin 5-6 in eyeshot
grained 6-8 in eyeshot
waxen 3-4 in eyeshot
Cells of kidney epithelium 3-5 in eyeshot
Patient, 30 years, suffers from edema. Rest nitrogen of blood is in a norm. BP is in a norm. Day's diuresis - 500 ml.
Conclusion:___________________________________________________________________________________
__________________________________________________________________________________________________
GENERAL URINE ANALYSIS №3
Color yellow
Reaction subacid
Transparense turbid
Specific gravity 1009
Albumen 1,65 ‰
MICROSCOPY OF SEDIMENT
Pavement epithelium 2-3 in eyeshot
Leukocytes 10-15 in eyeshot
Leached red corpuscles 5-10 in eyeshot
Cylinders:
hyalin 1-2 in eyeshot
grained 5-6 in eyeshot
waxen 3-4 in eyeshot
Cells of kidney epithelium 3-4 in eyeshot
Conclusion:___________________________________________________________________________________
__________________________________________________________________________________________________
GENERAL URINE ANALYSIS №4
Color straw-coloured
Reaction subacid
Transparense absolute
Specific gravity 1012
Albumen 0, ‰
MICROSCOPY OF SEDIMENT:
Pavement epithelium 1-2 in eyeshot
Leukocytes 2-3 in eyeshot
Leached red corpuscles 3-4 in eyeshot
Cylinders:
hyalin 1-2 not in every eyeshot
grained 1-2 not in every eyeshot
Patient, 48 years. Rest nitrogen of blood - 53 micromile/l. BP - 180/100 mm Hg. Day's diuresis - 1000 ml. Fluctuation of specific gravity during conducting of Zimnitskiy's test - 1008-1012.
Conclusion:___________________________________________________________________________________
__________________________________________________________________________________________________
GENERAL URINE ANALYSIS №5
Color yellow
Reaction acid
Transparense absolute
Specific gravity 1039
Albumen absent
Acetone ++
MICROSCOPY OF SEDIMENT:
Pavement epithelium 3-4 in eyeshot
Leukocytes 2-3 in eyeshot
Red corpuscles absent
Cylinders absent
Salts oxalate, urate, crystals of urinary acid
Patient F, 59 years, suffers from general weakness, promoted appetite, thirst, frequent defeats of abscesses of skin. Day's diuresis is 4,5 l.
Conclusion:___________________________________________________________________________________
__________________________________________________________________________________________________
GENERAL URINE ANALYSIS №6
Color straw-coloured
Reaction acid
Transparense absolute
Specific gravity 1008
Albumen 0,99 ‰
MICROSCOPY OF SEDIMENT:
Pavement epithelium 1-2 in eyeshot
Leukocytes 2-3 in eyeshot
Leached red corpuscles 6-8 in eyeshot
Cylinders:
hyalin 2-3 in eyeshot
grained 1-2 in eyeshot
Patient D., 45 years. In anamnesis: disease of kidney during 10 years. He suffers from great headache, weakness. BP - 180/120 mm Hg. Day's diuresis - 1000 ml. Fluctuation of specific gravity - 1004-1008 (Zimnitskiy's test).
Conclusion:___________________________________________________________________________________
__________________________________________________________________________________________________
GENERAL URINE ANALYSIS №7
Color yellow
Reaction subacid
Transparense turbid
Specific gravity 1009
Albumen 1,65 ‰
MICROSCOPY OF SEDIMENT:
Pavement epithelium 3-4 in eyeshot
Leukocytes 10-15 in eyeshot
Leached red corpuscles 5-10 in eyeshot
Cylinders:
hyalin 1-2 in eyeshot
grained 5-6 in eyeshot
waxen 3-4 in eyeshot
Patient, 38 years, suffers from hearache, weakness. BP is 145/105 mm Hg. RN - 46,9 micromole/l.
Conclusion:___________________________________________________________________________________
__________________________________________________________________________________________________
GENERAL URINE ANALYSIS №8
Color yellow
Reaction subacid
Transparense absolute
Specific gravity 1012
Albumen -0,65 ‰
MICROSCOPY OF SEDIMENT:
Pavement epithelium 2-3 in eyeshot
Leukocytes 2-3 in eyeshot
Leached red corpuscles 3-4 in eyeshot
Cylinders:
hyalin 1-2 in eyeshot
grained 1-2 in eyeshot
Patient I., 52 years, suffers from headache, weakness. BP - 180/110, hypertrophy of heart. RN -38,2 micromole/l.
Conclusion:___________________________________________________________________________________
__________________________________________________________________________________________________
GENERAL URINE ANALYSIS №9
Color pigwashes of meats
Reaction alkaline
Transparense turbid
Specific gravity 1022
Albumen 1,65 ‰
MICROSCOPY OF SEDIMENT:
Pavement epithelium 3-4 in eyeshot
Leukocytes 10-12 in eyeshot
Red corpuscles
fresh 20 in eyeshot
leached cover all eyeshot
Cylinders
hyalin 1 in eyeshot
bloody 1-2 in eyeshot
Patient D., 17 years. Became ill 2 weeks ago acute.. Day's diuresis - 250ml.
Conclusion:___________________________________________________________________________________
__________________________________________________________________________________________________
GENERAL URINE ANALYSIS №10
Color yellow
Reaction acid
Transparense turbid
Specific gravity 1015
Albumen 2,2 ‰
MICROSCOPY OF SEDIMENT:
Pavement epithelium 2-3 in eyeshot
Leukocytes 5-8 in eyeshot
Leached red corpuscles 8-10 in eyeshot
Cylinders
hyalin 10-15 in eyeshot
grained 3-4 in eyeshot
Patient I., 45 years. Edema of feet, astsit. Hypertrophy of heart, shortness of breathing, cyanosys. BP -200/100 mm Hg. Day's diuresis - 1000 ml.
Conclusion:___________________________________________________________________________________
__________________________________________________________________________________________________
GENERAL URINE ANALYSIS №11
Color straw-coloured
Reaction subacid
Transparense turbid
Specific gravity 1011
Albumen 50 ‰
MICROSCOPY OF SEDIMENT:
Pavement epithelium 2-3 in eyeshot
Leukocytes 2-3 in eyeshot
Red corpuscles absent
Cylinders
hyalin 2-3 in eyeshot
grained 2-3 in eyeshot
waxen 6-9 in eyeshot
Patient D., 55 years. Osteomyelitis of ribs after a wound. Purulent fistula. He is ill during 10 years.
Conclusion:___________________________________________________________________________________
__________________________________________________________________________________________________
Mark the changes of the urograme. Make a conclusions.
GENERAL URINE ANALYSIS №12
|Diuresis |2800 ml |
|Specific gravity |1,009 |
|Albumen |2 g/l |
|Glucose |absent |
|Keton bodies |absent |
|MICROSCOPY OF SEDIMENT |Single leached red corpuscles; |
| |Single hyalinic cylinders |
| |
|Additional datas: |
|Arterial pressure |185/100 mm Hg |
|Rest nitrogen of blood |80 mg% |
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
GENERAL URINE ANALYSIS №13
|Diuresis |800 ml |
|Specific gravity |1,029 |
|Albumen |1 g/l |
|Glucose |absent |
|Keton bodies |absent |
|MICROSCOPY OF SEDIMENT |Leached red corpuscles 40–50 in the eyeshot; single hyalinic and |
| |erythrocyte cylinders |
| |
|Additional datas:: |
|Arterial pressure |165/105 mm Hg |
|Rest nitrogen of blood |50mg% |
| |High level of antistreptolisine О in the blood plasma |
____________________________________________________________________________________________________________________________________________________________________________________________________
GENERAL URINE ANALYSIS №14
| | |
|Diuresis |1000 ml |
|Specific gravity |1,037 |
|Albumen |33 g/л |
|Glucose |absent |
|Keton bodies |absent |
|MICROSCOPY OF SEDIMENT |Grained and waxen cylinders in a big number |
|Additional datas: |
|Arterial pressure |120/65 mm Hg |
|Rest nitrogen of blood |35 mg% |
____________________________________________________________________________________________________________________________________________________________________________________________________
GENERAL URINE ANALYSIS №15
|Diuresis |1600 ml |
|Specific gravity |1,025 |
|Albumen |absent |
|Glucose |2,5% |
|Keton bodies |absent |
|MICROSCOPY OF SEDIMENT | |
|Additional datas: |
|Glucose of blood plasma |80 mg%. |
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
GENERAL URINE ANALYSIS №16
| | |
|Diuresis |340 ml |
|Specific gravity |1,035 |
|Albumen |1,5 g/l |
|Glucose |absent |
|Keton bodies |absent |
|MICROSCOPY OF SEDIMENT |Red corpuscles 20–30 in the eyeshot; grained and waxen cylinders 2 – 3 in the |
| |eyeshot. |
| |
|Additional datas: |
|Rest nitrogen of blood | 210 mg%. |
|Arterial pressure |145/100 mm Hg |
____________________________________________________________________________________________________________________________________________________________________________________________________
GENERAL URINE ANALYSIS №17
| | |
|Diuresis |5500 ml |
|Specific gravity |1,040 |
|Albumen |absent |
|Glucose |4% |
|Keton bodies |present |
|MICROSCOPY OF SEDIMENT | |
| | |
|Additional datas: |Glucose of blood plasma 300 mg% |
____________________________________________________________________________________________________________________________________________________________________________________________________
GENERAL URINE ANALYSIS №18
|Diuresis |165 ml |
|Specific gravity |1,015 |
|Albumen |3,5 g/l |
|Glucose |absent |
|Keton bodies |absent |
|MICROSCOPY OF SEDIMENT |Single leached red corpuscles; |
| |Single hyalinic cylinders |
|Additional datas: |Arterial pressure - 145/90 mm Hg |
| |Rest nitrogen of blood 58 mg% |
____________________________________________________________________________________________________________________________________________________________________________________________________
GENERAL URINE ANALYSIS №19
|Diuresis |3800 ml |
|Specific gravity |1,014 |
|Albumen |absent |
|Glucose |absent |
|Keton bodies |absent |
|MICROSCOPY OF SEDIMENT |Single hyalinic cylinders |
|Additional datas: |Arterial pressure - 115/80 mm Hg |
| |Rest nitrogen of blood 35 mg% |
___________________________________________________________________________________________________________________________________________________________________________________________________
GENERAL URINE ANALYSIS №20
|Diuresis |1600 ml |
|Specific gravity |1,020 |
|Albumen |absent |
|Glucose |1,5% |
|Keton bodies |absent |
|MICROSCOPY OF SEDIMENT |Cristals of solts in a big amount |
|Additional datas: |Positive reaction on the arginine and cysteine of urine |
| |Increased amount of phosphates |
| |Glucose of blood plasma 95 mg% |
______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
For the notes_________________________________________________________________________________
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