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THE MINISTRY OF PUBLIC HEALTH OF UKRAINE
VINNITSIA NATIONAL MEDICAL UNIVERSITY
named after M.I.PIROGOV
EDUCATIONAL-METHODICAL RECOMMENDATION
FROM PATHOPHYSIOLOGY
FOR THE 3RD YEAR
MEDICAL FACULTY STUDENTS
Module N 2 PATHOLOGY OF ORGANS
AND SYSTEMS
Practical training N 6 PATHOLOGY OF DIGESTION, LIVER AND KIDNEYS
VINNITSIA – 2012
The educational-methodical recommendation from Pathophysiology is approved and confirmed for the introduction into the educational process at Pathophysiology department meeting according to the protocol of meeting №10 from 10.01.12.
Compilers: Head of Department, Dr. of Med.Sc. Rikalo N.A.
as. Grytsenko A.S.
as. Guminska O.Y.
as. Androschuk O.V.
The educational-methodical recommendation is recommended for the foreign students of medical faculty (3rd course).
Thematic plan of the practical lessons:
Theme 1 «Pathophysiology of digestion»
Theme 2 «Pathology of liver»
Theme 3 «Kidneys pathology»
Theme 4 «Kidneys pathology. Urograms analyzing»
THEME:PATHOPHYSIOLOGY OF DIGESTION.
Actuality of theme.
A function of the digestive system is providing of an organism by the nutrition, 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 and mechanisms of development of violations which arise up at digestive system pathology 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 mark typical pathological states at the digestive system: insufficiency of digestion (maldigestion) and disorder of reabsorption (malabsorption);
➢ To use different principles for classification of main forms of digestive system pathology;
➢ To analyze the ulcer disease of stomach and duodenum as multifactorial disease;
➢ To characterize the risk factors for ulcer disease origin;
➢ To use modern views about the mechanisms of injury and protective abilities of digestive tract for analyzing the pathogenesis of ulcers;
➢ To analyze the experimental modeling of different forms of digestive system pathology for discovering the reasons for them origin and mechanisms of their development;
➢ To use the knowledges about nervous and humeral regulation of digestive tract different parts for analyzing of their motive, secretory and reabsorptive functions disorders;
➢ To know the indexes of secretory function and use it for the analyzing of its typical disorders;
➢ To analyze the reasons for origin and mechanisms of pancreatitis development;
➢ To analyze cause-effective relationships, to be able explain the pathological and compensatory-adaptative reactions, local and general signs at pathogenesis of pancreatic shock;
➢ To analyze the disorders of intestine digestion, development of maldigestion and malabsorption;
➢ To explain the pathogenesis of malabsorption main clinical signs;
➢ To analyze clinical variants of intestinal impassability origin and development, explain its possible consequences and complications.
For realization of purposes of lesson it is necessary to have the base knowledges-skills:
1. Features of digestive channel (Histology Department)
2. Functions of stomach, intestine and pancreas (Normal Physiology Department)
Checking of the primary level of knowledges.
Give the answer on the next questions:
1. Digestion insufficiency, definition.
2. Classification of the digestion insufficiency.
3. Disorders of saliva secretion.
4. Reasons and mechanisms of hypersalivation development.
5. Reasons and mechanisms of hyposalivation development.
6. Functions of the stomach.
7. Main manifestations of dyspepsia.
8. Mechanisms of dyspepsia manifestations development.
Theoretical questions at the base of which the execution of purpose types of activity is possible.
1. General concept about digestion insufficiency, principles of its classification.
2. Reasons for digestion insufficiency origin (maldigestion).
3. Disorders of appetite. Anorexia.
4. Reasons and mechanisms of digestion disorders in the oral cavity.
5. Reasons, mechanisms and consequences of saliva secretion disorders.
6. Disorders of esophagus motive function. Etiology. Pathogenesis.
7. Disorders of digestion in the stomach.
8. General characteristic of motive and secretory function of stomach.
9. Types of pathological gastric secretion, reasons for origin and mechanisms of development.
10. Etiology, pathogenesis of ulcer disease of stomach and duodenum. Role of helicobacter pylory.
11. Disorders of digestion in the intestine. Etiology. Pathogenesis.
12. Disorders of digestion, resulted by insufficiency of pancreatic juice production.
13. Etiology, pathogenesis and complications of acute and chronic pancreatitis.
14. Pathogenesis of pancreatic shock.
15. Intestine dyskinesias. Reasons for origin, mechanisms of development.
16. Disorders of cavitary and parietal digestion.
17. Malabsorption syndrome, definition, main clinical signs.
18. Intestinal enzymopathy.
Literature.
1. Handbook of general and Clinical Pathophysiology/ Edited by prof.A.V.Kubyshkin, CSMU, 2005, p.265-280.
2. Pathophysiology/ Edited by prof.Zaporozan, OSMU, 2005, p.230-247.
3. General and clinical pathophysiology/ Edited by Anatoliy V/ Kubyshkin – Vinnytsia: Nova Knuha Publishers – 2011. p.520-546.
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.
Independent students work.
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 PATHOLOGICAL GASTRIC SECRETION
Norm Inhibit Inert
[pic] [pic] [pic]
Asthenic Excitable
[pic] [pic]
Testing according system “Krok-I”
Tests of an open database (2010)
1. A patient ill with enteritis accompanied by massive diarrhea has low water rate in the extracellular space, high water rate inside the cells and low blood osmolarity. What is such disturbance of water-electrolytic metabolism called?
A Hypo-osmolar hypohydration
B Hyperosmolar hypohydration
C Osmolar hypohydration
D Hypo-osmolar hyperhydration
E Hyperosmolar hyperhydration
2. 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
All correct answers: A.
2009 –
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. 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
3. 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
4. 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
5. 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
6. 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 hereditary insufficiency of galaktose. 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
7. 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.
8. 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
9. 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
10. 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
11. 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
12. 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
13. 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
14. 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
15. 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
16. 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
17. 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
18. 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
19. 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
20. 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
21. 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
22. 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
23. 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
24. 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
25. 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
26. 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
27. 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
28. 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
29. 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
30. 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
31. 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
32. 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
33. 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
Correct answers:
1-A; 2-A; 3-A; 4-A; 5-A; 6-A; 7-A; 8-A; 9-D; 10-C; 11-A; 12-C; 13-D; 14-E; 15-B; 16-D; 17-B; 18-A; 19-C; 20-C; 21-C; 22-A; 23-C; 24-E; 25-A; 26-E; 27-B; 28-A; 29-A; 30-A; 31-A; 32-C; 33-A.
Situational tasks
1. Patient K., 35 years old, entered into the clinic after the poisoning by organophosphorous substances. Objectively: without consciousness, hyperkinesia of face muscles, increased sweating, tachycardia, disorder of saliva secretion.
1. What disorder of saliva secretion can be observed at the patient?
____________________________________________________________________
2. Reasons for described disorder origin.
____________________________________________________________________________________________________________________________________
3. What consequences of this disorder can develop?
________________________________________________________________________________________________________________________________________
2. Tumour of brain that characterized by disorder of saliva secretion (5 l per day) was founded at the patient H., 37 years old.
1. What is the disorder of saliva secretion at the patient?
____________________________________________________________________
2. Reasons for described disorder origin.
________________________________________________________________________________________________________________________________________
3. What disorders of water-electrolyte metabolism and acid-base balance can be observed at the patient? Explain your answer.
________________________________________________________________________________________________________________________________________
3. Patient M., 24 years old, suffers on the dryness of oral cavity. Objectively: parotid and submandibularis salivary glands increased from the both side, dense consistent, painful at palpation. Mikulich’s disease was diagnosed.
1. What is the disorder of saliva secretion at the patient?
____________________________________________________________________
2. Reasons for described disorder origin.
________________________________________________________________________________________________________________________________________
3. What consequences of this disorder can develop?
________________________________________________________________________________________________________________________________________
4. Patient P., 36 years old, entered to the clinic with complaints on dryness of the mouth, especially during meals. Objectively: oral mucosa is dry, saliva secreted baldly from the ducts of the salivary glands. An examination of the secretory function of salivary glands (after intake of pilocarpine) a significant reduction of salivation (to 0.2-0.5 ml for 20 minutes from each parotid gland) is observed.
1. Xerostomia, definition.
________________________________________________________________________________________________________________________________________
2. At what disorder of saliva secretion xerostomia observed?
____________________________________________________________________
3. Consequences of described disorder of saliva secretion.
____________________________________________________________________________________________________________________________________________________________________________________________________________
5. The patient complains on dry eyes and mouth. Objectively: oral mucosa is hyperemic and dry, with cracks, tongue is dry, swelling around the parotid glands, the glands are painfull ander palpation. Shegren’s syndrome was diagnosed.
1. What disorder of saliva secretion is observed at the patient?
____________________________________________________________________
2. Reasons for described disorder origin.
____________________________________________________________________
3. Consequences of described disorder of saliva secretion.
____________________________________________________________________________________________________________________________________________________________________________________________________________
6. The patient entered to the infectious department with suspected epidemic parotitis. From anamnesis: he suffered from epidemic parotitis in childhood. The examination revealed swelling of the left submandibular gland, at palpation painfull and dense formation, the size of a peawas foinded. At the x-ray examination of the ductus of salivary gland formation (diameter 0.5 to 0.5 cm) revealed.
1. What pathology is observes at the patient? Explain the answer.
____________________________________________________________________
________________________________________________________________________________________________________________________________________
2. What disorder of saliva secretion can be observed at the patient?
____________________________________________________________________
3. Clinical manifestations of the described disorder of saliva secretion.
____________________________________________________________________________________________________________________________________________________________________________________________________________
7. At the examination by the ophthalmologist atropine was introduced to patients pupil.
1. What disorder of saliva secretion can be observed at the patient?
____________________________________________________________________2. Consequences of described disorder of saliva secretion.
____________________________________________________________________________________________________________________________________________________________________________________________________________
8. The patient 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 disorder of the secretory function in a patient.
____________________________________________________________________
2. Specify the mechanisms of development of the symptoms.
____________________________________________________________________________________________________________________________________________________________________________________________________________
9. 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.
________________________________________________________________________________________________________________________________________________________________________________________________________
10. 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.
________________________________________________________________________________________________________________________________________________________________________________________________________
11. 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.
________________________________________________________________________________________________________________________________________________________________________________________________________
12. The patieny for 10 years 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
________________________________________________________________________________________________________________________________________________________________________________________________________
13. Patient complaints of heartburn, frequent constipation. Investigation of gastric content: total acidity – 88 mmol/l, total HCl – 83 mmol/l, free HCl – 50 mmol/l, bound HCl – 33 mmol/l, acid phosphates and organic acid - 5 mmol/l/.
1. Analyse the state of gastric acidity.
_______________________________________________________________________________________________________________________________________________________________________________________________________
2. Explain the reasons and mechanism of the main dyspeptic signs.
________________________________________________________________________________________________________________________________________________________________________________________________________
14. Diarrhea on the background of the manifestations of the general neurosis is observed at the patient M., during prolonged neuro-emotional overload. Objective: there is growing peristalsis and intestinal noises.
1. What disorder of intestine motive function is observed at the patient?
____________________________________________________________________
2. Explain the mechanism of described disorder development.
____________________________________________________________________________________________________________________________________________________________________________________________________________3. What else disorder of intestine motive function do you know?
________________________________________________________________________________________________________________________________________
15. Delay of gases and feces, vomiting are observed at the patient, operated for appendicitis complicated by peritonitis in the postoperative period. Objectively: abdomen uniformly swollen, peristalsis is absent, intestinal sounds aren’t auscultated ("dumb belly"). Intestinal obstruction was diagnosed.
1. What kind of intestinal obstruction is observed at the patient?
____________________________________________________________________
2. What kind of intestinal obstruction do you know else? Reasons for their development.
____________________________________________________________________________________________________________________________________________________________________________________________________________3. Consequences of intestine obstruction.
____________________________________________________________________________________________________________________________________________________________________________________________________________
16. Increase of glucose levels in the blood, resulted by the reduced insulin secretion, is observed at the patient suffers from epidemic parotitis.
1. Reasons for pancreatic hyposecretion.
____________________________________________________________________________________________________________________________________________________________________________________________________________2. Consequences of pancreatic hyposecretion.
____________________________________________________________________________________________________________________________________________________________________________________________________________
17. Disorder of digestion, resulted by pancreatic hyposecretion, developed at the patient with chronic pancreatitis on the base of chronic alcoholism.
1. Reasons for pancreatic hyposecretion.
____________________________________________________________________________________________________________________________________________________________________________________________________________2. Consequences of pancreatic hyposecretion.
____________________________________________________________________________________________________________________________________________________________________________________________________________
18. Acute pancreatitis with sharp pancreatic hypersecretion developed at the patient after intake of alcohol and fatty food in a big amount.
1. Kind of acute pancreatitis.
____________________________________________________________________________________________________________________________________________________________________________________________________________2. Reasons for origin and mechanisms of acute pancreatitis development.
____________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
3. Consequences of acute pancreatitis.
____________________________________________________________________________________________________________________________________________________________________________________________________________
19. Frequent and liquid feces, signs of intoxication, dehydration appear at the newborn on 5-6 days. The bottle-feeding resulted disappearance of these manifestations.
1. Insufficiency of what enzyme developed at the patient?
____________________________________________________________________2. Disorder of what process is the complication of this enzymopathy?
________________________________________________________________________________________________________________________________________3. What syndrome developed at the child? What are the reasons for this syndrome origin?
____________________________________________________________________________________________________________________________________
20. The patient complaines of the attacks of sudden weakness that develops immediately after the meal eating or during the first 15-20 minutes after the food intake. The attacks are accompanied by hot flashes, increased sweating, general weakness, dizziness, noise in the ears, palpitations, tremor of the limbs. Sometimes the intensity of the symptoms is so high that the patient has to go to bed. From anamnesis: resection of the stomach was made to the patient because of ulcer disease of stomach.
1. What syndrome developed at the patient?
____________________________________________________________________2. Machanism of described syndrome development.
____________________________________________________________________________________________________________________________________________________________________________________________________________
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 characterize the concepts, evaluate the criteria and apply them to the classification of hepatic failure, hepatic coma, jaundice, portal hypertension;
➢ To analyze the types of hepatic failure according to the reasons and mechanisms of development, clinical course, severity;
➢ To characterize etiological factors for the hepatic failure, jaundice, portal hypertension origin;
➢ To explain the metabolic (proteins, lipid, carbohydrates, electrolyte, xenobiotics metabolism) and hormonal disorders in the organism in case of hepatic failure;
➢ To apply modern advancements of neurophysiology for the explanation af the pathogenesis of encephalopathy and coma at hepatic failure;
➢ To explain the mechanisms of jaundices development;
➢ To analyze the causes and mechanisms of the most important clinical syndromes in different types of jaundices development;
➢ To analyze the 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. Structure of the liver and biliary ways (Human Anatomy Department).
2. Basic functions of liver (Normal Physiology Department).
3. Composition of bile and its role in of digestion (Normal Physiology Department).
The checking of primary level of knowledges.
Give the answers to the following questions:
1. Jaundice, definition.
2. Classification of jaundices according to 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. Hepatic insufficiency, definition.
12. Classification of hepatic insufficiency according to pathogenesis, clinical 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. Concept 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
Differentiative diagnostic of the different kind of jaundice
|Indexes |Hemolytic jaundice |Hepatocellular jaundice |Mechanic jaundice |
|Unconjugated bilirubin of blood |↑ |↑ |N |
|Conjugated bilirubin of blood |N |↑ |↑ |
|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 to the FMC 2.
1. Hepatic failure: definition, principles of classification.
2. Etiology, pathogenesis, experimental models of hepatic failure.
3. Typical metabolic violation at hepatic failure.
4. Insufficiency of antitoxic liver function, the mechanism of the main manifestations development.
5. Types, causes, pathogenesis of hepatic coma.
6. Role of cerebrotoxic substances.
7. Insufficiency of excretory liver function, main manifestations.
8. Types of jaundice, its causes and mechanisms of development.
9. Comparative characteristics of pigmentary disorders sharing with jaundice.
10. Cholemic, acholic syndromes.
11. Cholelithiasis.
12. The syndrome of portal hypertension: etiology, pathogenesis, manifestations.
13. Mechanisms of ascites.
Literature.
1. Handbook of general and Clinical Pathophysiology/ Edited by prof.A.V.Kubyshkin, CSMU, 2005. p.281-290.
2. Pathophysiology/ Edited by prof.Zaporozan, OSMU, 2005, p.248-259.
3. General and clinical pathophysiology/ Edited by Anatoliy V/ Kubyshkin – Vinnytsia: Nova Knuha Publishers – 2011. p.546-566.
Independent students work
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:______________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
Testing according system “Krok-I”
Tests of an open database (2010)
1. A patient being treated for viral hepatitis type B got symptoms of hepatic insufficiency. What blood changes indicative of protein metabolism disorder will be observed in this case?
A Absolute hypoalbuminemia
B Absolute hyperalbuminemia
C Absolute hyperfibrinogenemia
D Proteinic blood composition is unchanged
E Absolute hyperglobulinemia
2. Hepatitis has led to the development of hepatic failure. Mechanism of edemata formation is activated by the impairment of the following liver function:
A Protein-synthetic
B Barrier
C Chologenetic
D Antitoxic
E Glycogen-synthetic
3. A patient presents with icteritiousness of skin, scleras and mucous membranes. Blood plasma the total bilirubin is increased, stercobilin is increased in feces, urobilin is increased in urine. What type of jaundice is it?
A Haemolytic
B Gilbert's disease
C Parenchymatous
D Obturational
E Cholestatic
4. A 48 y.o. patient was admitted to the hospital with complaints about weakness, irritability, sleep disturbance. Objectively: skin and scleras are yellow. In blood: conjugated bilirubin, cholalemia. Feces are acholic. Urine is of dark colour (bilirubin). What jaundice is it?
A Mechanic
B Hemolytic
C Parenchymatous
D Gilbert's syndrome
E Crigler-Najjar syndrome
All correct answers: A.
2009
1. .In patients with the biliary tract obstruction the blood coagulation is inhibited; the patients have frequent haemorrhages caused by the subnormal assimilation of the following vitamin:
A. A
B. K
C. E
D. D
E. C
2008 - 2004
1. Patient suffers on chronic calculus’s choletsistitis complain about sharp pain in right hypochondrium, an itch and icteric of skin covers, plural petexial hemorrhages, excrement is fat and discolored (steatorrhea). What type of icterus is observed for a patient?
A. Hemolytic
B. Hepatocellular
C. Gemic
D. Mechanical
E. Circulatoric
2. Alcoholic cirrhosis is diagnosed in a patient. Ascyt and edemas on lower extremities are observed. What blood changes will be found out for a patient?
A. Hypoalbiminemia
B. Hypogamaglobulinemia
C. Hypoalfaglobulinemia
D. Dysproteinemia
E. Hypocholesterinemia
3. In a patient found out the tumor of pancreas head which is accompanied with disorder of general bilious channel communicating. The contents of what matter will be multiplied in blood here?
A. Urea
B. Hemoglobin
C. Insulin
D. Bilirubin
E. Adrenalin
4. Patient suffers from the portal cirrhosis, during abdominocentesis 8l. of liquids are got, that led to weakness and loss of consciousness. What mechanism of development of this complication?
A. Ischemia as a result of blood redistribution
B. Angiospastic ischemia
C. Embolism of cerebral arteries
D. Thrombosis of cerebral arteries
E. Sharp venous hyperemia of cerebrum
5. Patient N. complaint about dyspeptic disorders, melena, hemorrhoid bleeding. At an inspection found out expansion of venous vessels on a front abdominal wall and multiplying the stomach size. What pathology of digestive system can show up such symptoms?
A. Intestinal autointoxication
B. Ulcer disease
C. Colitis
D. Enteritis
E. Portal hypertension
6. A patient complain about head pain, crabbiness, rapid fatigueability, pain in right hypochondrium, itch of skin. At an inspection: yellow coloring of skin and mycoses, increased liver, pain during palpationi, AP - 80/40 mm Hg, heart rate – 46 /min. In blood: level of direct bilirubin - 34 mcmol/L, level of indirect - 35,2 mcmol/L, in urine - bilious acids, direct bilirubin, urobilin; the content of stercobilin in an excrement is diminished. What type of icterus is there?
A. Hemolytic
B. Parenchimatous
C. Subhepatic
D. Obturative
E. Prehepatic
7. A woman works on a production linked with phenilgydrazin (production of amidopirin), complaints about icteric color of skin and skler, weakness, fatigueability, multiplying a spleen. What type of icterus take place at patient?
A. Mechanical
B. Hepatic
C. Subhepatic
D. Hemolytic
E. Obturative
8. Disorder of what liver functions of liver at its insufficiency causes hemorrhagic syndrome?
A. Barrier
B. Antitoxic
C. Excretion of bile
D. Depositing of glycogen
E. Protein synthesis
9. What disease can caused the development of suprahepatic icterus?
A. Viral hepatitis B
B. Cirrhosis of liver
C. Hemolytic disease of new-born
D. Pancreatitis
E. Ulcer disease of stomach and duodenum
10. What diseases can causes the development of hepatic icterus?
A. Gastritis
B. Cholecystitis
C. Pancreatitis
D. Enteritis
E. Viral hepatitis B
11. What diseases can causes the development of subhepatic icterus?
A. Hepatitis
B. Gastritis
C. Pancreatitis
D. Gallstone disease
E. Cirrhosis of liver
12. To the doctor a patient appealed concerning icteric sclera and skin. During inspection it was not discovered encephalopatia and signs of cholemic and acholic syndromes. What icterus did develop?
A. Parenchymatous
B. Nuclear
C. Mechanical
D. Subhepatic
E. Hemolytic
13. Arterial hypertension can develop at hepatic insufficiency. What factors does conduct the increase of arterial pressure in such cases?
A. Аldosteron.
B. Adrenalin
C. Renin
D. Noradrenalin
E. Angiotenzin - II.
14. 32A female patient with chronic hepatitis complains of increase sensitivity to barbiturates which she used previously without any symptoms of intoxication. The disorder of what hepatic jaundice is responsible for this state?
A. Bile formation
B. Hemodynamic
C. Metabolic
D. Hemopoetic
E. Phagocytotic
15. A patient with jaundice complains of erythrism, headache, and insomnia. Objectively: pulse-54 beats/min. AP- 90/60 mmHg. Coagulation of blood decreases. There are traces scratching on skin. The action of what component causes these symptoms?
A. Bilirubin
B. Cholesterol
C. Bile pigment
D. Bile acid
E. Fatty acid
16. Patient D., 48 years, during long time disturb the frequent mycotic feet diseases and rashes of abscesses on the body. In anamnesis is alcoholism. What did assist development of disease in this case?
A. Damage of gematoecnhephalic barrier
B. Decrease of liver barrier function
C. Primary immunodeficiency
D. Allergy
E. Chronic intoxication
17. Patient L., 55 years, with the sharp attack of hepatic colic entered to gastroenterology department. Objectively: temperature- 380С, sclers, mucus and skin of icterus, urine is dark, an excrement is light. Complain is about the skin itch of skin. What is the reason of icterus for this patient?
A. Obturation of bilious channels
B. Destruction of hepatocytes
C. Increased hemolysis
D. Lipid exchange disorder
E. Protracted reception of products, rich on a carotin
18. The cirrhosis of liver is diagnosed; he is accompanied by ascit and common hemodynamic disorder. What pathological syndrome does determine these disorders?
A. Hepatolienal syndrome
B. Hepatocardial
C. Hepatorenal
D. Portal hypertension
E. Hepatointestinal
19. Patient N., 46 years, complaine about absence of appetite, nausea, pain in right hypochondrium, which increases at adopting rich food, yellow coloring of scler, darkening of urine. Intravenous injections were conducted one and a half months ago. In blood: increase of indirect and direct bilirubin. In urine direct bilirubin and urobilin is determined in great quantity. What mechanism of indirect bilirubinu absence in urine:
A. Strengthening of indirect bilirubinu inactivation by macrophag
B. Decrease of indirect bilirubinu conjugation in hepatocytes
C. Binding of indirect bilirubin with proteins
D. Indirect bilirubin don’t filtered through a kidney membrane
E. Connection of indirect bilirubin by immune complexes
20. A patient 48 years, is in a reanimation after poisoning a chetirikhloristim carbon. The state is heavy, patient without consciousness, a pulse is threadlike, weak filling, heart rate - 40 /min., AP - 75/40 mm Hg. Breathing is periodic (Biota). In blood: decrease of albumen (16 g/l), direct bilirubin - 155 mcmol/L. In urine high quantity of ammonium and bilirubin. What caused the development of the described state for a patient?
A. Cardiogenic shock
B. Respiratory insufficiency
C. Heprtic insufficiency
D. Cardiac insufficiency
E. Kidney insufficiency
21. It is discovered for a patient: yellow coloring of skin and mycoses membraness, there are traces scratching on skin, depressing reflexes of tendons and pain sensitiveness. Urine is “color of beer”, excrement is “acholic”. AT is 90/40 mm Hg., heart rate - 52 b/min. In blood increased cholesterol, direct bilirubin and bilious acids, in urine - bilious acids, direct bilirubin, and stercobilin is not found. Name a process which caused the absence of stercobilin in urine and excrement?
A. Stercobilin destroy in an intestine
B. Stercobilin is sucked back in blood
C. Stercobilin destroy in urine
D. There is no bile in intestine and stercobilin does not appear
E. The predecessor of stercobilin din liver
22. In a patient which suffers on gallstone disease, the discoloured fat excrement appears as a result of obturation of bile ways. Absence of what component of bile caused the phenomenon of steatorea?
A.Cholesterol
B. Bile acids
C. Bilious pigments
D. Lipid acids
E. Alcaline phosphatas
23. For a woman, 57 years, after the protracted pain attack in right hypochondrium an icterus appeared. There was suspicion on a sharp gallstone disease. What index does testify about impassability of bilious channels?
A. Protein fractions of blood plasma
B. General lipid of blood plasma
C. Urinary acid of blood plasma
D. Remaining nitrogen of blood
E. Free and linked bilirubin in plasma.
24. Boy, 15 years, the diagnosis of sharp viral hepatitis is set. Research of what index must be conducted for confirmation of sharp defeat of hepatic cell?
A. Contents of free and linked bilirubin in plasma
B. Speed of zsidannya of red corpuscles [SHZE].
C. Activity of aminotransferas [ALT and AST] in blood.
D. A level of cholesterol in plasma.
E. Contents of protein fractions of blood plasma
25. Patient, 25 years, the diagnosis of chronic hepatitis is set. Patients complain about the loss of body mass on 10 kg during 2 months. Objectively: a skin is dry, peels, pale with a rather yellow tint, petexial hemorrhages on a skin, gums hemorrhages. Violations of what liver function of represents promoted hemorrhages?
A. Synthesis of bile pigments
B. Synthesis of glycogen
C. Detoxication
D. Synthesis of protein
E. Depositing
26. After taking a fatty food a patient feels nausea, flaccidity, later the sign of steathorrhea has appeared, cholesterol in the blood 9,2ml/c. The cause of this state is the deficiency of:
A. Chylomicrones.
B. Triglyceroides.
C. Bile acids.
D. Fatty acids.
E. Phopholipids
27. Sick 48th years delivered to the clinic with complaints about a weakness, crabbiness, sleep disorder. Objectively: skin and sclers are yellow. In blood: an increase of general bilirubin with prevalation of direct. Acholic excrements. Urine - dark color. What icterus does take place?
A.Hemolitic
B. Syndrome of Gylbera
C.Parenchimatos
D. Syndrome Kriglera-Nayyara
E. Mechanical
28. For a patient the signs of hepatic insufficiency appeared during treatment of viral hepatitis B. What changes of blood testify to protein exchange disorder will be observed in this case?
A. Absolute hyperfibrinogenemia
B. Protein composition of blood is not changed
C. Аbsolute hypoalbuminemia
D. Absolute hyperalbuminemia
E. Absolute hyperglobulinemia
29. In a patient which appealed to the doctor, there is the yellow coloring of skin, urine is dark, excrement of darkly yellow. The increase of what matter concentration will be observed in the blood?
A. Free bilirubin
B. Mesobilirubin
C. Conjugated bilirubin
D. Biliverdin
E. Verdoglobin
30. Patient with liver cirrhosis. What matter, that excreating with urine, can characterize the state of liver antitoxic function?
A. Urinary acid
B. Hypur acid
S. Ammonium salt
D. Creatinin
E. Amino
Correct answers:
1-D; 2-A; 3-D; 4-A; 5-E; 6-A; 7-D; 8-E; 9-C; 10-E; 11-D; 12-E; 13-A; 14-C; `5-D; 16-B; 17-A; 18-D; 19-D; 20-C; 21-D; 22-B; 23-E; 24-C; 25-D; 26-C; 27-E; 28-C; 29-A; 30-B.
Situate 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 thready, 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) Hepatic insufficiency, definition.
________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
2) Classification of hepatic insufficiency according pathogenesis.
________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
3) What type of hepatic insufficiency developed at a patient?
____________________________________________________________________
4) 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) Hepatic insufficiency, definition.
____________________________________________________________________________________________________________________________________________________________________________________________________________
2) Classification of hepatic insufficiency according pathogenesis.
________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
3) What type of hepatic insufficiency developed at a patient?
____________________________________________________________________
4) Mechanisms of clinical signs development.
________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
3. Patient is suffers from headache, irritability, rapid fatigueability, pain in the right hypochondrium, itching of skin. Objectively: icteritiousnessof skin and mucuses, multiplying of liver, palpatory 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) Hepatic insufficiency, definition.
____________________________________________________________________________________________________________________________________________________________________________________________________________
2) Classification of hepatic insufficiency according pathogenesis.
________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
3) What type of hepatic insufficiency developed at a patient?
____________________________________________________________________
4) 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) Hepatic insufficiency, definition.
____________________________________________________________________________________________________________________________________________________________________________________________________________
2) Classification of hepatic insufficiency according pathogenesis.
________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
3) What type of hepatic insufficiency developed at a patient?
____________________________________________________________________
4) 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) Hepatic insufficiency, definition.
____________________________________________________________________________________________________________________________________________________________________________________________________________
2) Classification of hepatic insufficiency according pathogenesis.
________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
3) What type of hepatic insufficiency developed at a patient?
____________________________________________________________________
4) 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) Jaundice, definition.
____________________________________________________________________________________________________________________________________________________________________________________________________________
2) Classification of jaundices according pathogenesis.
____________________________________________________________________________________________________________________________________________________________________________________________________________
3) What type of jaundice developed at a patient?
____________________________________________________________________
4) 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 thebiomaterial.
|7. |Blood |Urine |Feces |
|Common bilirubin |61,56 mcmol/l |— |— |
|Conjugated bilirubin |42,75 mcmol/l |Present |— |
|Urobilin |Absent |Absent |— |
|Stercobilin |Absent |Absent |«Trace» |
|Bile acids |Absent |Absent |— |
|Activity of ALT |Norm |— |— |
________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
|8. |Blood |Urine |Feces |
|Common bilirubin |35,91 mcmol/l |— |— |
|Conjugated bilirubin |3,42 mcmol/l |Absent |— |
|Urobilin |Absent |Absent |— |
|Stercobilin |Increased |Increased |Increased |
|Bile acids |Absent |Absent |— |
|Activity of ALT |Norm |— |— |
____________________________________________________________________________________________________________________________________________________________________________________________________________
|9. |Blood |Urine |Feces |
|Common bilirubin |75,24 mcmol/l |— |— |
|Conjugated bilirubin |5,98 mcmol/l |«Trace» |— |
|Urobilin |Present |Present |— |
|Stercobilin |Increased |Increased |Norm |
|Bile acids |Absent |Absent |— |
|Activity of ALT |Increased |— |— |
____________________________________________________________________________________________________________________________________________________________________________________________________________
|10. |Blood |Urine |Feces |
|Common bilirubin |59,85 mcmol/l |— |— |
|Conjugated bilirubin |35,91 mcmol/l |Present |— |
|Urobilin |Absent |Absent |— |
|Stercobilin |«Trace» |«Trace» |Decreased |
|Bile acids |Present |Increased |— |
|Activity of ALT |Increased |— |— |
____________________________________________________________________________________________________________________________________________________________________________________________________________
|11. |Blood |Urine |Feces |
|Common bilirubin |30,78 mcmol/l |— |— |
|Conjugated bilirubin |3,42 mcmol/l |Absent |— |
|Urobilin |Absent |Absent |— |
|Stercobilin |Norm |Norm |Norm |
|Bile acids |Absent |Absent |— |
____________________________________________________________________________________________________________________________________________________________________________________________________________
|12. |Blood |Urine |Feces |
|Common bilirubin |82,08 mcmol/l |— |— |
|Conjugated bilirubin |5,98 mcmol/l |«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 |44,46 mcmol/l |— |— |
|Conjugated bilirubin |2,55 mcmol/l |Absent |— |
|Urobilin |Present |Present |— |
|Stercobilin |Increased |Increased |Increased |
|Bile acids |Absent |Absent |— |
________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________________
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 the typical violations of quantitative and qualitative composition of urine;
➢ To characterize the causes and mechanisms of processes glomerular filtration, tubular reabsorption and secretion disorders;
➢ To know the renal clearance, be able to calculate and apply it to analyze violations of various parts of the nephron;
➢ To analyze the mechanisms of pathological proteinuria, explain which kidney disease may be linked to the development of certain species;
➢ To identify the acute renal failure, its criteria and principles of Pathophysiological classification;
➢ To analyze the causes and mechanisms of acute prerenal, renal and postrenal kidney insufficiency;
➢ To be able to explain the mechanism of glomerular filtration rate reduction at different variants of acute renal failure;
➢ To evaluate the different approaches to experimental modeling of acute diffuse glomerulonephritis in determining the causes and mechanisms of its development;
➢ To identify nephrotic syndrome by its clinical and pathophysiological manifestations, explain the etiology of primary and secondary nephrotic syndrome;
➢ To apply the acute tubular necrosis as a main cause of acute renal failure;
➢ To identify the chronic renal failure (CRF), its criteria in terms of renal function depending on the stage and the clinical manifestations;
➢ To characterize the causes and mechanisms of chronic renal failure;
➢ To analyze reactive changes in the kidneys at them injury;
➢ To explain the metabolic disturbances (exchange of sodium and water, exchange of potassium, acid-base balance, mineral metabolism, metabolism of xenobiotics / drugs) and endocrine changes in renal function at chronic renal failure;
➢ To evaluate the importance of retention azotemia and other metabolic disorders at the development of poliorganic insufficiency;
➢ 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 (Human Anatomy Department).
2. To name the basic functions of kidney and explain their mechanisms (Normal Physiology Department).
3. To name the basic components of urine (Normal Physiology Department).
The checking of primary level of knowledges.
Give the answers to the following questions:
1. Basic quantitative urinary symptoms which arise up at the diseases of kidney.
2. Concept about poly-, oligo-, anuria, mechanisms of their development.
3. Concept about hyper-, hypo-, isosthenuria, mechanisms of their development.
4. 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. Concept about leukocyteuria. Reasons and mechanism of development.
9. Cylindruria, definition. Reasons of origin. Types of cylinders, mechanism of their education.
10. 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. Concept about urolithiasis. Reasons, mechanisms of development. Consequences.
Theoretical questions for the FMC 2:
1. Concept of kidneys insufficiency, principles of classification.
2. Preren, renal and postrenal mechanisms of renal processes disorders.
3. Causes and mechanisms of blood circulation in the kidneys disorders.
4. Causes and mechanisms for violations of glomerular filtration disorders.
5. Causes and mechanisms of tubular reabsorption and secretion disorders.
6. Main indexes of kidney functions.
7. Use of functional tests for the determination of the type of renal function disturbances.
8. Quantitative and qualitative changes of the urine.
9. Pathological components of urine.
10. General signs of renal failure .
11. Causes, manifestations and mechanisms of retention azotemia.
12. Pathogenesis of renal edema.
13. Violation of acid-base balance: azotemic renal acidosis, proximal and distal tubular acidosis.
14. Pathogenesis and manifestations of renal osteodystrophy.
15. Mechanisms of hypertension, anemia, disorders of hemostasis at renal disease.
16. Syndromes of acute and chronic renal failure: criteria, causes and mechanisms of development, clinical manifestations.
17. Pathogenesis of uremic coma.
18. Principles of renal failure treatment.
19. Concept of extracorporeal hemodialysis and peritoneal, lymphodialisis, their diagnostic significance.
20. Glomerulonephritis: definition, principles of classification.
21. Experimental models and modern understanding of the etiology and pathogenesis of diffuse glomerulonephritis.
22. Nephrotic syndrome, primary and secondary.
23. Causes and mechanisms of formation of kidney stones, 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. p.281-290.
2. Pathophysiology/ Edited by prof.Zaporozan, OSMU, 2005, p.248-259.
3. General and clinical pathophysiology/ Edited by Anatoliy V/ Kubyshkin – Vinnytsia: Nova Knuha Publishers – 2011. p.566-587.
Testing according system “Krok-I”
Tests of an open database (2010)
1. Shock and signs of acute renal failure (ARF) developed in the patient due to permanent injury. What is the leading cause of development of ARF in the case?
A Decreased arterial pressure
B Urine excretion violation
C Increased pressure in the nephron capsule
D Increased pressure in the renal arteries
E Decreased oncotic BP
2. Arterial hypertention is caused by the stenosis of the renal arteries in the patient. Activation of what system is the main link in the pathogenesys of this form of hypertension?
A Renin-angiotensin
B Sympathoadrenal
C Parasympathetic
D Kallikrein-kinin
E Hypothalamic-pituitary
3. Chronic glomerulonephritis was diagnosed in a 34-year-old patient 3 years ago. Edema has developed in the last 6 monthes. What caused it?
A Proteinuria
B Hyperproduction of vasopressin
C Disorder of albuminous kidneys function
D Hyperosmolarity of plasma
E Hyperaldosteronism
4. Two weeks after lacunar tonsillitis a 20-year-old man started complaining about general weakness, lower eyelid edemata. After examination the patient was diagnosed with acute glomerulonephritis. What are the most likely pathological changes in the urine formula?
A Proteinuria
B Cylindruria
C Presence of fresh erythrocytes
D Pyuria
E Natriuria
5. On the 6th day of treatment a patient with acute renal insufficiency developed polyuria. Diuresis intensification at the beginning of polyuria stage of acute renal insufficiency is caused by:
A Renewal of filtration in nephrons
B Volume expansion of circulating blood
C Growth of natriuretic factor
D Reduction of aldosteron content in plasma
E Reduction of vasopressin content in plasma
6. A 30 year old woman has face edemata. Examination revealed proteinuria (5,87 g/l), hypoproteinemia, dysproteinemia, hyperlipidemia. What condition is the set of these symptoms typical for?
A Nephrotic syndrome
B Nephritic syndrome
C Chronic pyelonephritis
D Acute renal failure
E Chronic renal failure
7. A patient with nephrotic syndrome has massive edemata of his face and limbs. What is the leading pathogenetic mechanism of edemata development?
A Drop of oncotic blood pressure
B Increase of vascular permeability
C Rise of hydrodynamic blood pressure
D Lymphostasis
E Increase of lymph outflow
8. A driver who got a trauma in a road accident and is shocked has reduction of daily urinary output down to 300 ml. What is the main pathogenetic factor of such diuresis change?
A Drop of arterial pressure
B Drop of oncotic blood pressure
C Increased vascular permeability
D Decreased number of functioning glomerules
E Secondary hyperaldosteronism
9. A patient with massive burns developed acute renal insufficiency characterized by a significant and rapid deceleration of glomerular filtration. What is the mechanism of its development?
A Reduction of renal blood flow
B Damage of glomerular filter
C Reduction of functioning nephron number
D Rise of pressure of tubular fluid
E Renal artery embolism
All correct answers: A.
2009
1. A patient complains about dyspnea provoked by the physical activity. Clinical examination revealed anaemia and presence of the paraprotein in the zone of gammaglobulins. To confirm the myeloma diagnosis it is necessary to determine the following index in the patient's urine:
A.Antitrypsin
B.Ceruloplasmin
C.Bilirubin
D.Haemoglobin
E. Bence Jones protein
2. Two weeks after lacunar tonsillitis a 20-year-old man started complaining about general weakness, lower eyelid edemata: After examination the patient was diagnosed with acute glomerulonephritis. What are the most likely pathological changes in the urine formula?
A. Presence of fresh erythrocytes
B. Natriuria
C. Pyuria
D. Cylindruria
E. Proteinuria
3. A patient with massive burns developed acute renal insufficiency characterized by a significant and rapid deceleration of glomerular filtration. What is the mechanism of its development?
A. Damage of glomerular filter
B. Rise of pressure of tubular fluid
C. Reduction of functioning nephron number
D. Reduction of renal blood flow
E. Renal artery embolism
Correct answers:
1-E; 2-E; 3-D.
2008 – 2004
1. For a patient as a result of nephron tubule pathology by Zymnitski test found out the substantial decrease of kidney ability to the osmotic concentration of urine. How are these changes named?
A. Proteinuria
B. Hematuria
C. Chsilindruria
D. Іsоhypostenuria
E. Leukocyturia
2. For a patient with mieloma protein discovered. What form of proteinuria does take place for this patient?
A. Renal glomerular.
B. Suprarenal
C. Renal tubular
D. Subrenal tumor
E. Subrenal uretral
3. Patient 30 years, delivered to the clinic with a diagnosis “sharp glomerulonephritis”, there was proteinuria. What violations in an organism caused this phenomenon?
A. Delay of nitrogen exchange products destroying
B. Decrease of oncotic blood pressure
C. Increase of glomerular membrane permeability
D. Increase of hydrostatical pressure on the capillaries wall
E. Decrease of functional nephrons quantity
4. For a patient A., 38 years, with 3 year of lupus disease found out the diffuse damage of kidney, which is accompanied massive edemas, expressed proteinuria, hyperlipidemia, dysproteinemia. What is the most reliable mechanism of proteinuria development in this clinical situation?
A. Nephrons inflammatory damage
B. Tubule ischemic damage
C. Increase the level of blood proteins
D. Nephron autoimmune damage
E. Impression of urine ways
5. Acute glomerulonephritis developed for a patient. What mechanism of his development?
A. Damaging action of complex IgA or IgD with an antigen
B. Damaging action of complex IgE or IgA with an antigen
C. Damaging action of complex IgG or IgM with an antigen
D. Damaging action of complex IgG or IgA with an antigen
E. Damaging action of complex IgD or IgM with an antigen
6. Patient A, 27 years, delivered in a hospital with the massive gastric bleeding in a grave condition. AT - 80/60 mm Hg. A patient selects 60 - 80 ml urine for day, relative specific gravity - 1,028-1,036. In blood plasma increased: remaining nitrogen, urea, creatinin. What pathogenetic mechanism of day's diuresis diminishing more credible in this clinical situation?
A. Increase of urine osmotic pressure
B. High level of blood remaining nitrogen
C. Increase of colloid-osmotic blood pressure
D. Decrease of glomerular capillaries hydrostatical pressure
E. An increase of hydrostatical pressure in the Boumen capsule
7. For a patient with chronic diffuse glomerulonephritis chronic insufficiency of kidney developed. In the terminal stage of insufficiency develops oligo-, anuria, which predefined:
A. By the ischemia of kidney cortex as vessel spasm result
B. Diminishing of filtrative pressure and filtration
C. Multiplying reabsorbtion of water in distal tubules
D. Disseminated intravascular blood coagulation
E. Decrease the quantity of active nephrons
8. To the rabbit intravenouswas entered nephrotoxic plasma of the Guinean piggy, which was preliminary immunized by rabbit kidney suspension. What pathology of kidney is designed thus?
A. Pyelonephritis
B. Glomerulonephritis
C. Uremia
D. Nephrotic syndrome
E. Tubular insufficiency
9. For a patient with a primary nephrotic syndrome the maintenance of general protein of blood makes 40 g/l. What reason of hypoproteinemia?
A. An exit of protein from vessels to tissues
B. A decrease of protein synthesis in liver
C. Promoted proteolys
D. Proteinuria
E. Disorder of protein suction in an intestine
10. At an inspection of patient is set that clirens of endogenous creatinin after collection of 24th portion of urine for him makes 50 ml/min (at a norm - 110-150 ml/min.). About the decrease of what function does the presence of such sign testify?
A. Kidney tubule reabsorbtion
B. Kidney incretoric function
C. Export from the organism of ions.
D. Export from the organism of urinary acid.
E. Kidney tubular filtrations
11. For a patient with sharp kidney insufficiency (day's diurez - 50 ml) anuria developed. What is the main mechanisms lie in basis of its origin?
A. Na reabsorbtion increased
B. Difficulty of urine outflow
C. Disorder of kidney blood circulation
D. Increase of kidney tubular filtrations
E. Water reabsorbtion increased
12. At a pyelonephritis mainly damaged:
A. Kidney tubule
B. Kidney glomerular
C. Interstitial tissue
D. Kidney vascular system
E. Uxtaglomerular vehicle
13. The basic displays of chronic kidney insufficiency are:
A. Metabolic acidosis
B. Intoxication by the products of nitrous exchange;
C. Tissue hypoxia
D. Anemia;
E. Immunodepression
14. At the inherited phosphate kidney diabetes violated:
A. Reabsorbtion of chlorides
B. Reabsorbtion of potassium
C. Ecscretion of sodium
D. Selection of water
E. Reabsorbtion of phosphates
15. Edemas and arterial hypertension appeared for a patient in one and a half weeks after a heavy streptococcus angina, in urine are hematuria and moderate proteinuria. In blood are antibodies to antistreptococcus and decrease of complement components. In what structures microvessels the most reliable localization of immune complexes which caused the development of nephropatia?
A. Pyramids
B. Bowls
C. Ureters
D. Urinary bladder
E. Glomerular
16. What main pathogenetic factor in development of edemas at a nephrotic syndrome?
A. An increase of capillaries hydrostatical pressure
B. An increase of intercellular liquid oncotic pressure
C. Decrease of blood plasma oncotic pressure
D. A decrease of blood plasma osmotic pressure
E. An increase of intercellular liquid osmotic pressure
17. In an experiment, at the design of kidney pathology for an animal, observed the followings signs: edemas, massive proteinuria, hypoproteinemia, dysproteinemia, hyperlipemia. What kidney pathology are such signs characteristic for?
A. Sharp diffuse glomerulonephritis
B. Pyelonephritis
C. Sharp kidney insufficiency.
D. Nephrotic syndrome.
E. Chronic kidney insufficiency
18. For a patient, as a result of sulema poisoning, sharp kidney insufficiency which includes 4 stages developed: first - initial, second - oliguria, fourth is convalescence. How is the third stage of sharp kidney insufficiency named?
A. Metabolic
B. Hemodynamic
C. Ischemic
D. Pathochemical
E. Polyuria
19. For a patient, as a result of sulema pathogenic action, sharp kidney insufficiency developed with the anuria, uremia and kidney necrosis. What is the localization of kidney necrotic damage in this case?
A. Cerebral matter
B. Ureters
C. Kidney bowls
D. Kidney cups
E. Cortex
20. Syndrome of Fankoni with disorder of sodium ions reabsorbtion, glucose, amino acid, hydrocarbonats, phosphates found out for a patient. What part of nephron will be damaged here?
A. Proximal
B. Distal
C. Genle loop
D. Collapsible tubule
E. Glomerular
21. A patient, 19 years, carried angina. In 2 weeks appealed to the doctor with complaints about oliguria, discoloration of urine (“pigwashes of meats”). AP - 190/100 mm Hg. What is the starting mechanism of arterial hypertension development at glomerulonephritis?
A. Aldosteron hypersecretion
B. Renin hypersecretion
C. ADG production is increased
D. Kidney glomerular Ischemia
E. Neurogenic component of vascular tone is increased
22. For a patient with a nephrotic syndrome development of edema is linked with:
A. Anemia
B. Urine selection disorder
C. Vasclar wall permeability disorder
D. Hyperaldosteronism
E. Massive proteinuria
23. A patient entered to the clinic with complaints about a general weakness, polyuria. It is discovered at an inspection: skin covers are pale, AP is a 180/110 mmHg; blood test : er- 3,2х1012/l, Hh - 90 g/l ; analysis of urine: specific gravity - 1,006, albumen -5g/l, leucocytes - 30 in п/з. What pathology these symptoms are characteristic for?
A. Kidney amyloidosis
B. Glomerulonephritis
C. Prostatitis
D. Pielonephritis
E. Kidney mieloma
24. Anuria developed, hypernitrogenemia and interstitial lung edema developed for a patient which was in a shock state. Disorder of what kidney function is main in development of sharp kidney insufficiency?
A. Reabsorbtion of water increased in tubules
B. Increased of sodium reabsorbtion
C. Decrease of glomerular filtration speed
D. Urinary acid secretion disorder in tubules
E. Potassium reabsorption is decreased
25. What is the mechanism of filtration diminishing in the case of suprarenal form of sharp renal insufficiency?
A. Damage of glomerular filter.
B. Kidney blood stream decreased
C. Active nephron quantity is diminished.
D. Tubules liquid pressure is increased
E. Decrease of oncotic blood
26. In the blood plasma of patient with urolithiasis there is increased the level of urinary acid. Contents of remaining nitrogen in blood - 20 mcmole/l. What change of blood composition found out for a patient?
A. Kidney hypernitrogenemia
B. Kidney hypoazotemia
C. Dysproteinemia
D. Hyperuricemia
E. Hyperacidemia
27. Anoreksia, dyspepsia, disorder of heart rhythm, itch of skin appeared for a patient symptoms with chronic kidney insufficiency. What main mechanism of these disorder development?
A. Disorder of lipid exchange
B. Changes of carbohydrate exchange
C. Accumulation of products of nitrous exchange in blood
D. Kidney acidosis
E. Disorder of water-electrolyte exchange
28. What origin of albumen more credible at selective proteinuria – 12g/d?
A. Тubular
B. Suprarenal.
C. Glomerular.
D. Uretral
E. Subrenal
29. A patient suddenly had pains in the kidney area with an irradiation in a groin, nausea, vomit, day's diuresis - 50 ml. What is the define the mechanism of anuria.
A. Disorder of filtration.
B. Increase of reabsorbtion.
C. Exception of nephron parts
D. Reflectory anuria.
E. Obturation of ureter.
30. Persons 72, is suffers on chronic glomerulonephritis. At an inspection: absence of appetite, vomit, diarrhea, itch of skin, anemia, maintenance of remaining nitrogen in blood -45 - mmole/l. Indicated signs are caused:
A. By the increase glomerular membrane permeability
B. By the kidney ischemia
C. Deleting of nephron functions
D. Autoimmune damage of glomerular membrane
E. Disorder of concentrating mechanism
31. Patient 32 years, with sharp glomerulonephritis which did not adhere the limitations of NaCl and water, suddenly lost consciousness, there were cramps. AP - 220/120 mm. Hg. Pupils are extended. Bradycardia. What complication did arise up for a patient?
A. Sharp cardiac insufficiency
B. Еclampsia
C. Hypertensive crisis
D. Kidney comma
E. Epilepsy
32. The frequent protracted angina took place in anamnesis for the patient 25 years. He complains about periodic head pains, rapid fatigueability, edemas of periorbital area. Found out moderate arterial hypertension, proteinuria, hypoproteinemia, hyperlipidemia. At kidney ultrasound: a bilateral defeat with the insignificant increase of kidney parenchyma echogenic. What disease is most reliable in this case?
A. Sharp glomerulonephritis
B. Chronic pielonephritis
C. Lipoid nephrosis
D. Chronic glomerulonephritis
E. Sharp kidney insufficiency
33. For physically healthy youths soldier after the heavy physical loading in one-day pedestrian transition on a 50 km in urine found out an albumen (to 1 g/l). What variety of proteinuria did take place?
A. Dehydratation proteinuria
B. Alimentary proteinuria
C. Organic proteinuria
D. Unreal proteinuria
E. Long going (mаrsh) proteinuria
34. Unselective unmassive proteinuria is characteristic for?
A. Uretritis
B. Chronic kidney insufficiency
C. Sharp kidney insufficiency
D. Nephritic syndrome.
E. Nephrotic syndrome.
35. How is the terminal stage of kidney insufficiency, which is accompanied development of metabolic acidosis, azotemia, grey color of skin, itch, smell of ammonia, by disorder of vital function, named?
A. Sharp kidney insufficiency
B. Tubulopatia
C. Glomerulopatia
D. Uremia
E. Kidney colic
36. Patient, 58 years complaints about growth of AP. At a clinical inspection found out chronic kidney disease with disorder of renal blood stream. Activating of what regulator mechanism did become reason of growth of AP for this patient?
A. Parasympathetic nervous system
B. Sympathetic nervous system
C. Cardio-vascular system
D. Damade of thyroid gland
E. Renin- angiotensin system
37. Woman, 55 years, with kidney insufficiency arterial pressure makes 170/100 mm.Hg. The hyperactivation of what systems caused the proof increase of arterial pressure?
A. Sympato - adrenal system
B. ypotalamo - hypophysar
C. Renin- angiotensin – aldosteron system
D. CNS
E. Kalicrein – kinin system
38. Woman 25 years, complain after cooling: pain in the back, disuric displays (leucocyturia, cylindruria, bacteriuria, day's diuresis without changes). It can be linked with development of?
A. Glomerulonephritis
B. Sechekam’yana illness
C. Radiculitis
D. Adnexsitis
E. Pyelonephritis
39. What quantitative changes of diuresis can result in uremia?
A. Polyuria
B. Dysuria
C. Аnuria
D. Nicturia
E. All foregoing changes
40. In what case it will be diminishing of glomerular filtration?
A. Pleasure in capillaries - 60 mmHg, oncotic blood pressure - 35 mm Hg, pressure in capsule 20 mm Hg
B. Pressure in capillaries - 80 mm Hg, oncotic blood pressure - 30 mm Hg, pressure in capsule - 20 mm Hg
C. Pressure in capillaries - 100 mm Hg, oncotic blood pressure - 30 mm Hg, pressure in capsule - 20 mm Hg
D. Pressure in capillaries - 80 mm Hg, oncotic pressure - 20 mm Hg, pressure in capsule 10 mm Hg
E. Pressure in capillaries - 100 mm Hg, onkotic pressure - 20 mm Hg, pressure in a capsule - 20 mm Hg
41. At research of urine for a patient found out proteinuriya (5 g/l) due to lowmolecular albumens, hematuria with the lixiviated red corpuscles. For disorder of what kidney function are such indexes characteristic ?
A. Disorder of tubule secretory function
B. Disorder of glomerular excretory function
C. Disorder of tubular reabsorbtion
D. Disorder of glomerular permeability
E. Extrarenal disorders
42. Reason of anuria in extrarenal of sharp kidney insufficiency is:
A. Necrosis of tubules epithelium
B. Glomerulonephritis
C. Poisoning with heavy metals
D. Hypoproteinemia
E. Obturation of urine ways
43. Kidney insufficiency is characterized anemia. What mechanism of its development?
A. Hematuriya
B. Hemoglobinuria
C. Erytropoetin production is decreased
D. Hypoproteinemia
E. Albuminuria
44. Kidney diabetes is diagnosed for the patient (renal glycosuria). A diagnosis is linked:
A. Decrease of glucose reabsorbtion in kidney
B. Diminishing of paratgormon secretion
C. Diminishing of insulin secretion
D. Diminishing of insulin reception
E. Hyperglucemia
45. Patient N., 55 years suffers from chronic glomerulonephrtis during 15 years. What changes of laboratory indexes are most characteristic for the kidney filtration decrease?
A. Hyperglucemia
B. Hypernitrogenemia
C. Hypoproteinemia
D. Proteinuria
E. Hypo-, isostenuria
46. What transferred indexes are characteristic for a nephrotic syndrome?
A. Proteinuria 400 mg/day
B. Hematuria
C. Proteinuria more than 3,5 g/daу
D. Leucocyturia
E. Piuria
47. A girl after the casual consumption of uneatable mushrooms entered to the reanimation department with the arterial hypotension, anuria, hyperazotemia, consciousness disorder. What pathology does take place in this case?
A. Acute glomerulonephritis
B. Acute pyelonephritis
C. Urolithiasis illness
D. Acute kidney insufficiency
E. -
48. As a result of accident prevention violation poisoning by sulema took place. In 2 days daily diuresis made 620 ml. Head pain, vomit, cramps, appeared for a patient, dysphnoe, in lungs are moist wheezes. What pathology does take place?
A. Pyelonephritis
B. Chronic kidney insufficiency
C. Glomerulonephritis
D.Acute kidney insufficiency'
E. Uremic coma
49. There were face edemas for a woman 30 years. At an inspection discovered: hypoproteinemia, dysproteinemia, hyperlipidemia, proteinuria (5,87 g/l). Such combination of symptoms is characteristic for?
A. Acute kidney insufficiency
B. Nephrotic syndrome
C. Nephritic syndrome
D. Pyelonephritis
E. Chronic kidney insufficiency
50. As a result of the protracted starvation glomerular speed filtration grew on 20%. What is the most reliable mechanism of filtration changes:
A. Increased arterial pressure
B. Decreased blood plasma oncotic pressure
C. Increased coefficient of filtration
D. Increased kidney plasma flow
E. Increased kidney filter permeability
Correct answers:
1-D; 2-B; 3-C; 4-D; 5-C; 6-D; 7-E; 8-B; 9-D; 10-E 11-D; 12-C; 13-B; 14-E; 15-E; 16-C; 17-D; 18-E; 19-E; 20-A; 21-D; 22-E; 23-D; 24-C; 25-B; 26-D; 27-C; 28-A; 29-D; 30-C; 31-B; 32-D; 33-E; 34-D; 35-D; 36-E; 37-C; 38-E; 39-C; 40-A; 41-D; 42-E; 43-C; 44-A; 45-B; 46-C; 47-D; 48-D; 49-D; 50-B.
Situate task:
1. Patient, 25 years, who had frequent tonsillitis syffers 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 arised 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 arised 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.
• Аналізувати типові порушення кількісного та якісного складу сечі;
• Характеризувати причини та механізми порушень процесів клубочкової фільтрації, канальцевої реабсорбції і секреції;
• Розуміти про нирковий кліренс, вміти його розраховувати та застосовувати для аналізу порушень різних відділів нефрону;
• Аналізувати механізми розвитку патологічної протеїнурії, пояснювати, з якими захворюваннями нирок може бути пов'язаний розвиток її окремих видів;
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 cloudy
Specific gravity 1010
Albumen 1,3‰
MICROSCOPY OF SEDIMENT
Pavement epithelium 2-3 in eyeshot
Leucocytes 1-2 in eyeshot
Leached erythrocytes 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 cloudy
Specific gravity 1015
Albumen 10,6 ‰
MICROSCOPY OF SEDIMENT
Pavement epithelium 3-4 in eyeshot
Leukocytes 6-10 in eyeshot
Leached erythrocytes single in eyeshot
Cylinders:
hyalin 5-6 in eyeshot
grained 6-8 in eyeshot
waxy 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 cloudy
Specific gravity 1009
Albumen 1,65 ‰
MICROSCOPY OF SEDIMENT
Pavement epithelium 2-3 in eyeshot
Leukocytes 10-15 in eyeshot
Leached erythrocytes 5-10 in eyeshot
Cylinders:
hyalin 1-2 in eyeshot
grained 5-6 in eyeshot
waxy 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 0,6 ‰
MICROSCOPY OF SEDIMENT:
Pavement epithelium 1-2 in eyeshot
Leukocytes 2-3 in eyeshot
Leached erythrocytes 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
Erythrocytes 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 erythrocytes 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 erythrocytes 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 cloudy
Specific gravity 1022
Albumen 1,65 ‰
MICROSCOPY OF SEDIMENT:
Pavement epithelium 3-4 in eyeshot
Leukocytes 10-12 in eyeshot
Erythrocytes
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 cloudy
Specific gravity 1015
Albumen 2,2 ‰
MICROSCOPY OF SEDIMENT:
Pavement epithelium 2-3 in eyeshot
Leukocytes 5-8 in eyeshot
Leached erythrocytes 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 cloudy
Specific gravity 1011
Albumen 50 ‰
MICROSCOPY OF SEDIMENT:
Pavement epithelium 2-3 in eyeshot
Leukocytes 2-3 in eyeshot
Erythrocytes absent
Cylinders
hyalin 2-3 in eyeshot
grained 2-3 in eyeshot
waxy 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 erythrocytes; |
| |Single hyalinic cylinders |
| |
|Additional datas: |
|Arterial pressure |185/100 mm Hg |
|Rest nitrogen of blood |80 mcmol/l |
____________________________________________________________________________________________________________________________________________________________________________________________________________
GENERAL URINE ANALYSIS №13
|Diuresis |800 ml |
|Specific gravity |1,029 |
|Albumen |1 g/l |
|Glucose |absent |
|Keton bodies |absent |
|MICROSCOPY OF SEDIMENT |Leached erythrocytes 40–50 in the eyeshot; single hyalinic and |
| |erythrocyte cylinders |
| |
|Additional datas:: |
|Arterial pressure |165/105 mm Hg |
|Rest nitrogen of blood |50mcmol/l |
| |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 waxy cylinders in a big number |
|Additional datas: |
|Arterial pressure |120/65 mm Hg |
|Rest nitrogen of blood |35 mcmol/l |
____________________________________________________________________________________________________________________________________________________________________________________________________________
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 |4,5 mcmol/l. |
________________________________________________________________________________________________________________________________________
GENERAL URINE ANALYSIS №16
|Diuresis |340 ml |
|Specific gravity |1,035 |
|Albumen |1,5 g/l |
|Glucose |absent |
|Keton bodies |absent |
|MICROSCOPY OF SEDIMENT |Erythrocytes 20–30 in the eyeshot; grained and waxy cylinders 2 – 3 in the |
| |eyeshot. |
|Additional datas: |
|Rest nitrogen of blood | 210 mcmol/l. |
|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 13 mcmol/l |
____________________________________________________________________________________________________________________________________________________________________________________________________________
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 erythrocytes; |
| |Single hyalinic cylinders |
|Additional datas: |Arterial pressure - 145/90 mm Hg |
| |Rest nitrogen of blood 58 mcmol/l |
________________________________________________________________________________________________________________________________________
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 mcmol/l |
________________________________________________________________________________________________________________________________________
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 4,4 mcmol/l |
________________________________________________________________________________________________________________________________________
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