METHODICAL INSTRUCTION FOR STUDENTS OF THE third COURSE
Medical Faculty
Lesson 13 (PRACTICAL – 6 hours)
Theme: 1. Kidney illnesses: glomerulonephritis, acute kidney insufficiency, pyelonephritis, amyloidosis (lardaceous), nephrosclerosis, uraemia.
2. Kidney-stoning illness.
3. Diseases of reproductive system.
Actuality of theme: Pathology of the kidney, male and female sex organs – a large group of diseases, which is a common cause of temporary disability and disability. Timely diagnosis of these diseases is important in the prevention of renal impairment, reproductive, child health and population in general.
Feature of renal diseases is the relationship of disorders in other organs and systems, including cardiovascular. At the present stage of particular importance in their diagnosis is percutaneous renal biopsy supravital.
Aim: to learn morphology of acute renal insufficiency, pyelonephritis, renal-stony disease, nephrosclerosis, polycystic kidneys, uremia, amyloidos of rens.
Professional orientation of students: Pyelonephritis, particularly in its chronic form, is a common, important and dangerous disease. It is the most frequent cause of death from uremia. In the experience of Brod of Prague, whose paper should be consulted, fatal uremia occured in 36 per cent of cases of chronic pyelonephritis, but in only 19 per cent of glomerulonephritis and 14 per cent of arteriolar nephrosclerosis. The disease used to be regarded as the province of the urologiist, but it is now very much the concern of the internist.
Initial level of knowledge and skills:
1. Normal anatomy of kidney (department of normal human anatomy).
2. Function of the glomerulus ( department of normal physiology).
3. Microscopic structure of the glomerulus ( department of histology, cytology and embryology).
4. Productive inflammation. Ways of infection spreading ( department of pathological anatomy).
5. Answer the questions of the theoretical part, which are offered in the album for class-room and extra-class-room work of students
Macropreparations: acute renal insufficiency (shock ren), cortical necrosis, acute necrotic nephrosis with mechanical jaundice, abscess-formed pyelonephritis, pustules of ren (apostematous nephritis), pustural nephritis, chronic pyelonephritis, arteriosclerotic kidney (after pyelonephritis), chronic pyelonephritis with papillonecrosis, contracted kidney, aterosclerotic wrinkled kidney, polycystic kidney, coral stone in the pelvis, fibrinous pericarditis, fibrinous-ulcerative colitis, hypernephroid carcinoma.
Micropreparations: Nephrosclerosis, granular dystrophy of epithelium of the convoluted tubules, atrophia of ren from compression, adenoma of the ren, embolic pustular nephritis, fibrinous pericarditis, lipoid nephrosis, nephrosclerosis.
Tables: cystic disease of the kidney, amyloid nephropathy, chronic pyelonephritis, renal cell carcinoma.
Questions for self-preparation:
Pathogenesis of pyelonephritis.
Morphology of acute pyelonephritis.
Morphology of chronic pyelonephritis.
Morphogenesis of acute tubular necrosis.
Morphology of ischemic acute tubular necrosis.
Morphology of toxic acute tubular necrosis.
Morphology of urate nephropathy.
Morphology of nephrocalcinosis.
Etiology and mechanism hydronephrosis.
Pathogenesis of renal stones ( calcium stones, magnesium ammonium phosphate stones, uric acid stones, cystine stones).
Patological anatomy of malignant tumor (Wilms tumor).
12.Morphology of renal cell carcinoma.
Methodology of Practical Class.
Individual Students Program.
I. Practical work – 9.00 – 12.00
Work 1.
Practical work with album & micropreparations
– Students must answer the questions, draw the micropreparations or microslides in album and describe the micropreparates with pathology, designate the main signs of pathologic process.
Class equipment by Illustrative material:
Micropreparations or microslides:
1. Necrotic nephrosis №218,№248. Preparation is coloured by hematoxylin-eozin.
In the epithelium of convoluted tubules almost along whole length the nuclei are absent. Cytoplasm is coloured into homogeneous pink colour. The cells of epithelium are edematic, partially destroyed, fill up the lumen of canaliculi. Cerebral layer is sharply hyperemic, in the lumen of straight canaliculi there are blood here and there – it is hematuria.
2.Granular dystrophy of epithelium of the convoluted tubules № 48. The cells of epithelium of the convoluted tubules are edematic, high, partially destroyed, coloured in homogeneous pink colour. In the lumen of convoluted tubules here and there one can see homogeneous pink massa – these are scaled off cells of epithelium. Nuclei of epithelium are absent, here and there one can see them weakly, contours are washed up. The vessels are plethoric.
3.Atrophia of ren from compression №136. Preparation is coloured by van Gison’s method, the connective tissue is coloured in red colour. Learning the preparation with the naked eye one can see expressed atrophia of renal parenchyma, the width from the capsule (salient side) to dilated pelvis (curved side) is 2-
4.Adenoma of the ren №
5.Embolic pustular nephritis № 120. Preparation is coloured by hematoxylin and eozin. One can see numerous pustules, microabscesses, placed at most in the cortical layer. Pustules are represented by leukocytic infiltration with complete damaging of renal tissue. Here and there on the territory of pustules one can see septic emboles – it is intensively blue coloured homogeneous massa.
6.Fibrinous pericarditis № 189. Preparation is coloured by hematoxylin and eozin. On the core there is fibrinous deposit in look of thick dark-brown coloured threads.
7.Lipoid nephrosis №122,№312. In №122 – coloration is by sudan III, in the preparation one can see yellow coloured tubes, these are renal canaliculi, in the epithelium of which there are deposits of neutral fat. With lipemia the fat is taken out through the rens and on account of reabsorption it is accumulated in the epithelium of canaliculi.
№312 – coloration is by hematoxylin and sharlah-red. One can see depositions of neutral fat (red colour) in the epithelium of canaliculi.
8.Nephrosclerosis №83. Coloration is by van Gison’s method. Glomeruli are red coloured – this is connective tissue, so, glomerulosclerosis takes place. Glomeruli have different sizes, that tells about that not all glomeruli are affected at the same time, about different length of development of the pathological changes in different glomeruli. The walls of vessels are considerably thickened, sclerosed. Plethora and dilation of canaliculi take place – it is “thyroid ren”.
Work 2.
Practical work with macropreparations near stands.
– Students must recognize the pathology of organs which are presented on the stand.
Macropreparations:
1.Acute renal insufficiency (shock ren). It is represented by several macropreparations with same changes. The ren has usual sizes. On the section one can see clear border between cortical and cerebral layers: cortical layer is pale, dilated; pyramids of cerebral layer are plethoric, dark-red coloured and they clearly stand out against a white background. Pallor of cortical layer is stipulated by ischemia, which is developed on account of spasm of afferent arterioles. Blood, passing the cortical layer, is droped by juxtamedullar shunts to cerebral layer.
2.Cortical necrosis. The ren of child has small sizes. Cerebral layers is plethoric, the cortical layer is pale. In the cortical layer one can see big white sites of necrosis, that are placed under the capsule. Necrosises of cortical layer are stipulated by long ischemia.
3.Acute necrotic nephrosis with mechanical jaundice. The surface and the section of ren are pale-yellow coloured. The border between layers are absent, in the cerebral layer one can see punctate and linear hemorrhages, more rare the hemorrhages on the border between layers (in the intermedial zone). The cortical layer is dilated and blanched. In the porta renis there is excessive growing of fatty tissue. With jaundice the level of bilirubin, biliary acids, which are not endotoxins, is increased considerably. Bilirubinemia and cholalemia are the starting device of development of the acute renal insufficiency with jaundice. So, renal insufficiency joins hepatic insufficiency.
4. Abscess-formed pyelonephritis. On the section one can see that in the renal tissue numerous big abscesses are placed in the cortical and cerebral layers, the border between layers is washed out, in the porta renis there is excessive growing of fatty tissue. The fatty tissue in the porta renis tells about long inflammation of mucous of the pelvis, calyces of ren. So, renal abscesses are complications of upper pielonephritis.
5.Pustules of ren (apostematous nephritis). It is represented by two macropreparations, that have the same changes. The ren has usual sizes, it is plethoric. One the surface (in the cortical layer) there are multiple not big pustules with red contours at expense of hyperemia. Localization of pustules in the cortical layer of ren tells about hematogenic pyelonephritis. Septic emboli with arterial blood come, as a rule, into cortical layer of ren, because the cortical layer is better vascularized. Emboli are stoped in the capillaries, diameter of which is less then size of embol, and here focal purulent inflammation, that is pustule, is developed.
6.Pustural nephritis (moulage). Against pale-pink background one can see numerous light-yellow coloured not big pustules. The pustules have red contours.
7.Chronic pyelonephritis. It is represented by two macropreparations:
the sizes of ren are considerably decreased, the surface is bigtuberous, the upper pole is atrophied, on the section one can see small pustules and multiple hemorrhages. In the porta of organ, in the pelvises and calyces there is excessive growing of fatty tissue. Bigtuberous surface of ren tells about big zones of sclerosis, which were developed after inflammation. Deformed upper pole of organ tells about that the inflammation was focal, that is peculiarly to pyelonephritis. Probably abscesses or carbuncle of upper pole took place. Excessive growing of fatty tissue in the porta renis also is consequence of chronic inflammation of pelvis, calyces. So, atrophy and sclerosis were developed on account of upper pyelonephritis.
The ren is some increased, the surface is bigtuberous, the border between layers is absent. In the porta of organ one can see excessive growing of fatty tissue. One can see that from the porta renis bands of connective tissue grow into the parenchyma. Especially near porta renis the sclerosis is expressed. Explain, why does the nephrosclerosis prevail near porta renis?
8.Arteriosclerotic kidney (after pyelonephritis). It is represented by two macropreparations:
the sizes of ren are some decreased, the surface is bigtuberous, the upper pole is sharply atrophied and sclerosed. In the porta there is excessive growing of fatty tissue. Explain, why is the upper pole more atrophied and sclerosed?
The sizes of ren are usual, the surface is evenly smalltuberous, in the porta there is excessive growing of fatty tissue.
9.Chronic pyelonephritis with papillonecrosis. The ren is some increased, pale-yellow coloured; one can see single cicatrices, on the surface there are numerous light-yellow coloured with red contour small pustules besides one can see punctate hemorrhages. On the section one can see dilation of cortical layer, the border between layers is not clear. On the top of pyramid there are light-white coloured with red contours sites – it is necrosis of papillae (papillonecrosis). In the porta there is excessive growing of fatty tissue. Explain the reasons of papillonecrosis and with what pathology is this complication possible?
10.Contracted kidney. The ren is decreased, the surface is small tuberous. White coloured cicatrices deform the organ, forming the sulci, cavitates; between them there are small dark-red coloured colliculi. Small cicatrices were developed on the place of sclerosed glomeruli. Next glomeruli are increased, that is compensatory hypertrophy is developed. Dark-red colour of colliculi is stipulated by plethora of capillaries of the glomerule. Smalltuberous ren can be contracted or arteriosclerotic. Arteriosclerotic kidney is developed after previous inflammation of glomeruli; that is after glomerulonephritis. Contracted kidney is developed without previous damaging of glomeruli. It can be with damaging of afferent arteriole (its narrowing). With hypertonia arteriosclerosis is developed, including and of afferent arterioles of ren. From hypoxia the glomerule is atrophied and sclerosed. Macroscopically contracted ren and arteriosclerotic kidney are almost the same.
11.Aterosclerotic wrinkled kidney. The ren has usual sizes, the surface is bigtuberous. Deformed cicatrices are wide, they form wide sulci, cavitates. Colliculi have almost the same sizes. The form of organ is preserved. Bigtuberous deformation of ren is stipulated by that the big arteries are affected by aterosclerosis, that is why there are big sites of atrophia and sclerosis and of compensatory hypertrophy.
12.Polycystic kidney. It is represented by three preparation. The sizes of ren are considerably increased, from the surface and on the section it is represented by cysts, that have diameter equal 1-3 sm. The cysts are filled by transparent liquid (urine) or dark-red liquid (blood). The walls of cysts are thin and half-transparent. Between the cysts here and there are growing of fatty tissue. It is congenital anomaly, that is appeared in embryonal period and is displayed by underdevelopment of renal canaliculi and by narrowing or absence of connection of canaliculi with collective tubes. That is why some canaliculi devastate, other are transformed into the retention cysts. Parenchyma of ren, in particular glomeruli, for this is atrophied, and child dies from renal insufficiency. Polycystosis of ren often is united with polycystosis of the liver, pancreas, ovaries.
13.Coral stone in the pelvis. Renal pelvis is some dilated, filled up by the big stone, that from the pelvis gives processes to calyces, that is its configuration repeat the form of the pelvis with calyces. It is called coral, because is like to underwater coral growings.
14.Calculous pyelonephritis. In the preparation the part of ren is represented – these are opened pelvis and calyce, in the lumen of which there are stones. Mucous membrane of pelvis is hyperemic (it is sign of inflammation) with single hemorrhages. Pelvis and calyce are increased (stretched), parenchyma of ren is thinned, atrophied.
15.Nephrolithiasis and hydronephrosis. On the section one can see that the pelvis and cavice of ren are considerably increased (stretched), parenchyma of ren is considerably atrophied. In the lumen of pelvises and cavices one can see stones. So, nephrolithiasis was complicated by hydronephrosis and by atrophia of parenchyma from pressure.
16.Hydronephrosis. In the preparation one can see big fibrous sac, filled up by transparent liquid. Fibrous sac quite is not like for form to ren. The stone obstructes ureter, hydronephrosis is developed, complete atrophy of ren from pressure comes.
17.Fibrinous pericarditis (hairy heart). Core is covered with threads of fibrin, that is why “hairy” heart. With uremia urea begins to exude from the organism through the skin, serous and mucous membranes. With stimulation core by urea aseptic fibrinous pericarditis is developed. Pericardial murmur with uremia is a bad prognostic sign.
18.Fibrinous-ulcerative colitis. The mucous membrane of large intestine is covered with fibrinous film, here and there it is ulcerous. With uremia the urea exudes from organism through the skin, serous and mucous membranes. From stimulation by urea in the mucous membranes necrotic changes, ulcering, depositions of fibrinous films appear. Ulcerative stomatitis, ulcerative-fibrinous esophagitis, gastritis, enteritis, colitis are developed.
19. Hypernephroid carcinoma. The tissue of ren is destroyed by tumor, only on the border of preparation one can see partially preserved parenchyma of ren. Tissue of tumor is heterogeneous by density. One can see hemorrhages. Tumor is developed from tissue, which is the base of renal laying (metanephrogenic tissue). The cells of tumor sometimes form the tubes, liked canaliculi. In it different derivative mesoderms, such as cross-striated and smooth muscular fibrae, fatty tissue, vessels, cartilagines can met. It metastasizes into the lungs, grows into next tissue and organs.
20. Carcinoma of urinary bladder. One can see on the mucous membrane the big tumor that has look as cauliflower with papillary vegetations. Tumor has origin from transitional epithelium to next tissue and organs. It metastasizes into regional lymph nodes.
Work 3.
Analyzing work.
– Students must analyze the pathology of organs of gross preparations and micropreparations and explain the possible reasons of their beginning (etiology), basics of morphological change and mechanism of their development (pathomorphosis & pathogenesis).
Brake time: 12.00 – 12.30
I. Seminar discussion of practical work – 12.30 – 13.45
List of theoretical questions for the discussion:
1. Classification of prostate adenoma.
2. Morphogenesis endocervicoses.
3. Hemorrhagic glomerulonephritis.
4. Chronic glomerulonephritis.
5. Secondary-wrinkled kidney.
6. Adipoid-amiloidnyy nephrosis.
7. Kidney stones with hydronephrosis.
8. Fibrinous pericarditis in uremia.
9. Classification of diseases of genital organs.
10. Etiopathogenesis of background and precancerous diseases of the cervix.
11. Endocervicoses morbid anatomy.
12. Morphology of cervical cancer.
13. Causes of and morphological characteristics of endometrial hyperplasia.
14. The morphology of endometrial cancer.
15. Classification and histological characteristics of ovarian tumors.
16. Morphology mastopatiy.
17. Classification and pathology of prostate pathomorphology.
18. Reasons for development and morphology of ectopic pregnancy.
19. Etiology, pathogenesis and morphology of kidney disease.
20. Morphological changes of various kinds of glomerular nephritis.
21. To change the different departments of nephrons in nephrosis and pyelonephritis?
22. The morphological changes that occur in various organs in these diseases, causes of death.
TEST EVALUATION AND SITUATIONAL TASKS
Situation Tasks:
1. In the body section of vascular collapse deceased male, 48 years, revealed increased pigmentation of skin, reduced in size adrenal glands, enlarged liver, a brownish yellow color. In histological studies in the adrenal glands revealed necrotic tuberculosis with granulation tissue. In the liver – fatty phenomenon. Indicate the diagnosis and possible complications.
Answers to the Situation Tasks:
1. In the patient developed Addison’s disease. The most threatening complications is a state of collapse and the development of shock due to adrenocorticotropic hormone deficiency.
Tests
1. Most forms of chronic renal failure produce increased serum levels of all of the following substances, EXCEPT:
a) Calcium. b) Aldosterone. c) Phosphate. d) Parathormone. e) Renin.
2. Uremia is associated with all of the following abnormalities, EXCEPT:
a) Peripheral neuropathy. b) Gastritis. c) Polycythemia. d) Pericarditis. e) Diffuse alveolar damage.
3. Diabetes mellitus is associated with all of the following renal disorders, EXCEPT:
a) Diffuse glomerulosclerosis. b) Nodular glomerulosclerosis. c) Benigh nephrosclerosis. d) Urate nephropathy. e) Acute pyelonephritis.
4. All of the following conditions predispose to urolithiasis, EXCEPT:
a) Sickle cell nephropathy. 2. Hyperparathyroidism. 3. Gout. 4. Proteus pyelonephritis. 5. Enteric hyperoxaluria.
5. The factor least likely to cause acute pyelonephritis is which of the following:
a) Pregnancy. b) Nephrolithiasis. c) Catheterization of the bladder. d) Prostatic hypertrophy. e) Septicemia.
6. All of the following statements correctly describe chronic pyelonephritis, EXCEPT:
a) It causes asymmetrically scarred kidneys. b) It is associated with vesicoureteral reflux in most cases. c) It spares the calyces and pelvis. d) It may produce thyroidization of tubules. e) It is an important cause of secondary nephrosclerosis.
7. All of the following statements correctly describe analgesic abuse nephropathy, EXCEPT:
a) It is characterized by tubulo-interstitial component. b) It is often caused by phenacetin. c) It causes inability to concentrate urine. d) It often improves with drug with drawal. e) It predisposes to the development of renal cell carcinoma.
8. Renal diseases producing systemic hypertension include all of the following, EXCEPT:
a) Acute glomerulonephritis. b) Renal amyloidosis. c) Chronic glomerulonephritis. d) Chronic pyelonephritis. e) Renal vasculitis.
9. Histologic features of malignant nephrosclerosis include all of the following, EXCEPT:
a) Fibrinoid necrosis of arterioles. b) Medial thickening of arterioles. c) Fibromuscular dysplasia of the renal artery. d) Renal artery thrombosis. e) Focal renal parenchymal infarction.
10. Obstetrically related renal disease includes all of the following disorders, EXCEPT:
a) Nephrocalcinosis. b) Diffuse cortical renal necrosis. c) Acute ischemic tubular necrosis. d) Acute glomerulonephritis. e) Hydronephrosis.
11. Hematuria is a characteristic clinical feature of all of the following diseases, EXCEPT:
a) Glomerulonephritis. b) Malakoplakia. c) Nephrolithiasis. d) Renal cell carcinoma. e) Bladder papilloma.
12. What pathologic condition of the kidneys is caused by mercury poisoning?
a) Acute tubular necrosis. b) Renal papillary necrosis. c) Crescentic glomerulonephritis. d) Acute interstitial nephritis. e) Renal cell carcinoma.
a) Arterial bloodstream. b) The lymphatics. c) Venous bloodstream. d) Vesicoureteral reflux. e) Aberrant arteriovenous shunts.
14. All of the following statements regarding Goodpasture’s syndrome are true, EXCEPT:
a) Patients present with hemoptysis and hematuria. b) Death occurs due to uremia and pulmonary hemorrhage. c) Electron microscopy shows the absence of electron-dense deposits. d) Immunofluorescence reveals granular deposits of IgG in the glomeruli. e) Immunofluorescence reveals linear deposits of IgG in the glomeruli.
15. Hydronephrosis is caused by all of the following, EXCEPT:
a) Chronic renal vein thrombosis. b) Large uterine leiomyoma. c) Renal calculi. d) Benign prostatic hypertrophy. e) Papillary transitional cell carcinoma of the ureter.
16. Benign nephrosclerosis is characterized by all of the following, EXCEPT:
a) Narrowing of the lumen of the arterioles and small arteries. b) Thickening and hyalinization of the vessels’ walls. c) Deposition of amyloid within the Bowman space. d) Foci of tubular atrophy. e) Deposition of collagen within the Bowman space.
17. The tubular epithelial cells in acute tubular necrosis are characterized by all of the following pathologic features, EXCEPT:
a) Karyolysis. b) Plasmolysis. c) Plasmorrhexis. d) Plasmocoagulation. e) Tubulorrhexis.
18. Hydronephrosis is characterized by all of the following, EXCEPT:
a) Kidney infarct. b) Thinning of the renal parenchyma. c) Dilatation of the renal pelvis. d) Dilatation of the renal calyces. e) Progressive atrophy of the kidney.
a) Dilatation of the pelvis and calyces. b) Ischemic tubular necrosis. c) Interstitial inflammation. d) Interstitial fibrosis. e) Glomerular and tubular atrophy.
Answers for the tests
1) a; 2) c; 3) d; 4) a; 5) e; 6) c; 7) e; 8) b; 9) c; 10) a; 11) b; 12) a; 13) d; 14) d; 15) a; 16) c; 17) e; 18) a; 19) b.
III. TESTING of KNOWLEDGES of STUDENTS – 14.15 – 15.00
References:
А – Basic:
1. Ya. Bodnar, A. Romanyuk, R. Bodnar, K. Romanyuk, V. Voloshyn. Short cours of patomorphology: Textbook. – Ternopil: TSMU,2011. – 544 p.
2. Practical classes materials.
3. Anderson’s Pathology //Edited by Jonh M. Kissane. The C.V. Mosby Company. – Toronto – Philadelphia, 1990. – 2196 p.
4. Emanuel Rubin, John L. Farber. Pathology. – Philadelphia, 1994. –1200 p.
5. Harsh Mohan. Textbook of Pathology. — Jaypee Brothers, Medical publishers (P) LTD., New Delhi, 1995. — 980 p.
6. Ramzi S. Kotran, Vinay Kumar, Stanley S. Robbins. Robbins Pathologic Basis of Disease, W.B. Saunders Company, USA, 1994. – 1400 p.
7. Robbins and Contran Kumar. Pathologic Basis of Disease /Eighth edition. – Saunders, Elsevier, 2010. – 1450 p.
8. Thomas C. Histopathology. – B.C. Decker Inc. – Toronto – Philadelphia, 1989. – 386 p.
9. Thomas C. Macropathology. – B.C. Decker Inc. – Toronto – Philadelphia, 1990. – 355 p.
10. Zagoruyko A.K. Short lectures on pathology (pathological anatomy). – Simferopol: 2 ed. CSMU, 2002 – 196 p.
11. Lectury presentation. http://intranet.tdmu.edu.ua/data/kafedra/internal/index.php?&path=patologanatom/presentations/en/stomat/ptn/Pathomorphology/2-3/ ….
B – Additional :
1.Sorokina I. Pathological anatomy. Kharkov: Fact, 2005, P. 564
2.Струков А.И., Серов В.В. Патологическая анатомия. – М.: Медицина, 1993. – C. 47-59.
3.Серов В.В., Ярыгин Н.Е., Пауков В.С. Патологическая анатомия. Атлас. – М., 1986. – C. 5-25.
4.Ramzi S. Kotran, Vinay Kumar, Stanley S. Robbins. Robbins Pathologic Basis of Disease, W.B. Saunders Company, USA, 1994 – P. 24-28.
Methodical instruction has been worked out by: assistant Petro Vavrukh
Methodical instruction was discussed and adopted at the Department sitting
01 june___ 2011. Minute № _16
Methodical instruction was adopted and reviewed at the Department sitting
__07 june__2012 . Minute № __15_
