LAB 7
URINARY SYSTEM DISEASES


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OBJECTIVES

1. List factors contributing to calculi formation and prevention. (pp. 664-665, Table 45-1).

2. Describe the procedure and uses of an intravenous pyelogram (IVP). (p. 671, Fig. 45-9).

3. Name the general physiological purposes (to evaluate filtration, reabsorption, etc.) of the following : plasma creatinine, blood urea nitrogen (BUN), concentration and dilution tests and renal arteriogram. (Ch 45)

4. Briefly describe the basic structural and/or functional changes in the kidney produced in each of the following : pyelonephritis, glomerulonephritis, hypertensive kidney, polycystic kidney. (Ch 46).

5. Name and briefly describe various factors/conditions which can obstruct urine flow. Name 2 conditions which can result from obstruction of urine flow (pp. 664, 681).

6. Know all underlined terms and * questions, including * case study questions.

MICROSCOPE SLIDES 

Normal Kidney Cortex - (H3490 or H3495) Click here 

The cortex or outer region of the kidney contains the glomeruli and Bowman's capsules where filtration occurs and the proximal and distal convoluted tubules where reabsorption and secretion take place. Observe these structures, using the diagram provided. Note the even appearance of the glomeruli and tubules.

                    84. Normal glomerulus, microscopic *

Normal Kidney Medulla - (H3490) Click here 

The medulla or inner region of the kidney contains the loops of Henle and collecting ducts where water reabsorption occurs. Note the even appearance of these structures.  

Acute (Hematogenous) Pyelonephritis - (PH 1726) (p. 683) Click here 

In pyelonephritis, infection of the kidney causes inflammation and damage to the tubules. Note the scattered patches of inflammatory white blood cells. Using high power, notice that the tubular cells have indistinct outlines because they are damaged. The glomeruli appear normal. Compare this slide with that of the normal kidney.

            23. Acute pyelonephritis, medium power microscopic *

* Which of the 3 main processes in urine formation would be most affected in this kidney? (pp. 649, 683) 

Chronic Pyelonephritis - (PH 1728) (pp. 683-685) Click here 

In chronic pyelonephritis, not only the tubules but also the glomeruli have been damaged. Some of the tubules are filled with casts, some of the glomeruli have become hyalinized (appear solid and pink) and there are scattered patches of white blood cells. Compare this slide with the slide of normal kidney and with Fig. 46-6, p. 684, Fig. 46-11, p. 689

26. Chronic pyelonephritis, low power microscopic

Chronic Pyelonephritis -(Chronic Pyelitis and Pyonephrosis - PH 1730) Click here 

This slide emphasizes the presence of protein casts in the tubules. (See Fig. 46-6, p. 684, Fig. 46-11, p. 689). The damaged tubules have leaked proteins which have coagulated into the round pink casts. (Pyelitis means the renal pelvis is infected and pyonephrosis means hydronephrosis which has become infected. You do not have to know these two terms). Do not confuse casts in tubules with hyalinized glomeruli even though they are similar in appearance.

26. Chronic pyelonephritis, low power microscopic

End-Stage Kidney - (Kidney in Diabetes - PH 1765) Click here 

            43. End stage renal disease, gross
            44. End stage renal disease, microscopic *

Regardless of the starting point of each specific type of chronic renal disease, the end is the same, destruction of all parts of the nephron. This final stage is called end-stage kidney. This particular slide shows end-stage kidney due to diabetes. (pp. 696-698, Fig. 46-18)

Compare this slide with that of the normal kidney and with Fig. 46-11 on page 689 of the text. Note that both the glomeruli and tubules are abnormal. Many of the glomeruli are hyalinized (replace by pink protein material) and many of the tubules show fibrosis. There is also blood present within the tubules.

* Which of the 3 main processes in urine formation would be abnormal in this kidney? (pp. 647-650)

SPECIMENS AND RADIOGRAPHS
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Urinary Bladder Calculi
(pp. 664-665, 40-41, Fig. 3-11)

Urinary tract calculi (stones) are lumps of crystallized salts present in the kidney, ureters or bladder. A major contributing factor in calculi formation is urine which is too acid or too alkaline. Altered pH of the urine causes salts which are normally in solution to precipitate out of solution. Urinary stones may also result from excessively high concentrations of certain compounds in the urine and from urinary infections.

            1.Synovial fluid with sodium urate crystals, polarized light with red compensator, microscopic. *
            7. GIF animation of urinary tract lithiasis
            10. Hydronephrosis with calculus at ureteropelvic junction, gross
            9.  Hydronephrosis, severe, gross [CT]
            8. Hydronephrosis from obstruction by calculus, gross
            11. Hydroureter and hydronephrosis, gross [XRAY]

* What are three materials commonly found in calculi formed in acid urine? (pp. 664-665, Table 45-1)

* What are three materials commonly found in calculi formed in alkaline urine? (p. 665, Table 45-1)

* What is the main way an individual can prevent stone formation? (p. 665)

Kidney with cyst (p. 695)

This specimen is a sectioned pig kidney. Note the single large, round, empty cyst which may result from enlargement of a tubule. A kidney with polycystic kidney disease would have many large and small cysts throughout its substance.

            62. Dominant polycystic kidney disease, gross
            63. Dominant polycystic kidney disease, gross
            64. Dominant polycystic kidney disease, gross [CT]
            67. Multiple simple renal cysts, gross
            62.Dominant polycystic kidney disease with polycystic liver, gross [CT]
            62. Dominant polycystic kidney disease with polycystic liver, gross [CT]

* What is the usual cause of the adult form of polycystic kidney in humans? (p. 695)

Kidneys with Nephrosclerosis (pp. 692-694)

Long standing hypertension often results in arteriosclerosis of the small arteries and arterioles of the kidney. This results in renal ischemia which in time leads to destruction of the glomeruli and atrophy of the tubules. These microscopic changes result in the granular and pitted surfaces of the kidneys you see here. Notice that the aorta of this patient also shows extensive atherosclerosis.

            37. Benign nephrosclerosis, gross
            38. Malignant nephrosclerosis, gross

* Which of the 3 main processes in urine formation would be affected in these kidneys? (pp. 649, 683)

Preserved Kidney with Neoplasia (pp. 111-113)

Observe the longitudinally cut surface of the kidney. Note that only a small portion shows the normal structure of cortex and medulla. The remainder is mainly tumor tissue.

                Transitional cell carcinoma of bladder, gross
            Transitional cell carcinoma of renal pelvis, gross
            Transitional cell carcinoma of renal pelvis, gross
            Transitional cell carcinoma, low power microscopic *
            Transitional cell carcinoma, high power microscopic *
            Renal cell carcinoma, gross [MRI]
            Renal cell carcinoma, gross [MRI]
            Renal cell carcinoma, gross
            Renal cell carcinoma with renal vein invasion, gross
            Renal cell carcinoma, microscopic *
            Metastases to kidney, gross
            Wilm's tumor of kidney, gross
            Wilm's tumor of kidney, low power microscopic *
            Wilm's tumor of kidney, high power microscopic *
            Angiomyolipoma of kidney, gross
            Angiomyolipoma of kidney, microscopic

* Is this neoplasm benign or malignant? Give reasons for your answers. (pp. 111-113, Fig. 8-3)

Intravenous Pyelogram of Urinary System (p. 671)

* How is an intravenous pyelogram (IVP) performed? (p. 671)

Note the outlines of the kidney, calces, renal pelvises, ureters and bladder. Note that one ureter appears smaller than the other. The kidney above smaller ureter is malfunctioning and producing abnormally small amounts of urine. The catheter inserted into the bladder is collecting the radiopaque material from the bladder.

CASE STUDY

Three weeks after recovering from a sore throat, Sara, a five year-old was brought to her pediatrician by her parents. Sara had a fever and had vomited several times. Her parents mentioned that during the previous week, she had not eaten well and was much less energetic than usual. Examination revealed the following : soft tissues were somewhat swollen, her urine contained blood and protein and it had a high specific gravity.

*1. What kidney condition does Sara probably have? (pp. 685-686)

*2. Explain the cause of each of the following : swollen tissues, hematuria and proteinuria. (pp. 685-688, Fig. 46-8)

*3. Name 3 other signs or symptoms which would be expected in this condition. (p. 685)

*4. The doctor prescribed penicillin and a diet with low salt content. What is the reason for each of these? (p. 687)

*5. How good are Sara's chances for complete recovery? (p. 687)

The story of the illness was told by Sara's parents many times over the following years. At age 25, Sara gradually became aware of having symptoms similar to those which she had during her previous kidney disease. She took some penicillin given her by a friend and cut down on salt in her diet. Her symptoms did not subside, as she had expected, but gradually became worse. She lost her appetite and often felt nauseous. She was weak, felt little motivation for any activities, and got out of breath quickly during mild exercise. She also noticed that the small amount of urine which she voided contained blood. Sara finally went to her doctor for help.

*6. Summarize Sara's current symptoms.

Clinical tests on Sara revealed the following :

Blood : hypoalbuminemia, azotemia, high BUN,
high creatinine, low serum bicarbonate

Urine : hematuria, proteinuria, no bacteria,
casts, specific gravity of 1.010 constantly

Sara was diagnosed as having Chronic Glomerulonephritis (CGN)

*7. What are the chances that her present condition was caused by her childhood kidney disease? What usually causes her present disease? (pp. 685, 688)

*8. What effect would CGN have on her glomerular filtration rate (GFR)? (Fig. 46-13, p. 691)

*9. What is causing her edema in this case? (p. 691, Fig. 46-13)

*10. What is causing her azotemia? (p. 691, Fig. 46-13)

*11. Besides the glomeruli, what other parts of her kidneys are damaged ? How do you know? (p. 678)

12. List five bodily systems, other than urinary, which are likely to be damaged by Sara's kidney disease and for each system named, tell one pathological change expected. (Table 47-1, p. 705)

*13. What are Sara's chances for recovery from CGN? (pp. 688, 714-715)

*14. What general treatment strategies might be suggested for Sara? (pp. 691, 714-715)

8Copyright 2001 - Augustine G. DiGiovanna - All rights reserved.

This material may not be reproduced or distributed in any form or by any means, or stored in any data base or retrieval system without prior written permission is obtained from Augustine G. DiGiovanna, Ph.D.,  Professor of Biology, Salisbury University, Salisbury, MD  21801.