PYELONEPHRITISPYELONEPHRITISPYELONEPHRITIS.pptx

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1. Glomerulonephritis PREPARED BY DAYANA SIVAN ASSISTANT PROFESSOR MALIK DEENAR COLLEGEOF NURSING KASARAGOD

2. It is an inflammatory and damage to the filtering part of the kidney(glomerulus).Toxins, metabolic wastes and excessive fluid are not filtered properly into urine . Instead, they build up in the body causing swelling and fatigue. Epidemiology It is the third most common cause for End-Stage Renal Disease (ESRD).

3. Etiology Humoral Immunological Mechanism: The response is mediated by antibody molecules that are secreted by plasma cells. Eg : Mother’s antibodies are passed from her body to the body of fetus . 2. Cellular Immunological Mechanism: Destruction of infected cells by Cytotoxic T-cells, or destruction of intracellular pathogens by macrophages. 3. Abnormalities in metabolism. 4. Hereditary diseases. 5. Vascular diseases.

4. Pathogenesis The Glomerular lesion may involve either in all glomeruli OR focal: some , not all glomeruli OR segmental: any part of an individual glomerulus. If so, they seem to be proliferative or overgrowth of epithelium or endothelium and membranous thickening of Glomerulus basement Membrane(GBM). Here, antigens; such as Endogenous antigens; which include Heymann antigen on the epithelial cells or Goodpasture antigen, which causes kidney damage and lung damage on Glomerulus basement Membrane(GBM) And/or Exogenous antigen such as viral, bacterial, parasite or fungal Or Previously sequestered antigens such as Deoxyribonucleic acid (DNA) or thyroglobulin are the first step in Humoral Immunologic damage to the Glomerulus.

5. Antineutrophil cytoplasmic auto antibody( ANCAs) that is autoantibodies reacting to cytoplasmic components to neutrophils and monocytes are found in Glomerulonephritis. Complex of these antigens and antibodies are formed in the circulation and entrapped in the glomerular capillary. Humoral and Cell mediated immune reaction gets damaged due to the parenchymal damage because of high blood flow and capillary hydrostatic pressure in glomerulus. This cause a complexity and increases the likelihood of Glomerular damages.

6. Treatment Early treatment is needed to remove the circulating anti glomerular basement membrane and reduce renal inflammation. Immunosuppressive therapy, except for those with minimal renal involvement or irreversible kidney disease without lung involvement. Corticosteroids: Intravenous methylprednisolone upto 1000 mg/day for 3 consecutive days, followed by oral prednisolone of 1 mg/kg/day tapered to 20 mg/ day for 6 weeks. Contd ………………

7. 4. Oral Cyclophosphamide (CYC) 2mg/kg/day. 5. Plasmapheresis: Daily exchange of plasma, Human Albumin for 14 days ; if patient is affected by Glomerular basement membrane. Oral prednisolone and Cyclophosphamide are discontinued after 6 and 3 months. Plasmapheresis is continued for atleast 14 days or until Glomerular basement membrane become undetectable.

8. PYELONEPHRITIS Infection of Kidney, due to : Inability to empty the Bladder Urinary stasis Urinary Obstruction due to tumour or Benign Prostatic Hypertrophy. Seen mostly in females, because of short urethra and urinary meatus to vagina and rectum- which allow bacteria to enter into the bladder.

9. Etiology Bacterial infection causing causative organisms are Escherichia coli, Pseudomonas, Staphylococcus aureus, Streptococcus faecalis.

10. Morphology Gross: It may involve one or both kidneys. Kidneys show small abscesses in the renal parenchyma. Microscopy • Glomeruli: Glomeruli appear normal. • Tubules — Intratubular aggregates of neutrophils form abscess. — Tubular necrosis in later stages.

11. CYSTITIS Cystitis is a medical condition that refers to the inflammation of the bladder, usually caused by a bacterial infection, especially, Urinary Tract Infection.

12. Purulent or suppurative exudate consists of plasma with both active and dead neutrophils, fibrinogen, and necrotic parenchymal cells. This kind of exudate is consistent with more severe infections, and is commonly referred to as pus. Chronic cystitis Microscopically, the bladder wall shows chronic inflammatory infiltrate.

13. Clinical Features Both acute and chronic cystitis are characterized by a triad of symptoms: Frequency Lower abdominal pain localized over the bladder region or in the suprapubic region Pain or burning on urination “ Recognition of cystitis is important as it may cause pyelonephritis.”

14. 2. )Emphysematous cystitis: This form is characterized by the presence of bullae, seen in diabetic individuals.

15. 3.)Malakoplakia This occurs in infection with E. coli, Proteus and in immunocompromised patients. It is a peculiar form of chronic cystitis with formation of yellowish raised lesions within a pink mucosa. Histologically it typically shows the presence of foamy macrophages (von Hansemann cells) and laminated mineralized concretions with targetoid appearance (Michaelis-Gutmann bodies).

16. Yellow, soft, slightly raised mucosal plaque 3-4cm diameter. Malakoplakia is a rare inflammatory condition which makes its presence known as a papule, plaque or ulceration that usually affects the genitourinary tract.

17. RENAL CELL CARCINOMA RCC is a type of kidney cancer that affects the cells in the lining of the small tubes (tubules) in the kidneys that filter and clean the blood.” The origin is from renal tubular epithelium, predominantly in the cortex. Men are affected about twice as commonly as women.

18. Histopathology The gross and microscopic appearance of renal cell carcinomas is highly variable. The renal cell carcinoma may present reddened areas where blood vessels have bled, and cysts containing watery fluids. The body of the tumor shows large blood vessels that have walls composed of cancerous cells.

19. Gross examination often shows a yellowish, multilobulated tumor in the renal cortex, which frequently contains zones of necrosis, hemorrhage and scarring. In a microscopic context , there are four major histologic subtypes of renal cell cancer: clear cell (conventional RCC, 75%), papillary (15%), chromophobic (5%), and collecting duct (2%). Chromophobe cells are a histological structure that does not stain readily, and thus appears pale. Sarcomatoid changes (spindle cells) can be observed within any RCC subtype and are associated with more aggressive clinical course and worse prognosis. Under light microscopy, these tumour cells can exhibit papillae, tubules or nests, and are quite large, atypical, and polygonal.

20. RENAL CALCULI

21. INTRODUCTION Renal calculi are a common cause of blood in the urine (hematuria) and pain in the abdomen groin. They occur in 1 of every 11 people in the United States, with men affected 2 to 1 over women. Development of the stones is related to decreased urine volume or increased excretion of stone-forming components such as calcium, oxalate, uric acid, cystine, xanthine, and phosphate. Calculi may also be caused by low urinary citrate levels (an inhibitor of stone formation) or excessive urinary acidity.

22. TYPES MORPHOLOGICAL Calcium oxalate  stones are the most common type of renal calculi, comprising 70% to 75% of all urinary stones. They may present as 2 different crystalline forms: Calcium oxalate monohydrate Calcium oxalate dihydrate These stones typically form in acidic urine.

23. Calcium oxalate monohydrate calculi are extremely hard and usually present with a smooth, rounded surface. They are typically dark brown. Calcium oxalate dihydrate stones will be quite brittle with small, sharp, jagged edges. They are usually yellow to light brown.

24. HISTOPATHOLOGY Calcium oxalate: envelope, spindles, ovals, octahedral, picket fences, or dumbbell shaped. They often appear to have an "X" in their center.

25. MORPHOLOGICAL Calcium phosphate calculi They account for about 10% of all renal calculi. They tend to grow faster and larger than calcium oxalate calculi. These stones are off-white, grayish - white,or yellowish in color . Calcium phosphate stones form in alkaline urine and are typically associated with abnormal metabolic factors, such as hyperparathyroidism and renal tubular acidosis.

26. HISTOPATHOLOGY They are colorless, they often appear as plates, stars, or as a collection of needles.

27. MORPHOLOGY Uric acid calculi only form in acidic urine, usually with a pH less than 5.5. This acid is the most common composition of bladder stones and is typically radiolucent. Uric acid accounts for 8% to 10% of urinary calculi, and the incidence is increasing worldwide. This condition is most closely associated with diabetes, morbid obesity, metabolic syndrome, and older age at presentation

28. This is the only kidney stone that can be reasonably expected to dissolve if the urinary pH is sufficiently elevated and maintained. This type of stone is also more likely to form from excessive urinary acidity rather than hyperuricosuria. Uric acid stones may be yellow, orange, reddish, or brown, depending on the amount of blood-derived pigment they may have accumulated.

29. HISTOPATHOLOGY It is Rhomboidal-shaped crystals, rosettes, or plates.

30. MORPHOLOGY Struvite or triple phosphate (calcium, ammonium, magnesium phosphate) stones are always associated with infection and increased pH levels. It comprises of 7% to 8% of all urinary calculi worldwide. Struvite stones are caused by the action of urease from bacteria, which increase the urinary pH and generate ammonia, leading to triple phosphate precipitation and stone formation. Struvite stones appear chalky, white, or grayish. Their surface is usually smooth and relatively brittle.

31. HISTOPATHOLOGY appears coffin-lid-shaped.

32. MORPHOLOGICAL Cystine   stones are caused by genetic defect and account for only 1% to 2% of all urinary stones. They tend to be amber, tan, or yellowish in color with a waxy appearance. Cystine stones may turn somewhat greenish after exposure to air.

33. HISTOLOGICAL hexagonal-shaped crystals. They appear as almost perfect benzene rings under the microscope.