GROUP FIVE GENERAL PATHOLOGY PRESENTATION

Presentation

1. Group 5. presented By: KABUUKA RICHARD KOBUSINGYE PHIONA KAGOYA AGNES NOURELDEIN ABDALLA MOHAMED

2. Acute Renal Failure (ARF) Definition: Acute renal failure, also known as acute kidney injury (AKI), is characterized by a sudden decrease in kidney function, leading to the accumulation of waste products and disturbances in fluid and electrolyte balance.

3. Pathophysiology: ARF can be classified into three main categories based on its etiology: Pre-renal ARF: Caused by reduced blood flow to the kidneys (renal hypoperfusion), which may occur due to factors such as dehydration, heart failure, or sepsis. The decrease in perfusion pressure results in decreased glomerular filtration rate (GFR).

4. Intrinsic (renal) ARF: Due to direct damage to the nephron (the functional unit of the kidney) from various insults such as ischemia, nephrotoxins (e.g., drugs, contrast agents), or glomerulonephritis. Tubular injury, especially to the proximal convoluted tubules, can lead to tubular cell death, obstruction of tubules, and impaired urine concentration.

5. Post-renal ARF: Caused by obstruction of the renal outflow tract, which can occur due to kidney stones, tumors, or enlarged prostate. Back pressure on the kidneys can impair GFR and lead to renal damage if prolonged.

6. Clinical Manifestations: Azotemia (elevated blood urea nitrogen and creatinine) Oliguria or anuria (low or absent urine output) Fluid overload leading to edema or hypertension Electrolyte imbalances (e.g., hyperkalemia)

7. Chronic Renal Failure (CRF)   Definition: Chronic renal failure, or chronic kidney disease (CKD), is characterized by a gradual loss of kidney function over months to years, often due to underlying conditions.

8. Pathophysiology; Progressive Nephron Loss: The common causes include; diabetes mellitus. Hypertension. Glomerulonephritis. polycystic kidney disease. Nephrons are lost over time, leading to compensatory hyperfiltration in the remaining nephrons, which can accelerate damage.

9. Glomerulosclerosis: Damage to the glomeruli can lead to scarring (sclerosis), further reducing filtration capacity.  Tubulointerstitial Fibrosis: Chronic inflammation and ischemia lead to fibrosis of the tubules, impairing function. Complications: Development of secondary hyperparathyroidism due to imbalances in calcium and phosphate metabolism. Accumulation of uremic toxins causing systemic effects

10. Clinical Manifestations: Progressive decline in GFR Symptoms of uremia (fatigue, nausea, itching, etc.) Anemia due to erythropoietin deficiency Bone disease (renal osteodystrophy) due to disturbances in mineral metabolism  

11. Nephrotic Syndrome:   Definition: Nephrotic syndrome is characterized by a triad of symptoms: proteinuria (>3.5 g/day), hypoalbuminemia (low serum albumin), and edema.

12. Pathophysiology: Glomerular Damage: The primary mechanism involves damage to the glomerular filtration barrier, leading to increased permeability to proteins. Common causes include minimal change disease, focal segmental glomerulosclerosis, diabetic nephropathy, and membranous nephropathy.

13. Proteinuria : Loss of albumin and other proteins in the urine leads to decreased oncotic pressure in the plasma, resulting in edema. Compensatory Mechanisms: Increased liver production of lipoproteins (hyperlipidemia) in response to low albumin levels. Activation of the renin-angiotensin-aldosterone system (RAAS) due to fluid retention.

14. Immunologic Factors: Some forms of nephrotic syndrome (e.g., minimal change disease) may have an underlying immunologic cause.   Clinical Manifestations: Edema, particularly in the face and legs Foamy urine due to proteinuria Increased susceptibility to infections Hyperlipidemia