GENITO-URINARY SYSTEM

• Organs of the urinary system

  • Kidneys
  • Ureters
  • Urinary bladder
  • Urethra
• Renal functions


  • Formation of urine and elimination of metabolic waste
  • Acid base regulation; reclamation of bicarbonate from glomerular filtrate
  • Conservation of water through reabsorption by proximal convoluted tubules
  • Maintenance of normal extracelular potassium ion concentration through passive reabsorption in proximal convoluted tubules and tubular secretion in the distal tubules under the influence of aldosterone
  • Endocrine function (production of erythropoietin, renin, vitamin D)
• Responses to kidney injury

  • Azotemia
  • Uremia
  • Plasma protein loss
  • Water, electrolyte and acid/base imbalances
  • Hyperparathyroidism
  • Osteodystrophies
  • Drug retention
• Primary glomerular damage


  • Deposition of immune complexes, thrombosis, embolism, or direct viral bacterial infection of glomerular components
  • Lesions: necrosis/proliferation of cells or membranes of glomerulus, infiltration of leukocytes, reduced vascular perfusion/leakage of large quantities of proteins or other macromolecule in glomerular filtrate
  • Chronic lesions: atrophy and fibrosis, secondary atrophy of renal tubules
• Tubular damage


  • May occur as a result of tubular epithelial damage from infection, direct toxic damage or ischaemia
  • Response to injury by cellular degeneration, necrosis and atrophy
  • Damage or loss of nephron leads to compensatory hypertrophy of tubules to maintain overall renal function
  • Severe insult and loss of tubular membrane results in loss of tubular segments, failure of functional repair and permanent loss of entire nephron
  • Tubules may atrophy due to reduced oxygen tension, interstitial fibrosis or tubular obstruction or secondary to diminished glomerular perfusion and function
• Renal interstitium


  • Seen in ascending UTI (pyelonephritis), systematically derived infections of tubules and interstitium and secondary to injury or tubules and glomeruli
  • Acute lesions: edema, hemorrhage, inflammation (neutrophil infiltration)
  • Chronic lesions: less prominent neutrophils, fibrosis leading to decreased nephron function
• Diseases of the lower urinary tract

  • Infection
  • Obstruction
  • Intoxication
  • Congenital defects
  • Physical trauma
  • Neoplasia
• Renal failure


  Occurs when the kidneys fail to carry out their normal metabolic and endocrine function, leading to retention of constituents of plasma
• Types of renal failure

  • Pre-renal (e.g. decreased renal blood flow, circulatory collapse, obstruction of vascular supply, shock, severe hypovolemia)
  • Renal (e.g. renal disease)
  • Post-renal (e.g. obstruction of urine outflow)
• Impairment of renal function

  • Can lead to retention of constituents of plasma that are normally removed by the kidneys, including nitrogenous waste products (azotemia), other waste products (phenolic acids, guanidine, large molecular weight alcohols), reduced blood pH (metabolic acidosis), alterations of plasma ion concentration (particularly potassium, calcium, and phosphate), and hypertension
  • Results in a toxicosis called uremia, associated with multi-systemic clinical signs and lesions
• Lesions in uremia


  • Ulcerative and necrotic stomatitis
  • Ulcerative and hemorrhagic lesions in the stomach, colon
  • Fibrinous pericarditis
  • Uremic pneumonitis
  • Mucoarteritis
  • Soft tissue calcification
• Non-renal lesions in uremia

  • Pulmonary edema
  • Fibrinous pericarditis
  • Ulcerative and hemorrhagic gastritis
  • Ulcerative and necrotic stomatitis
  • Atrial and aortic thrombosis
  • Hypoplastic anemia
  • Soft tissue mineralization
  • Fibrous osteodystrophy
  • Parathyroid hyperplasia
• Developmental abnormalities of the kidneys

  • Agenesis/Aplasia
  • Hypoplasia
  • Renal dysplasia
  • Renal cyst
  • Ectopic kidney
  • Renal tubular dysfunction (cystinuria, glucosuria, hereditary generalized defect in tubular reabsorption)
• Circulatory disturbances of the kidneys

  • Hyperemia/Congestion
  • Hemorrhage
  • Infarction
  • Renal ischaemia
  • Anemia
  • Edema
• Disturbances in cell metabolism of the kidneys

  • Cloudy swelling
  • Hydropic degeneration
  • Amyloid deposition
• in the outer cortexas a means of conserving circulatorycompetence. The inner cortex vasoconstriction is mofidified by prostaglandin(PGE2) produced in the medulla which has a locai vasodilezory effect on theefferent arterioles of juxta-medullary nephrons.
• General anemia


  • oligemia
  • oligocythemia
  • oligochomemia
• General anemia


  Produced by hemorrhagic, hemolytic, hypochromic, aplastic or hypo plasticconditions
• Local anemia can also be seen if the thrombi/emboli becomeestablished in the renai artery or its branches.
• Edema-usually in association with inflammation.
• Cloudy Swelling


  Due to various inorganic, organic and bacterial or toxic substances that reached·the kidney via the blood stream. They injure glomerulus and convoluted tubulesfirst then followed by the collecting tubule.
• Hydropic Degeneration


  Characterized by formation of clear cytoplasmic vacuole that do not containglycogen, fat or mucin and are suspected to be tissue fluids.
• Amyloid


  Deposited on the capillary loops of glomeruli and around the intertubularcapillaries. Its presence usually leads to renal failure terminating to uremia.
• Fatty Degeneration


  Expression of severe injury to kidney cells; a result of intoxication
• Glycogen Infiltration


  Of little importance in domestic animals. The amount of glycogen in the tubular epithelium increase in diabetes.
• Pigmentation


  • Hemoglobin
  • Bile pigments
  • Muscle pigments
• Hemoglobin


  Due to excessive hemolysis of erythrocytes that can becaused by: Protozoan blood diseases, Bacterial diseases-bacillary hemoglobinuria, leptospirosis, Post parturient hemoglobin - seen in heavy milk producing cowsassociated with feeding ration low in phosphorus.
• Bile pigments


  A small amount of urobilinogen is normally excreted inurine but observed to be marked in case of hemolysis with normal liver.
• Organs of the urinary system

  • Kidneys
  • Ureters
  • Urinary bladder
  • Urethra
• Renal functions


  • Formation of urine and elimination of metabolic waste
  • Acid base regulation; reclamation of bicarbonate from glomerular filtrate
  • Conservation of water through reabsorption by proximal convoluted tubules
  • Maintenance of normal extracelular potassium ion concentration through passive reabsorption in proximal convoluted tubules and tubular secretion in the distal tubules under the influence of aldosterone
  • Endocrine function (production of erythropoietin, renin, vitamin D)
• Responses to kidney injury

  • Azotemia
  • Uremia
  • Plasma protein loss
  • Water, electrolyte and acid/base imbalances
  • Hyperparathyroidism
  • Osteodystrophies
  • Drug retention
• Primary glomerular damage


  • Deposition of immune complexes, thrombosis, embolism, or direct viral bacterial infection of glomerular components
  • Lesions: necrosis/proliferation of cells or membranes of glomerulus, infiltration of leukocytes, reduced vascular perfusion/leakage of large quantities of proteins or other macromolecule in glomerular filtrate
  • Chronic lesions: atrophy and fibrosis, secondary atrophy of renal tubules
• Tubular damage


  • May occur as a result of tubular epithelial damage from infection, direct toxic damage or ischaemia
  • Response to injury by cellular degeneration, necrosis and atrophy
  • Damage or loss of nephron leads to compensatory hypertrophy of tubules to maintain overall renal function
  • Severe insult and loss of tubular membrane results in loss of tubular segments, failure of functional repair and permanent loss of entire nephron
  • Tubules may atrophy due to reduced oxygen tension, interstitial fibrosis or tubular obstruction or secondary to diminished glomerular perfusion and function
• Renal interstitium


  • Seen in ascending UTI (pyelonephritis), systematically derived infections of tubules and interstitium and secondary to injury or tubules and glomeruli
  • Acute lesions: edema, hemorrhage, inflammation (neutrophil infiltration)
  • Chronic lesions: less prominent neutrophils, fibrosis - will result to decreased nephron function
• Diseases of the lower urinary tract

  • Infection
  • Obstruction
  • Intoxication
  • Congenital defects
  • Physical trauma
  • Neoplasia
• Renal failure


  Occurs when the kidneys fail to carry out their normal metabolic and endocrine function, leading to retention of constituents of plasma
• Types of renal failure

  • Pre-renal (e.g. decrease renal blood flow, circulatory collapse, obstruction of vascular supply to kidneys, shock, severe hypovolemia)
  • Renal (e.g. renal disease)
  • Post-renal (e.g. obstruction of urine outflow)
• Effects of renal failure

  • Retention of nitrogenous waste products (azotemia)
  • Intravascular accumulation of other waste products (phenolic acids, guanidine, large molecular weight alcohols)
  • Reduced blood pH (metabolic acidosis)
  • Alterations of plasma ion concentration (particularly potassium, calcium, and phosphate)
  • Hypertension
  • Toxicosis called uremia with multi-systemic clinical signs and lesions
• Lesions in uremia


  • Ulcerative and necrotic stomatitis
  • Ulcerative and hemorrhagic lesions in stomach, colon
  • Fibrinous pericarditis
  • Uremic pneumonitis
  • Mucoarteritis
  • Soft tissue calcification
• Mechanisms of non-renal lesions in uremia

  • Pulmonary edema (increased vascular permeability)
  • Fibrinous pericarditis (increased vascular permeability)
  • Ulcerative and hemorrhagic gastritis (ammonia secretion and vascular necrosis)
  • Ulcerative and necrotic stomatitis (ammonia secretion in saliva and vascular necrosis)
  • Atrial and aortic thrombosis (endothelial and subendothelial damage)
  • Hypoplastic anemia (increased erythrocyte fragility and lack of erythropoietin production)
  • Soft tissue mineralization (altered calcium-phosphorus metabolism)
  • Fibrous osteodystrophy (altered calcium-phosphorus metabolism)
  • Parathyroid hyperplasia (altered calcium-phosphorus metabolism)