Renal Disorders Unit 6 Intrarenal Disorders Occur primarily within the kidney and have the potential to result in renal insufficiency or failure Categories Infectious Obstructive Glomerular Congenital
Exam 3 Acute pyelonephritis Pathophysiology/Etiology/Pathogenesis Obstruction or ureteral reflux that allows contaminated urine to enter the kidney. Risk factors are diabetes mellitus, anatomic abnormalities of the urinary tract, and obstructive causes. Clinical Manifestations: Sudden onset of fever Chills CVA tenderness (classic sign- flank pain) nausea, vomiting anorexia, and fever-induced dehydration. Complications: abscesses, sepsis, acute respiratory distress syndrome, recurrent/chronic pyelonephritis, and chronic kidney disease. Diagnosis Urinalysis revealing significant amounts of bacteria and white blood cell (WBC) casts Obstruction Conditions that interfere with the flow of urine May be congenital (children) or acquired (adults) Changes results from: Location and degree of obstruction (i.e., partial or complete, unilateral or bilateral) Duration and timing (acute onset or chronic) of the obstruction
Chronic pyelonephritis Pathophysiology/Etiology/Pathogenesis: Chronic reflux of infected urine into the renal pelvis. Risks: renal calculi, neurogenic bladder, vesicoureteral reflux, or underlying intrarenal disease. Clinical Manifestations: Symptoms may be vague, inconsistent, or similar to acute pyelonephritis. Flank or abdominal pain, fever, malaise, or anorexia.
CHRONIC OBSTRUCTION
Diagnosis: Renal Ultrasound
BILATERAL OBSTRUCTION- Lajjet BOTH KIDNEYS CONGENITAL MALFORMATION OTERIOR URTHFALVALVE BENIGN PROSTATIC HYPERPLASIP CERVICAL CARCINOMA
Renal Calculi Nephrolithiasis: Stones formed in the kidneys Urolithiasis: Stones formed anywhere in the urinary tract Etiology and Pathogenesis: Urine becomes supersaturated with a specific solute. Urine is a solution of solvent (water) and solutes (particles). Some solutes have tendencies to form crystals when concentration of urine becomes supersaturated. Crystallization is enhanced with dehydration (decreased solvent) or with higher levels of solute in urine from excess excretion (calcium, uric acid). Adequate fluid intake is an inhibitor to stone
Kidney stones Clinical Manifestations: Acute renal colic or dull & localized flank pain. Renal Colic: spasmodic, intermittent sharp pain Nausea, vomiting, diaphoresis, tachycardia, and tachypnea, and hematuria Diagnosis: -Urinalysis to evaluate hypercalciuria and urinary pH Complete blood count (CBC) for dehydration -CT scan, x-ray -CMP to check Ca+ -Uric Acid -Parathyroid hormone level if Ca+ elevated.
formation. Glomerular Disorders Pathophysiology/Etiology/Pathogenesis: Proliferative and membranous lesions Tubulointerstitial damage Nephron's atrophy and the kidneys become small, scarred, and nonfunctional. Clinical Manifestations: Persistent proteinuria with or without hematuria a decline in GFR generalized edema or hypertension Glomerulus: cluster of nerve endings, blood vessels in a cluster of capillaries at the end of a kidney tubule where waste products are filtered from the blood.
Acute Glomerulonephritis Pathophysiology/Etiology/Pathogenesis: Abrupt onset of hematuria, proteinuria, oliguria, azotemia, edema, and hypertension Infectious organisms stimulate the production of antibodies and the initiation of the inflammatory process triggered by viruses or bacteria. Cause by infection in another part of the body causing the immune system to attack the glomeruli walls. Clinical Manifestations: Smoky or coffee-colored urine Increased circulating volume, producing edema, hypertension, and oliguria with increasing serum levels of creatinine and nitrogenous wastes (BUN). Diagnosis: Based on patient history, clinical manifestations, and urinalysis results BUN and Creatinine Renal biopsy Chronic Glomerulonephritis
Chronic Glomerulonephritis Glomerular diseases that as