Pathophysiology of Uti

PATHOPHYSIOLOGY OF UTI For infection to occur, bacteria must gain access to the bladder, attach to and colonize the epithelium of the urinary tract to avoid being washed out with voiding, evade host defense mechanisms, and initiate inflammation. Most UTIs result from fecal organisms that ascend from the perineum to the urethra and the bladder and then adhere to the mucosal surfaces. Bacterial Invasion of the Urinary Tract By increasing the normal slow shedding of bladder epithelial cells (resulting in bacteria removal), the bladder can clear itself of even large numbers of bacteria. Glycosaminoglycan (GAG), a hydrophilic protein, normally exerts a non-adherent protective effect against various bacteria. The GAG molecule attracts water molecules, forming water barrier that serves as defensive layer between the bladder and the urine. GAG may be impaired by certain agents (cyclamate, saccharin, aspartame, and tryptophan metabolites). The normal bacterial flora of the vagina and urethral area also interfere with adherence of Escherichia coli (the most common microorganisms causing UTI). Urinary immunoglobulin A (IgA) in the urethra may also provide a barrier to bacteria. Reflux An obstruction to free-flowing urine is a problem known as urethrovesical reflux, which is the reflux (backward flow) of urine from the urethra into the bladder. With coughing, sneezing, or straining, the bladder pressure rises, which may force urine from the bladder into the urethra. When the pressure returns to normal, the urine flows back into the bladder, bringing into the bladder bacteria from the anterior portions of the urethra. urethrovesical reflux is also caused by dysfunction of the bladder neck or urethra. The urethrovesical angle and urethral closure pressure may be altered with menopause, increasing the incidence of infection in postmenopausal women. Reflux is most often noted, however, in young children. Treatment is based on its severity. Ureterovesical or vesicoureteral reflux refers to the backflow of urine from the bladder into one or both ureters. Normally, the ureteroveical junction prevents urine from traveling back into the urether. The ureters tunnel into the bladder wall so that the bladder musculature compresses a small portion of the ureter during normal voiding. When the ureterovesical valve is impaired by congenital causes or ureteral abnormalities, the bacteria may reach and eventually destroy the kidney.

Schematic Diagram: Loss of integrity of the mucosal lining (caused by in indwelling catheter, tumor, parasites, or calculus)

Decreased resistance to invading organisms

Inflammatory changes occur in the affected portion of the Urinary tract.

Clumps of bacteria may be present.

Inflammatory changes in the renal pelvis and throughout the kidney.

Scarring of the kidney parenchyma (occurs in chronic infection), which interferes kidney function.

Etiology: Causative organism:  Escherichia Coli 90% of UTI in women.  Enterocobacter- Pseudomonas- Staphylococcus saprophyticus  Candida Route of entry:  Ascent from the urethra (most common)  Circulating blood. Contributing causes:  Obstruction usually congenital  vesicoureteral reflux  infections elsewhere in the body 1.) Upper respiratory 2.) Gastrointestinal diarrhea  poor perineal hygiene  short female urethra  catheterization  Inherent defect in the ability of the bladder mucosa to protect it from microbial infection.