Urinary Tract Infection & Interstitial Disease Flashcards
Common routes of infection of UTI
- ascending = most common
- organisms that colonize lower GI/perineal skin are introduced to urethral meatus and ascend into urinary tract
- most common = E.Coli
- hematogenous (blood-borne) infection
- debilitaed patients/previously damaged kidneys
- S. aureus, group A streo
- clinical setting: speticemia, endocarditis
Virulence factors that produce UTI
- certain strains of E. coli have P pili which allow attachment to receptors on urothelial cells
- “uropathogenic” ==> agglutinate human RBCs
- blood group P1 infections > blood group P2
- endotoxins by E. coli may inhibit ureteral peristalsis
Host defense mechanisms against UTI
- Secretions of urethral glands
- Mucosal factors
- Hydrokinetic factors - urine flow
- Functional “valve” between bladder and ureter that prevents retrograde flow.
- Urine (poor culture medium).
Predisposing factors to UTIs
- females = shorter urethra, more easily irritated + vagina often colonized by bacteria
- instrumentation = catheters, cystoscopy
- decreased urine flow
- calculi = obstruction => perpetuat/spread infection
- vesical-ureteral reflux
- pregnancy
- diabetes = high glucose in urine => good culture medium
Causes of decreased urine flow (==> UTI)
- Urinary tract obstruction
- Incomplete voiding
- Infrequent micturition
- Low flow
- Bladder/ureteral diverticula
- Neurologic diseases affecting bladder control
Clinical manifestations of UTIs
- covert bacteriuria
- F>>M
- some may have chronic pyelonephritis
- scarring occurs in young children
- symptomatic UTI
Symptoms of UTI @ urethra and vesical-urethral valve
- dysuria
- difficulty voiding
- incomplete emptying
- incontinence
Symptoms of UTI @ bladder (cystitis)
- frequency
- suprapubic pain
- sx of urethra UTI
Symptoms of UTI @ ureters and kidneys (acute pyelonephritis)
- flank pain + tenderness
- abdominal pain
- fever, chills
- oliguria
- sx of cystitis + sx of urethral infection
Lab features of UTI
- Urinalysis: Many WBC’s, WBC casts (pyelonephritis), RBC’s (variable).
- urine culture: usually > 100,000 bacteria/ml; always > 10,000 bacterial/ml
Major complications of UTIs
- Acute pyelonephritis = suppurative inflammation of kidney and renal pelvis from bacterial infection
- perinephric abscess = usually w/acute pyelonephritis
- renal scarring
- recorrence
- stones = esp. w/proteus infection
Characteristics of acute pyelonephritis
- Patchy, wedge-shaped regions of suppuration with microabscesses.
- Tubules filled with aggregates of PMNs
- Tubular destruction
- Interstitium – edema, PMNs, lymphs and plasma cells (may predominate in areas away from abscesses or during resolution).
- Glomeruli preserved until late in course
Major causes of chronic pyelonephritis
- when combined w/chronic or recurrent infections ==> renal scarring + progressive renal impairment
- urinary tract obstruction
- vesical-ureteral reflux (VUR)
Pathogenesis of chronic pyelonephritis caused by urinary tract obstruction
- obstruction predisposes to infection
- obstruction ==> difficult to eradicate; more recurrence
- obstruction + infection ==> structural kidney damage
- pressure-induced ischemia + tubular atrophy
- tissue injury due to bacteria/inflammation
Causes of obstruction ==> chronic pyelonephritis
- Intrinsic (intraluminal) masses of the urinary tract:
- exophytic tumors
- calculi
- blood clots
- Inflammation, stricture of urethra or ureters
- Urethral valves
- Extrinsic compression:
- tumors (esp. pelvis, retroperitoneal)
- retroperitoneal fibrosis
- hemorrhage (trauma)
- iatrogenic (surgical ligation, adhesions)
- Functional:
- neurological disease
- diabetes mellitus
- Idiopathic
Consequences of chronic obstructive pyelonephritis
- structural changes
- hydronephrosis
- atrophy + flattening of renal papillae/medulla
- fibrosis/atrophy of renal cortex
- microscopic: tubular atrophy + fibrosis w/patchy inflitrate of lymphs + edema/PMNs (if acute infection)
- functional changes
- decreased GFR
- HTN
Common causes of VUR
- normal: oblique course of ureter effectively forms “valve”
- if ureter enters perpindicularly ==> valve is lost ==> urine reflux into ureter
- most common: abnormality in infancy and resolves through childhood
- familial
Characteristics of reflux nephropathy
- = VUR + chronic/recurrent infection
- usually associated w/HTN
- organisms can gain access to renal parenchyma via reflux
- ==> scars @ calcyces
- thinning of cortex and medulla
- extensive scarring at poles of kidney
- small percentage of pts develop focal segmental glomerulosclerosis