Urinary Tract Infection & Interstitial Disease Flashcards

1
Q

Common routes of infection of UTI

A
  • 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
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2
Q

Virulence factors that produce UTI

A
  • 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
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3
Q

Host defense mechanisms against UTI

A
  1. Secretions of urethral glands
  2. Mucosal factors
  3. Hydrokinetic factors - urine flow
  4. Functional “valve” between bladder and ureter that prevents retrograde flow.
  5. Urine (poor culture medium).
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4
Q

Predisposing factors to UTIs

A
  • 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
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5
Q

Causes of decreased urine flow (==> UTI)

A
  1. Urinary tract obstruction
  2. Incomplete voiding
  3. Infrequent micturition
  4. Low flow
  5. Bladder/ureteral diverticula
  6. Neurologic diseases affecting bladder control
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6
Q

Clinical manifestations of UTIs

A
  • covert bacteriuria
    • F>>M
    • some may have chronic pyelonephritis
    • scarring occurs in young children
  • symptomatic UTI
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7
Q

Symptoms of UTI @ urethra and vesical-urethral valve

A
  • dysuria
  • difficulty voiding
  • incomplete emptying
  • incontinence
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8
Q

Symptoms of UTI @ bladder (cystitis)

A
  • frequency
  • suprapubic pain
    • sx of urethra UTI
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9
Q

Symptoms of UTI @ ureters and kidneys (acute pyelonephritis)

A
  • flank pain + tenderness
  • abdominal pain
  • fever, chills
  • oliguria
    • sx of cystitis + sx of urethral infection
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10
Q

Lab features of UTI

A
  1. Urinalysis: Many WBC’s, WBC casts (pyelonephritis), RBC’s (variable).
  2. urine culture: usually > 100,000 bacteria/ml; always > 10,000 bacterial/ml
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11
Q

Major complications of UTIs

A
  1. Acute pyelonephritis = suppurative inflammation of kidney and renal pelvis from bacterial infection
  2. perinephric abscess = usually w/acute pyelonephritis
  3. renal scarring
  4. recorrence
  5. stones = esp. w/proteus infection
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12
Q

Characteristics of acute pyelonephritis

A
  1. Patchy, wedge-shaped regions of suppuration with microabscesses.
  2. Tubules filled with aggregates of PMNs
  3. Tubular destruction
  4. Interstitium – edema, PMNs, lymphs and plasma cells (may predominate in areas away from abscesses or during resolution).
  5. Glomeruli preserved until late in course
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13
Q

Major causes of chronic pyelonephritis

A
  • when combined w/chronic or recurrent infections ==> renal scarring + progressive renal impairment
  • urinary tract obstruction
  • vesical-ureteral reflux (VUR)
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14
Q

Pathogenesis of chronic pyelonephritis caused by urinary tract obstruction

A
  • 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
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15
Q

Causes of obstruction ==> chronic pyelonephritis

A
  1. Intrinsic (intraluminal) masses of the urinary tract:
  • exophytic tumors
  • calculi
  • blood clots
  1. Inflammation, stricture of urethra or ureters
  2. Urethral valves
  3. Extrinsic compression:
  • tumors (esp. pelvis, retroperitoneal)
  • retroperitoneal fibrosis
  • hemorrhage (trauma)
  • iatrogenic (surgical ligation, adhesions)
  1. Functional:
  • neurological disease
  • diabetes mellitus
  1. Idiopathic
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16
Q

Consequences of chronic obstructive pyelonephritis

A
  • 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
17
Q

Common causes of VUR

A
  • 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
18
Q

Characteristics of reflux nephropathy

A
  • = 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