CLMD - UTI, pyelo, sepsis, changes in outflow/obstruction Flashcards
Risk factors for UTIs in women
Use of spermicide with diaphragm for contraception
Frequent sexual intercourse
Anatomic factors affecting bladder emptying: cystoceles, urinary incontinence, residual urine
Tissue effect of post-menopausal estrogen depletion
Diabetes
Risk factors for UTIs in males
Prostatic hypertrophy
Non-circumcised
DDX for dysuria in a female
Cystitis Cervicitis (Chlamydia, Neisseria) Vaginitis (candida, trichomonas) Urethritis (herpetic) Interstitial cystitis Non-infectious vaginal or vulvar irritation
When is asymptomatic bacteriuria worrisome and needing further workup and potential tx?
In a pregnant pt — untreated asymptomatic bacteriuria in pregnant pts more likely to result in symptomatic pyelonephritis which is also more likely to develop sepsis
Prostatitis can be chronic in prostatic hypertrophy; prolonged abx course may be necessary x ___ weeks
4-6
Pyelonephritis results in bacteremia in 20-30% of cases. Hematogenous spread is rare, but more likely with what 3 organisms?
Candida
Salmonella
Staph aureus
3 major complications of pyelonephritis
Papillary necrosis
Emphysematous pyelonephritis
Xanthogranulomatous pyelonephritis
Besides pyelonephritis, what other conditions may lead to papillary necrosis?
Obstruction
Diabetes
Sickle cell
Analgesic nephropathy
Emphysematous pyelonephritis is production of gas in nephric and perinephric areas. It occurs almost exclusively in pts with _____
Diabetes
______ pyelonephritis develops in cases of chronic obstruction or chronic infection and causes suppurative destruction of renal tissue and may lead to abscess formation
Xanthogranulomatous
Differentiate sepsis (septicemia) from septic shock
Sepsis = suspected or documented infection and acute increase in organ failure; dysregulated host response to infection leading to hypofunction of uninfected organs
Septic shock — progressive organ dysfunction leading to marked increase in mortality (subset of sepsis); vasopressor therapy needed to maintain MAP at 65+ mmHg, serum lactate greater than 2 mmol/L (18mg/dL) = AKA hypotension that cannot be reversed with infusion of fluids
Important considerations in tx of sepsis/septic shock
Volume resuscitation with IV fluids
Cultures — blood, urine, CSF, etc
Initiate abx for most likely cause (generally broad spectrum)
Pressor agents: NE, vasopressin, etc. for severe cases
Correct acid/base imbalance — fluids, oxygenation, monitor electrolytes
Preventative strategies for recurrent UTI
Consider PRN antibiotic therapeutic regimens — continuous, post-coital, or patient-initiated
Empty bladder as soon as reasonable after intercourse
Wipe front to back after toileting
Showers instead of tub baths
Lactobacillus probiotics
Cranberry products
Vitamin C
Increased fluid intake
3 phases of unilateral ureteral obstruction effects on renal function
- Urine backflow — increases intraluminal hydrostatic pressure; a simultaneous increase in glomerular capillary pressure induced by afferent arteriolar vasodilation which maintains GFR. Activation of RAAS leads to second phase
- [6+ hours] Decrease glomerular blood flow d/t afferent arteriole vasoconstriction
- Decreased luminal hydrostatic pressure AND renal blood flow baseline
[note that persistent obstruction >24 hours can cause a 50% drop in GFR]
2 phases of bilateral ureteral obstruction in renal injury
- Urine backflow — increases intraluminal hydrostatic pressure. Simultaneous increase in glomerular capillary pressure induced by afferent arteriolar vasodilation which maintains GFR. RAAS is activated which leads to second phase
- [6+ hours] Decrease glomerular blood flow due to afferent arteriole vasoconstriction; this persistent efferent and (partial) afferent arteriole vasoconstriction maintains GFR
[note that ANP may play a role in maintaining GFR/arteriole function]
Changes in Na+ regulation with unilateral tubular dysfunction
Inability to reabsorb Na+ throughout the nephron —> salt wasting
Downregulation of receptor and enzyme activity poorly understood — may be related to ischemia, decreased ATP or changes in PGE2 levels
Changes in fluid volume regulation in bilateral tubular dysfunction
Presence of volume expansion; ANP blocks effects of renin —> decreased angiotensin II —> net result is diuresis and natriuresis
Changes in urine concentrating ability with tubular dysfunction d/t obstruction
Inability to absorb Na+ in the TAL and dilute the filtrate in the DCT —> excretion of solutes
Defective urea recycling: transporter defect reduces concentrating effect and allows urea to be excreted
What changes in potassium take place in tubular dysfunction d/t obstruction?
Low-flow luminal state —> high urinary K+ concentrations in CD —> loss of gradient between cell and lumen —> HYPERKALEMIA
In terms of the “big picture”, a patient presenting with what 3 things should cause you to think about urinary tract obstruction?
Azotemia
Hyperkalemia
Metabolic acidosis
Congenital causes of ureteral obstructtion
Ureteropelvic junction narrowing or obstruction
Ureterovesical junction narrowing or obstruction and reflux
Ureterocele
Retrocaval ureter
Congenital causes of bladder outlet obstruction
Bladder neck obstruction
Ureterocele
Congenital causes of urethral obstruction
Posterior urethral valves Anterior urethral valves Stricture Meatal stenosis Phimosis
Acquired intrinsic defects causing ureteral obstruction
Calculi Inflammation Infection Trauma Sloughed papillae Tumor Blood clots
Acquired intrinsic defects causing bladder outlet obstruction
BPH Prostate Ca Bladder Ca Calculi Diabetic neuropathy Spinal cord dz Anticholinergic drugs and alpha adrenergic antagonists
Acquired intrinsic defects causing urethral obstruction
Stricture Tumor Calculi Trauma Phimosis
Acquired extrinsic defects causing ureteral obstruction
Pregnant uterus Retroperitoneal fibrosis Aortic aneurysm Uterine leiomyomata Ca of uterus, prostate, bladder, colon, rectum Lymphoma PID, endometriosis Accidental surgical ligation
Acquired extrinsic defects causing bladder outlet obstruction
Carcinoma of cervix, colon
Trauma
Acquired extrinsic defects causing urethral obstruction
Trauma
How might adults develop secondary VU reflux?
Adults with voiding difficulties may develop reflux that predisposes them to complciations like UTI, pyelo, and hydronephrosis
Although BPH is a benign process, eventually the pressure in the bladder will increase such that urine is forced into the ureters causing ______; it has a vague pain pattern that may include the low back, perineum, or suprapubic area
Hydronephrosis
_____ incontinence = neurogenic loss of detrusor function causing emptying phase abnormality; bladder empties when capacity is exceeded
Overflow/bypass
Overflow incontinence is often diagnosed based on what test?
Post-void residual — US eval to see how much is left in bladder after voiding
> 100 ml indicates incomplete emptying
Cause of stress incontinence
Increased intraabdominal pressure in those with defective fascial support of UV junction [may see bulging of anterior vaginal wall on straining, indicative of posterior rotation d/t defective support]
[note increased risk in women who have given birth]
Causes and description of neurogenic bladder
Spinal cord trauma
Spinal myelomeningocele
Less common: spinal stenosis, herniated discs
Disruption of coordination of relaxation of sphincter during bladder contraction — as volume increases, resting pressure rises [>40 cm H2O increases risk for hydronephrosis and subsequent decrease in GFR — so requires regular monitoring to avoid irreversible injury]
_____ is the imaging technique preferred for dx of renal lithiasis
CT
Patients with outlet obstruction d/t malignancy often present with constitutional symptoms. What types of cancer might be implicated?
Transitional cell CA obstructing ureter at UPJ or UVJ
Can also be GI or urogenital — colon cancer, ovarian cancer, lymphoma
Postobstructive diuresis is a normal physiologic event after bilateral ureteral obstruction — what does this process consist of?
Combination of fluid overload, urea accumulation, and electrolyte imbalance
Rate 250 mL/h but can be as high as 750 ml/h
Results from downregulation of Na transporters during obstruction; ANP released in response to cardiac preload during obstruction
Tx is fluid replacement in response to diuresis (75% of urine volume) and careful monitoring of urine and serum osmolality as well as serum electrolytes
