CLMD - UTI, pyelo, sepsis, changes in outflow/obstruction Flashcards

1
Q

Risk factors for UTIs in women

A

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

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2
Q

Risk factors for UTIs in males

A

Prostatic hypertrophy

Non-circumcised

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3
Q

DDX for dysuria in a female

A
Cystitis
Cervicitis (Chlamydia, Neisseria)
Vaginitis (candida, trichomonas)
Urethritis (herpetic)
Interstitial cystitis
Non-infectious vaginal or vulvar irritation
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4
Q

When is asymptomatic bacteriuria worrisome and needing further workup and potential tx?

A

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

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5
Q

Prostatitis can be chronic in prostatic hypertrophy; prolonged abx course may be necessary x ___ weeks

A

4-6

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6
Q

Pyelonephritis results in bacteremia in 20-30% of cases. Hematogenous spread is rare, but more likely with what 3 organisms?

A

Candida
Salmonella
Staph aureus

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7
Q

3 major complications of pyelonephritis

A

Papillary necrosis
Emphysematous pyelonephritis
Xanthogranulomatous pyelonephritis

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8
Q

Besides pyelonephritis, what other conditions may lead to papillary necrosis?

A

Obstruction
Diabetes
Sickle cell
Analgesic nephropathy

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9
Q

Emphysematous pyelonephritis is production of gas in nephric and perinephric areas. It occurs almost exclusively in pts with _____

A

Diabetes

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10
Q

______ pyelonephritis develops in cases of chronic obstruction or chronic infection and causes suppurative destruction of renal tissue and may lead to abscess formation

A

Xanthogranulomatous

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11
Q

Differentiate sepsis (septicemia) from septic shock

A

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

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12
Q

Important considerations in tx of sepsis/septic shock

A

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

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13
Q

Preventative strategies for recurrent UTI

A

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

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14
Q

3 phases of unilateral ureteral obstruction effects on renal function

A
  1. 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
  2. [6+ hours] Decrease glomerular blood flow d/t afferent arteriole vasoconstriction
  3. Decreased luminal hydrostatic pressure AND renal blood flow baseline

[note that persistent obstruction >24 hours can cause a 50% drop in GFR]

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15
Q

2 phases of bilateral ureteral obstruction in renal injury

A
  1. 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
  2. [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]

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16
Q

Changes in Na+ regulation with unilateral tubular dysfunction

A

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

17
Q

Changes in fluid volume regulation in bilateral tubular dysfunction

A

Presence of volume expansion; ANP blocks effects of renin —> decreased angiotensin II —> net result is diuresis and natriuresis

18
Q

Changes in urine concentrating ability with tubular dysfunction d/t obstruction

A

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

19
Q

What changes in potassium take place in tubular dysfunction d/t obstruction?

A

Low-flow luminal state —> high urinary K+ concentrations in CD —> loss of gradient between cell and lumen —> HYPERKALEMIA

20
Q

In terms of the “big picture”, a patient presenting with what 3 things should cause you to think about urinary tract obstruction?

A

Azotemia
Hyperkalemia
Metabolic acidosis

21
Q

Congenital causes of ureteral obstructtion

A

Ureteropelvic junction narrowing or obstruction

Ureterovesical junction narrowing or obstruction and reflux

Ureterocele

Retrocaval ureter

22
Q

Congenital causes of bladder outlet obstruction

A

Bladder neck obstruction

Ureterocele

23
Q

Congenital causes of urethral obstruction

A
Posterior urethral valves
Anterior urethral valves
Stricture
Meatal stenosis
Phimosis
24
Q

Acquired intrinsic defects causing ureteral obstruction

A
Calculi
Inflammation
Infection
Trauma
Sloughed papillae
Tumor
Blood clots
25
Q

Acquired intrinsic defects causing bladder outlet obstruction

A
BPH
Prostate Ca
Bladder Ca
Calculi
Diabetic neuropathy
Spinal cord dz
Anticholinergic drugs and alpha adrenergic antagonists
26
Q

Acquired intrinsic defects causing urethral obstruction

A
Stricture
Tumor
Calculi
Trauma
Phimosis
27
Q

Acquired extrinsic defects causing ureteral obstruction

A
Pregnant uterus
Retroperitoneal fibrosis
Aortic aneurysm
Uterine leiomyomata
Ca of uterus, prostate, bladder, colon, rectum
Lymphoma
PID, endometriosis
Accidental surgical ligation
28
Q

Acquired extrinsic defects causing bladder outlet obstruction

A

Carcinoma of cervix, colon

Trauma

29
Q

Acquired extrinsic defects causing urethral obstruction

A

Trauma

30
Q

How might adults develop secondary VU reflux?

A

Adults with voiding difficulties may develop reflux that predisposes them to complciations like UTI, pyelo, and hydronephrosis

31
Q

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

A

Hydronephrosis

32
Q

_____ incontinence = neurogenic loss of detrusor function causing emptying phase abnormality; bladder empties when capacity is exceeded

A

Overflow/bypass

33
Q

Overflow incontinence is often diagnosed based on what test?

A

Post-void residual — US eval to see how much is left in bladder after voiding

> 100 ml indicates incomplete emptying

34
Q

Cause of stress incontinence

A

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]

35
Q

Causes and description of neurogenic bladder

A

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]

36
Q

_____ is the imaging technique preferred for dx of renal lithiasis

A

CT

37
Q

Patients with outlet obstruction d/t malignancy often present with constitutional symptoms. What types of cancer might be implicated?

A

Transitional cell CA obstructing ureter at UPJ or UVJ

Can also be GI or urogenital — colon cancer, ovarian cancer, lymphoma

38
Q

Postobstructive diuresis is a normal physiologic event after bilateral ureteral obstruction — what does this process consist of?

A

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