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

(38 cards)

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
Acquired intrinsic defects causing bladder outlet obstruction
``` BPH Prostate Ca Bladder Ca Calculi Diabetic neuropathy Spinal cord dz Anticholinergic drugs and alpha adrenergic antagonists ```
26
Acquired intrinsic defects causing urethral obstruction
``` Stricture Tumor Calculi Trauma Phimosis ```
27
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 ```
28
Acquired extrinsic defects causing bladder outlet obstruction
Carcinoma of cervix, colon | Trauma
29
Acquired extrinsic defects causing urethral obstruction
Trauma
30
How might adults develop secondary VU reflux?
Adults with voiding difficulties may develop reflux that predisposes them to complciations like UTI, pyelo, and hydronephrosis
31
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
32
_____ incontinence = neurogenic loss of detrusor function causing emptying phase abnormality; bladder empties when capacity is exceeded
Overflow/bypass
33
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
34
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]
35
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]
36
_____ is the imaging technique preferred for dx of renal lithiasis
CT
37
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
38
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