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12 Renal  Sexually active (friction, high traffic).

Tuesday, July 28, 2009 ○ What orders would you expect to receive for
9:25 PM MaryJane?
 UA (urine analysis).
• Renal Disorders ○ What nursing considerations would you have
○ Julie Mann, NP for MaryJane?
○ N145  Void after sex
• Case #1  Hygiene.
○ Mrs. Jones an 83 y/o female returns to the • Urinary Tract Infections
clinic 3 days after discharge from the ○ Upper and Lower Urinary Tract Infections
hospital s/p (status post, after)  Upper UTI: Pylonephritis
hysterectomy. Her family states she has  Kidney/ureters have an infection.
been increasing confused and complaining  Lower UTI: Cystitis
about generalized abdominal discomfort.  Bladder gets infected
○ What might be the cause of her confusion? ○ distal urethra, vagina, and perianal area
 Infection (symptom for elderly) contains pathogens
 UTI ○ urine in the bladder is sterile
○ What orders would you expect to receive for • Cystitis
Mrs. Jones? ○ Uncomplicated (most common): health
 Sample of urine (WBCs, cultures) adult, normal urinary system, caused by e.
○ What nursing considerations would you have choli
for Mrs. Jones? ○ Complicated: r/t abnormality in urinary tract
 Fall risk. (enlarged prostate, tumor, unable to void)
 Infection. OR other health problem that compromises
 Someone with her to take antibiotics, defenses or responsiveness to treatment.
help.  Caused by Proteus mirabilis, Klebsiella,
• Case #2 and Enterobacter (gram neg.), and
○ Mary Jane is a recently married 25 year old Staph aureus (gram pos)
female who returns from her honeymoon to • Bodies Defenses
Costa Rica with complaints of dysuria, ○ Washout phenomenon (usually void it out)
frequency, and urgency.  Men longer urethra less likely to develop
○ What might be going on with MaryJane? vs women.
 UTI  Wash out pathogen.
○ Why would she be at higher risk for this ○ IgA and Phagocytic blood cells
condition?  Reside in ureters, help protect body.
○protective mucin layer of bladder: protects • Clinical Manifestations
against invasion ○ Frequency/urgency
 May bind to water that is part of urine. ○ lower abd. or back pain
○ local immune response: normal flora in ○ burning and pain on urination
periurethral area: Lactobacillus ○ Urine may be cloudy and foul smelling
 Help curb development of pathogens. ○ Very common for women, particular b/t 18-
• Who’s at risk? 40
○ urinary obstruction and reflux ○ Not common for men
 Women with children, cough/strain, ○ Elderly have different symptoms (might not
urine refluxes back into urethra. have pain, larger infection)
○ neurogenic disorders that interrupt  Will have confusion.
emptying ○ Sometimes blood in the urine.
 Flacid bladder, unable to empty
• Case #3
completely. ○ Mrs. Logan is a 63 y/o multiparous female
○ women who are sexually active (many pregnancies). (g 8, p 8) who presents
○ postmenopausal women with c/o frequency of urination, small weak
 Low levels of estrogen interrupt mucin stream, and states, “I feel like I don’t
lining. completely empty my bladder.”
○ men with diseases of the prostate ○ What might be going on with Mrs. Logan?
○ Elderly  Obstruction, possibly prolapsed uterus --
 Unable to maintain mucin lining. > pressure on urethra, unable to void.
○ diabetes ○ What contributing factors might have led to
○ pregnant women her condition?
 Obstruction/pressure on tissues  Blockage/prolapsed uterus.
○ instrumentation and catheterization (point ○ What are the risks associated with her
towards the navel when harder to find on condition?
women)  Pain, UTI, unable to void (distended
 Infection risk d/t tubes bladder-->backflow into kidneys)
• What mechanism caused Mrs. Jone’s UTI?
○ Likely from Instrumentation, catheter.
Almost 100% of indwelling catheter users
get UTI, antibiotics commonly used.
• What mechanism caused MaryJane’s UTI?
○ Sex & friction
functional (can't squeeze as efficiently --
>can't push out all of urine)
 overflow incontinence (leak urine [ie
when cough])
 Can scan to see how much pt is voiding,
or use catheter to pull off and measure.
 Need to remove obstruction if at all
possible.
• Who’s at risk?
○ Bladder CA
○ Neurogenic bladder
 Flacid/spastic bladder
○ Bladder stones
○ Prostatic hyperplasia or CA
 Either benign or otherwise.
• Urinary Tract Obstruction ○ urethral strictures
○ Any interference in the flow of urine at any  Narrowing of urethra, sometimes by
part of the urinary tract. inflammation.
○ Classified by: ○ congenital urethral defects
 cause (congenital or acquired) • Signs of obstruction
 degree (complete[more dangerous] or ○ bladder distention (feel during palpation,
partial) very uncomfortable)
 duration (acute or chronic [can lead to ○ Hesitancy (difficult to get stream started)
bilateral renal failure d/t backing up of ○ straining when initiating urination
urine])
○ small weak stream (if at all)
 level (upper or lower)
○ Frequency
• Lower Obstruction
○ feeling of incomplete bladder emptying
○ Compensatory Stage
○ overflow incontinence
 hypertrophy of the bladder muscle (push
harder) • Case #4
○ Heathcliff is a 32 y/o male MEPN student
 bladder wall thickens
 bladder muscle fatigue when chronic that is so dedicated to his studies and his
○ Decompensatory Stage patients that he often skips breaks during
 bladder may be overstretched and his 12 hour clinical rotation and long class
fibrotic, high residual volumes, not as days. He copes by drinking 4-5 venti lattes a
day and eating his favorite comfort food, ○ Calcium Stones (oxylate [more common] or
macaroni and cheese. phosphate)
○ He presents to the ED with severe right flank  most stones are this type (80%)
pain that radiates to his groin. He is afebrile, ○ Magnesium ammonium phosphate stones
his vital signs are normal except his HR is  also called struvite stones
115. He states he feels nauseated and might ○ uric acid stones
vomit.  People who have gout
○ What might be going on with Heathcliff? ○ cystine stones
 Kidney Stone  Younger individuals
○ Why would he have tachycardia, & n/v? ○ Determines Treatment
 Severe Pain.
○ What behaviors put him at risk for this
condition?
 Not voiding, not hydrating
 high calcium not a factor (actually
calcium oxylate in body is a risk [ie.
From spinach])

• Renal Calculi (kidney stones)


○ supersaturated urine
 Water absorbed out of it.
○ unilateral formation
 Tend to form in one kidney
○ natural stone inhibitors
 Reason why some people don't develop
but others do.
• Types of Stones  Once occur, more likely to reoccur.
○Stone lodged any where above the ○ ureteral strictures (narrowing)
ureteralvesical junction = kidney stone ○ tumors that compress the ureters
○ Mechanism of kidney damage by: ○ Pregnancy
 hydronephrosis ○ Renal Stones
 Hydroureter • Clinical Manifestations
• Complications ○ Renal colic
○ Hydroureter  acute, intermittent and excruciating
 obstruction blocks the outflow from the pain in the flank and upper outer
ureter and ureter dilates quadrant on affected side.
○ Hydronephrosis ○ Radiating pain to the lower abdomen,
 urine filled dilation of the renal pelvis bladder, perineum, or scrotum
and calices ○ Cool and clammy skin
 assoc. with progressive atrophy ○ n/v (from pain response)
○ Other probs - Electrolytes can't do their job. • Case #5
○ Processes can reverse if stone removed if ○ Mr. Johnson is a 68 y/o male with a pmh
caught before permanent damage. (past medical history) significant for DM
(Diabetes Mellitus). He is recovering at home
s/p prostatectomy. He develops chills and
fever and complains of a constant ache in
his left flank and generally feels sick.
○ What might be going on with Mr. Johnson?
 Inflammation over kidneys.
○ What might have put him at a higher risk of
developing his condition
 Instrumentation to urinary tract (three
way catheter, continuous irrigation of
bladder)
• Acute Pyleonephritis
○ Infection of the kidney parenchyma and
renal pelvis
○ Same agents as for lower UTI’s, ascending
up
○ May be acute or chronic (aren't as
• Who’s at risk for obstruction? symptomatic)
• Who’s at risk? (athersclerotic heart disease). He presents
○ DM (don't heal very well) to his primary care doctor with SOB and
○ urinary tract instrumentation and edema. The physician runs some lab work
catheterization and finds elevated renal function tests (BUN
○ vesicoureteral reflux (occurs at base of up), low hemoglobin, and hyperkalemia.
ureter and top of the bladder, when bladder ○ What might be causing Mr. Peabody’s
becomes overfilled, small amount refluxes symptoms?
into bladder)  Renal Failure (chronic - chronic
○ Pregnancy (blockage/pressure on ureters) predisposition)
 Higher risk for preterm labor (therefore, ○ What contributed to the development of this
follow condition closely) condition?
○ neurogenic bladder (spastic/flaccid bladders,  Diabetes, HTN, ASHD.
not voiding as well, backup of urine) ○ Is this an acute or chronic condition?
• Clinical Features  Chronic
○ Acute: • Renal Failure
 shaking chills and fever ○ Renal Insufficiency: a decline in renal
 constant ache in flank area (usually function down to 25% of normal GFR
unilateral, sometimes bilateral--> super (glomerular filtration rate) --> strain/stress
sick) on kidneys
 lower UTI infection symptoms ○ Renal Failure: significant loss of renal
(frequency, urgency, etc) function <25%. <10% is end stage renal
 malaise failure
 feeling of being ill  fail to regulate fluid, electrolyte and pH
○ Chronic: balance
 may be same as acute or more  occurs as an acute or chronic condition
commonly more insidious. • Acute Renal Failure Causes
 polyuria ○ PreRenal (most common)
 Nocturia (wake up at night to go to • Hypovolemia (ie. large blood loss,
bathroom) anaphylactic shock)
 Proteinuria (protein spills into urine) • decreased vascular filling
 significant cause of renal failure • heart failure and cardiogenic shock
• Case #6 • decreased renal perfusion
○ Mr. Peabody a 72y/o man with a pmh ○ IntraRenal
significant for diabetes, HTN, and ASHD
• Acute tubular necrosis (no more blood ○ Symptoms caused by decline in renal
supply, nephrotoxic drug [diuretics]) function and accumulation of toxins
○ Post-Renal ○ Who’s at risk?
• bilateral ureteral obstruction  DM (long term damage to kidneys)
 One kidney can compensate.  HTN (long term damage to kidneys)
• bladder outlet obstruction (pressure on  Glomerulonephritis
tubules)  other kidney diseases
• Acute renal failure  Polycystic renal disease & more!
○ Abrupt reduction in renal function
○ Elevated BUN (blood urea [urea backs up
first] nitrogen) and Creatinine levels
○ Oliguria: less than 30/ml day (reduction in
renal output)
○ Most types are reversible
○ Recovery in 3 phases
 Oliguria
 Diuresis over several days (once
underlying cause is gone)
 Recovery (several months b4 fully
recovered)
• Chronic renal failure
○ Hard to treat.
○ Progressive and irreversible loss of nephrons
 Electrolyte balance shot. Some
hormones as well.
 Asotemia Urea builds in blood-->
symptoms of urea in blood Uremia (very
itchy, confusion, headaches, see below)
○ Decreases GFR
○ decreased tubular reabsorptive capacity
○ decreased endocrine functions of the
kidneys
○ Erythropoietin hormone released --> Anemia