Welcome to the bed. We'll go ahead and give you
the story. This is all going to happen super
fast. Welcome to the emergency room. Welcome
back to the Deep Dive. Our mission today is really
laser focused and I think vital for a lot of
you. We know you're gearing up for one of the
toughest sections of the MedSurg exam. renal
and urologic disorders. So instead of trying
to boil the ocean and cover everything, we're
going with the Pareto principle. We're going
to dive deep into that critical 20 % of information,
the high yield stuff. That's going to give you
80 % of the understanding you need. That's exactly
right. And this isn't about just memorizing a
bunch of random facts. It's about really understanding
the why behind the disease, and more importantly,
what your nursing response has to be. Our sources
today really give us an intensive breakdown of
the big issues. We're talking infections that
can go septic, like UTIs and pyelonephritis.
Then there are the immunologic problems that
mess with fluid balance, like glomerulonephritis
and nephrotic syndrome. And then you've got the...
Well, the mechanical nightmares like kidney stones
and the functional issues like incontinence.
And to really guide this deep dive, we're setting
up three, let's call them non -negotiable overarching
nursing priorities. These apply to almost everything
we're gonna talk about today. So as you study,
for every single condition, you should be asking
yourself, one, does this cause a massive fluid
balance shift? Two, does it require urgent pain
control? And three, is there an immediate life
-threatening sepsis risk? Exactly. If you can
answer those three questions for each of these
diseases, you're already building that foundational
knowledge you need, not just for the exam, but
for the bedside. So let's unpack this. Let's
do it. All right, we have to start with the most
common urologic infection, the urinary tract
infection. I think it's one of those things that
can seem almost mundane, but the potential for
it to become a systemic illness is huge, right?
It is, especially in certain populations. So
to kick things off, let's talk about the basic
defenses that have to fail for a UTI to even
begin. So let's break down the pathophysiology.
The system above your urethra, so the bladder,
the ureters, the kidneys, that whole area is
inherently sterile. And nature has given us two
main defenses to keep it that way. First, you've
got the acidic pH of the urine. It's usually
somewhere between 4 and 7 .5, and most bacteria
just can't grow in that environment. OK, so it's
hostile territory for germs. Exactly. And the
second defense is purely mechanical. It's the
flushing action of urination. Every time you
void, you're physically washing out any bacteria
that might be trying to creep up the urethra.
So a UTI happens when a pathogen gets past those
defenses. Precisely. And overwhelmingly, in like
75 % of cases that don't involve some kind of
structural defect, that pathogen is E. coli.
It ascends from the perineal area, gets into
the bladder, and it overcomes those defenses,
usually because the bladder isn't emptying completely.
And that failure, that's what leads to cystitis,
the bladder infection. But I think the key here
for testing is identifying the risk factors that
set the stage for that to happen. Yeah, and they
fall into three really critical categories. First
is anything that compromises the immune response.
So think about aging patients, people with poorly
controlled diabetes. Because the sugar in the
urine feeds the bacteria. Right, it's fuel for
them, exactly. Or anyone on immunosuppressive
drugs. That's bucket number one. OK, and the
second? The second is anything that causes urinary
stasis. I mean, if the bladder doesn't empty
all the way, those bacteria just sit there and
multiply. They're not getting flushed out. So
that would be things like BPH in men. BPH is
a classic example. Or urethral strictures, a
neurogenic bladder from a spinal cord injury,
anything that obstructs the outflow. And then
there's the third category. And this is the one
where, I mean, nursing intervention is just absolutely
paramount. It is. We're talking about foreign
bodies. Indwelling catheters. Indwelling catheters.
CIUT's catheter -associated urinary tract infections
are the single biggest source of health care
-associated UTIs. Full stop. The sources are
so clear on this. The catheter itself, even with
perfect sterile technique, bypasses all the natural
defenses. And gives the bacteria a highway right
into the bladder. A highway and a... place to
live. It provides a surface for biofilm to develop.
So preventing CI -UTI isn't just a good idea.
It's a core daily nursing responsibility and,
you know, a massive exam topic. OK, so let's
shift to manifestations. For a younger, healthy
adult, the symptoms are pretty classic, right?
The lower urinary tract symptoms, or LUTs. Correct.
You're looking for dysuria, that burning, painful
feeling during urination. Then you have urinary
frequency, which is often defined as needing
to go more than every two hours. Urgency too.
Urgency, and sometimes a little suprapubic discomfort
or pressure. These are really the classic signs
of cystitis. But, and this is the big but, the
clinical priority cue, the thing that I think
really throws people off is the presentation
in the elderly. This is 100 % high -yield information
right here. In an older adult, their whole inflammatory
response can be blunted. They might not mount
a fever. They might not even complain about pain
when they urinate. So what do you see instead?
Instead, the absolute critical finding is often
a sudden, totally unexplained change in cognitive
function. New onset confusion, delirium, or even
just generalized malaise and fatigue. Sometimes
those are the only signs of a severe UTI, or
even the beginning of urosepsis. So take home
is, if you have an older patient with new confusion,
UTI has to be at the top of your differential.
Immediately, you have to rule it out. Let's talk
about meds for these uncomplicated UTIs. It's
usually a short course of antibiotics. What are
the common ones and what are the critical teaching
points for us? Okay, so the standard short course
is often trimethoprims sulfamethoxazole, which
is TMP SMX, nitroferantoin, or phosphomycin.
But let's really focus on the two big drug alerts
that the sources highlight. Give us the first
one, the absolute must -know detail for nitroferantoin.
Nitroferantoin is a fantastic drug for lower
UTIs, but its use completely hinders on the patient's
renal function. The key nursing consideration
is you must check the patient's creatinine clearance,
the CRCL. And what's the cutoff? If the CRCL
is less than 30 milliliters per minute, the drug
is contraindicated. And why is that? It's twofold.
When renal function is that poor, the drug doesn't
concentrate in the urine enough to actually kill
the bacteria, so it's ineffective. But worse,
it accumulates in the rest of the body systemically,
and that increases the risk of some really serious
side effects, like peripheral neuropathy. So
that lab value is a hard stop. It's an absolute
clinical barrier. You have to check it. OK, that's
the definite need to know. Now, for symptom relief,
because these patients are miserable. Phenazapyridine
or pyridium is often used. What's the mandatory
patient education for that one? The teaching
for phenazoperidine is so critical for, you know,
just preventing patient panic. It's a topical
analgesic. It basically coats the inside of the
urinary tract to reduce that burning and urgency.
And you have to warn them. You must warn them
that it causes a really dramatic but totally
harmless change in their urine color. We're talking
bright orange, sometimes a reddish brown. And
it will stain everything. Clothing, contact lenses,
the toilet bowl. If you forget to tell them that,
they're going to think they're bleeding to death
and they'll be right back in the ER. Excellent
point. OK, now let's get to the core nursing
implications. Beyond giving meds, how do we intervene
to manage this and prevent it from coming back?
Our management really comes down to three things,
hydration, hygiene, and adherence. OK, break
that down. So for a SES monitor, we're getting
a baseline mental status, especially in our older
adults, checking their pain level and monitoring
their hydration status with I's and O's. And
for intervene? We push fluids. aggressively.
The goal is at least eight large glasses of water
a day, or about two and a half liters. You want
to keep that system constantly flushing. We also
stress meticulous hygiene wiping front to back,
voiding after intercourse, and just teaching
them to empty their bladder completely every
single time. And then educate is the adherence
piece. Yes. We have to emphasize completing the
entire course of antibiotics, even if they feel
better in a day or two. If they stop early, it
can lead to resistance and relapse. We also advise
them to avoid bladder irritants, caffeine, alcohol,
carbonated drinks during that acute phase. Perfect.
So let's wrap this section with the highest yield
points for the exam. Okay. Quick review summary
for UTI. Priority assessment in the elderly.
New onset confusion or delirium. That mental
status change is key. Fluid intake goal. Minimum
eight glasses or 2 .5 liters a day. Flush the
system. Nitrofurenzoid alert. Contra indicated
if CRCL is less than 30, you have to check that
lab. And Fidesoperidine? Harmless but very intense
red or orange urine. Don't forget to teach that.
And finally, CIUTI prevention. Strict aseptic
technique on insertion, but more importantly,
as the nurse, you have to advocate for prompt
catheter removal. Get it out as soon as it's
no longer medically necessary. Now let's make
the jump from that lower tract infection, cystitis,
to an upper tract infection. Right. Acute pylonephritis.
And this is a total game changer, right? This
takes the infection from being a localized annoyance
to a systemic life -threatening crisis. It's
a huge leap. With pylonephritis, those ascending
bacteria, again, often E. coli, Proteus, or Klebsiella,
they've made it all the way up to the renal parenchyma
and the pelvis. They're inside the kidney itself.
And that causes widespread inflammation, edema,
even micro abscesses to form within the kidney
tissue. So unlike a bladder infection that's
kind of contained, this is a deep organ infection
and it triggers a much, much stronger systemic
inflammatory response. And if it's recurrent,
it can cause long -term damage. Absolutely. That
inflammation leads to scarring and over time
that scarring can lead to chronic kidney disease.
So because this is now a systemic disease, the
manifestations are radically different from a
simple UTI. What's the cardinal sign that tells
you, this is pilonephritis, not cystitis? It's
the combination of systemic symptoms and flank
pain. These patients present with a really rapid
onset of high fever. We're talking 103 degrees
or higher shaking chills, severe malaise, and
often pretty significant nausea and vomiting.
And the flank pain is key? It is the key local
sign. It's pain in the costovertable angle or
CVA tenderness. That flank pain means the infection
is literally stretching the capsule of the kidney.
Can you just briefly describe that CVA assessment?
I feel like that's a key physical finding we
have to know. For sure. CVA tenderness is assessed
by either palpation or light percussion. Sometimes
it's called a renal punch or a thumb break at
that angle formed by the 12th rib and the spine.
And if it's positive? If that light tap elicits
sharp, intense pain, it's a very strong indicator
of kidney involvement, either from infection
or an obstruction. That pain, plus the high fever
and chills, That paints a really critical picture.
And this level of infection immediately brings
up our third major priority. Sepsis risk. How
fast can this progress to UroSepsis and what
are the signs of impending septic shock? UroSepsis
is a massive, massive threat. The kidneys are
incredibly vascular organs, so it's very easy
for those bacteria to get into the bloodstream.
That's Bactremia. OK. The signs of septic shock
would be a rapid onset of hemodynamic instability,
so persistent low blood pressure or hypotension,
even after you give them IV fluids, an increased
heart rate, tachycardia, rapid breathing, and
critical labs like an elevated lactate level.
Recognizing the initial high fever and chills
as the first warning sign of sepsis is just paramount.
It requires immediate escalation. So given that
sepsis risk, the interprofessional management
has to be aggressive and usually hospital -based.
What does that initial antibiotic and fluid strategy
look like? Yeah, for severe cases, hospitalization
is definitely necessary. You're starting with
IV fluid replacement immediately. They're often
dehydrated from the vomiting and the fever. And
then you start empirical broad spectrum. IV antibiotics
before the cultures come back. Absolutely. You
can't wait. You're typically using a fluoroquinolone
like Cipro or maybe an extended spectrum cephalosporin.
You have to start targeting the most likely culprits,
those gram negative bacteria right away. And
once the patient starts to stabilize, I assume
the antibiotic course changes. It does. Once
they're a febrile and clinically improving, you
can transition them from IV to oral antibiotics.
But and this is a huge point, this is not a short
course like for a UTI. Pyelonephritis requires
a minimum of 14 days and often up to 21 days
of oral therapy. And that's to make sure you've
completely cleared the infection from the kidney
tissue itself. Exactly, to prevent abscesses
or a chronic recurrence. Okay, so for the nurse
managing this patient, monitoring for septic
shock is obviously number one. What else is essential
on, say, a four -hour assessment schedule? Okay,
so for a SES monitor, we're doing frequent temperature
and vital signs, always looking for that drop
in BP or spike in heart rate or respiratory rate.
We're monitoring their pain, specifically that
CVA tenderness. Strict I and O is crucial both
to track urine output for perfusion and to track
their fluid status with all the IV fluids we're
given. And interventions. Intervene is all about
prompt administration of those IV fluids and
antibiotics. That's a time -sensitive, life -saving
intervention. We're also giving aggressive pain
control with analgesics and using antipyretics
to bring that fever down and reduce the metabolic
demand. And what about patient education? Education
focuses on the risk of relapse. They have to
understand why they need to complete that long
course of antibiotics. And they also need to
know they'll need a follow -up urine culture
after treatment to make sure the urine is sterile.
Let's do a quick review summary for acute pilonephritis.
Okay. Defining sign. CVA tenderness or flank
pain combined with a high systemic fever, chills,
and usually nausea and vomiting. management priority.
Immediate fall dehydration and prompt empirical
broad -spectrum antibiotics to prevent uricepsis.
And the long -term risk. Recurrent infections
can lead to chronic scarring and eventually potential
end -stage renal disease. Okay, we are shifting
gears completely now. We're moving away from
bacterial invasion and into conditions where
the body is basically attacking itself. We're
looking at diseases where the glomerulus, the
kidney's tiny delicate filtration unit, is damaged
by an immune response. And this leads us directly
to our first major priority, massive fluid balance
shifts. Let's start with acute post -striptococcal
glomerulonephritis, or APSGN. The pathophysiology
of APSGN is really a classic example of what's
called a type 3 hypersensitivity. It's caused
by circulating antigen antibody complexes. Okay,
what does that mean in simple terms? It means
that after an infection, usually a group A beta
hemolytic strep infection like strep throat or
even a skin infection like impetigo, the body
creates these little immune complexes. And the
critical point is the timing. The kidney damage
happens five to 21 days after the initial infection
is already gone. So the body's own defense system
is causing the problem. Exactly. These complexes
get lodged in the glomerular basement membrane.
They trigger this big inflammatory reaction and
that severely reduces the glomerular filtration
rate or GFR. And when that filtration rate drops,
the kidney can't clear waste and more importantly,
it can't manage fluid. So what does that reduced
GFR look like clinically? It creates the classic
APSGN triad. fluid overload, hypertension, and
visible changes in the urine. The fluid overload
usually appears first as generalized edema. It
often starts with this really striking periorbital
edema, especially when they wake up in the morning.
Puffy eyes. Very puffy eyes. And then that progresses
to peripheral edema. Because the GFR is so low,
the body holds onto sodium and water, which leads
to a big rise in plasma volume and, as a result,
pretty severe hypertension. And the urine changes.
They must tell a clear story about the filter
being damaged. They do. First you see oliguria,
which is just reduced urine output. But the characteristic
sign is hematuria, where red blood cells are
leaking through those damaged glomeruli. The
urine is often described as looking smoky. T
-colored or rusty. And you see protein, too.
Yes, moderate proteinuria as well. And diagnostics,
particularly an ASO titer, can help confirm that
preceding strep infection. So the goals for interprofessional
management are really just supportive, right?
You're focused on controlling those two big complications,
the hypertension and the volume overload. That's
100 % correct. We're treating the symptoms while
the immune system recovers. Rest is actually
essential until the hypertension and hematuria
start to subside. And pharmacologically, we use
aggressive antihypertensives and, critically,
diuretics to pull off all that excess fluid.
Antibiotics are only used if, for some reason,
the original strep infection is still active,
which is pretty rare. So given the danger of
that uncontrolled hypertension, The nursing role
in monitoring fluid and pressure has to be meticulous.
What are the key measurements? OK, so for a SES
monitor, blood pressure has to be checked frequently,
often every two to four hours. Any significant
elevation needs to be reported immediately. But
the gold standard for tracking fluid status is
daily weights. Same time, same scale. Same time
every morning, same scale before they eat. It's
the most accurate indicator. And of course, strict
INO is mandatory. We also watch their BUN and
creatinine to track how well the filtration is
recovering. And intervention. For intervene,
strict adherence to sodium and fluid restrictions
is critical if they have that hypertension and
edema. The fluid restriction is often calculated
based on the previous day's urine output, plus
a little extra for insensible losses. What about
protein? Protein restriction is reserved only
for patients who are showing signs of severe
uremia, like a really high BUN. Otherwise it's
not restricted. And for education. is all about
adherence to that diet and fluid restriction
and really the importance of preventing future
strep infections by seeking prompt treatment
for sore throats or skin infections. Let's do
the quick review for APSGM. The classic triad,
edema, which is initially periobital, hypertension,
and hematuria, that smoky, tea -colored urine.
And the timing. It occurs one to three weeks
after a group A strep infection. And the number
one nursing priority. Aggressive monitoring and
control of blood pressure and fluid status. So
that means strict daily weights in I's and O's.
OK, now let's look into Frodeck syndrome. If
APSGN is about the filter getting clogged and
reducing GFR, Frodeck syndrome sounds like the
filter just becomes Leaky. That's a perfect way
to put it. The core pathophysiology here is a
massive increase in glomerular permeability.
It allows large molecules, specifically plasma
proteins, to just pour out into the urine. And
that's the definition of it, right? Massive proteinuria.
Exactly. Typically greater than three and a half
grams of protein loss per day. And this leads
to severe hypoalbuminemia, very low levels of
albumin circulating in the blood. And that profound
drop in albumin is what triggers the life changing
manifestation of this disease. It is. Albumin
is what's responsible for maintaining oncotic
pressure, which is what keeps fluid inside your
blood vessels. When all that albumin leaks out,
the oncotic pressure just plummets. And fluid
shifts out. aggressively. It shifts out of the
vascular space and into the interstitial space.
And the result is the hallmark sign of nephotic
syndrome. Severe generalized pitting edema. We
call it anisarca. It can be so severe, it actually
impairs mobility and breathing. And beyond the
edema, the body tries to compensate for this
protein loss, which leads to a secondary problem
we have to watch for. Yes, hyperlipidemia. The
liver senses this massive protein loss and it
tries to compensate by ramping up protein synthesis.
But unfortunately, it also ramps up the production
of lipoproteins, and that results in severe hyperlipidemia
and high cholesterol, which puts them at long
-term cardiovascular risk. critical associated
risks. One is susceptibility to infection. What's
the other less obvious, but really dangerous
one? The hidden danger, and this is a major testable
concept, is hypercoagulability. The blood clotting?
Yes. The massive protein loss doesn't just include
albumin. The patient is also losing their natural
anticoagulant proteins, specifically antithrombin
3, into the urine. This creates a severe prothrombotic
state. It puts them at a very high risk for DVTs,
pulmonary embol - and even renal vein thrombosis.
Wow. So given all that complexity, the management
involves a few different medication classes.
What are the main ones? The primary treatment
is to address the underlying inflammation, often
with corticosteroids like high -dose pritansone.
To manage the protein loss itself, we often use
ACE inhibitors or ARBs. How do those help with
protein loss? They actually reduce the filtration
pressure inside the glomerulus, which physically
reduces the amount of protein that can leak out.
And of course, we use diuretics to manage the
extr... and anti -hyperlipidemics for the high
cholesterol. And interprofessional management
has to include a dietitian here. What are the
nutritional considerations? A dietitian consult
is absolutely essential. The patient might need
a moderate protein intake to try and balance
a loss without overburdening the kidneys, but
the primary dietary focus is a strict low -sodium
diet to help manage all that edema and fluid
retention. So shifting to nursing management,
if a patient has Anisarca, their skin must be
incredibly vulnerable. What's our priority? Meticulous
skincare and integrity is paramount. The skin
over those edematous areas is stretched, it's
fragile, and it's so prone to breakdown and then
subsequent infection. So what does that look
like in practice? OK, so for a SES monitor, we
are checking their edema, looking for pitting,
measuring abdominal girth. We're constantly monitoring
their skin integrity. And we're always watching
for signs of infection or thrombosis. And interventions.
For intervene, it's frequent repositioning, gentle
handling. using pressure redistribution surfaces,
elevating edematous limbs. And because they often
have a poor appetite from all these sites, we
offer small, frequent, appealing meals to get
their calories in. And, you know, just providing
emotional support for the massive changes in
their body image. And education. We teach them
to monitor their weight daily and report any
signs of infection or swelling immediately. And
we really have to emphasize the importance of
that low sodium diet and sticking to their steroid
regimen. Let's do a quick review summary for
nephrotic syndrome. Okay. Defining feature. Massive
proteinuria, more than three and a half grams
a day leading to severe generalized edema or
anisarca and hypoalbuminemia. The hidden danger.
High risk of hypercoagulability because they're
losing anti -chrompin 3. And the nursing priority.
Meticulous skin care and vigilant infection prevention.
And the management is corticosteroids and ACE
inhibitors with a low sodium, moderate protein
diet. We have now reached our second major priority.
Acute, severe pain. And I don't think you can
talk about that without talking about kidney
stones. I mean, it's one of the most painful
conditions a person can experience. It really
is. So let's talk about the pathophysiology.
Why do these crystals even form in the first
place? It all revolves around something called
supersaturation. It's when the concentration
of certain salts in the urine gets so high that
they can't stay dissolved anymore. So they start
to precipitate out and form crystals that clump
together. And what causes that supersaturation?
It's complex. It can be low urine volume from
dehydration, genetics, diet, metabolic diseases.
It's really multifactorial. The source outlined
four major types of stones. And knowing the type
is key for prevention. It's everything for prevention.
So number one is calcium oxalate. That's the
most common. About 70 % to 80 % of stones. Number
two is uric acid. About 5 % to 10%. These are
associated with gout and high purine diets. Things
like red meat and alcohol. Exactly. Number three
is streuvite. About 10 % to 15%. And this is
the infection stone. Why is it called that? because
these are almost always caused by UTIs with certain
kinds of bacteria, mainly proteus. The bacteria
raise the UNPH, which allows these big, complex
staghorn stones to form that can fill the entire
renal pelvis. And the last one is rare. Yeah,
cysteine stones are rare. They are from a genetic
defect in amino acid metabolism. So let's talk
about the pain itself, renal colic. What causes
that sheer intensity? Well, the pain isn't actually
caused by the stone just sitting there. It's
caused by the obstruction when the stone tries
to pass. As the stone moves, it blocks the ureter
and urine backs up behind it. That's called hydronephrosis.
And that fluid retention stretches the sensitive
walls of the ureter and the kibbe capsule, causing
these intense agonizing spasms. That's why the
pain is so sudden and excruciating. And the location
of the pain can actually help you track where
the stone is. It can. Pain that's high up in
the flank suggests the stone is still in the
kidney or the upper part of the ureter. As the
stone moves down, the pain typically radiates
sharply down to the groin, the inner thigh, the
labia, or the testes. And nausea and vomiting
are super common because of the severity of that
pain reflex. We mentioned our third priority,
sepsis. What's the urologic emergency linked
to kidney stones? The life -threatening emergency
is an obstructed infected kidney. If a patient
comes with renal colic and a fever and chills,
that is a huge red flag. It means bacteria are
trapped behind that stone. A closed system infection.
Exactly. And that can escalate to Eurocepsis
incredibly fast. It requires immediate urgent
drainage with a stent or a nephrostomy tube before
you even think about treating the stone. For
acute management, our immediate priority is pain
control. You mentioned earlier that NSAIDs are
often preferred over opioids, which sounds counterintuitive
for such intense pain. Why is that? It's a great
question. And you often do need opioids for breakthrough
pain. But NSAIDs, like Toradol, are often preferred
because they treat two problems at once. They
manage the pain, but they also reduce the inflammation
and the swelling in the wall of the ureter. Which
might help it pass. By reducing that swelling,
they can potentially open up the ureter just
enough to help facilitate spontaneous stone passage.
And for bigger stones that won't pass? What are
the common procedures? For stones bigger than
about five millimeters, you'll need a procedure.
Lithotripsy, or ESWL, uses non -invasive shock
waves to break the stone up into smaller fragments
that can be passed. For larger impacted stones,
you might need a ureteroscopy to go up and grab
it, or a percutaneous nephrolithotomy, which
is a small surgical incision into the kidney
to remove it directly. Okay, now to the critical
nursing interventions. What is the single most
important action a nurse must take for a patient
with a suspected kidney stone? Strain all urine,
every single drop. This is completely non -negotiable.
And why is that so important? Because you have
to capture that stone or its fragments and send
it to the lab for analysis. Without knowing what
the stone is made of, you can't create an effective
long -term prevention plan, especially with diet.
And beyond straining. What are our fluid goals
once the acute crisis is over? Aggressive hydration.
We're encouraging a really high fluid intake,
often two to four liters a day, to get their
urine output way up. This volume helps flush
out any small fragments. Is there ever a time
you wouldn't push fluids? Yes. If the patient
has a complete... total obstruction and the kidney
is backing up with hydronephrosis, you have to
limit fluids until that obstruction is relieved
to prevent further kidney damage. Let's talk
about education, specifically after a procedure
like lithotripsy. What should the patient expect?
After lithotripsy, they need to be prepared.
Hematuria is expected. It's common for a few
days as the fragments pass. They might also have
some minor bruising on their back or flank where
the shock waves went in. We teach them to keep
forcing fluids, manage their pain, and to report
any signs of infection, like a fever or chills,
immediately. Or if the pain gets suddenly worse.
Right, because that could mean a fragment has
caused a new, complete obstruction. And finally,
let's revisit diet, tailored by that stone analysis.
What are the key restrictions? This is such a
high yield detail. The diet has to match the
stone. For calcium oxalate, you reduce foods
high in oxalate. Spinach, rhubarb, chocolate,
nuts, tea. For uric acid. You reduce purines.
So that's organ meats, shellfish, beer, and red
meat. They might also need allopurinol. And for
the streuvite infection stones. Prevention is
all about preventing and aggressively treating
UTIs. OK, let's do a quick review summary for
Calculi. Immediate nursing priority, pain management.
essential intervention, strain all urine for
analysis, fluid goal, high intake of two to four
liters a day unless there's an acute obstruction,
and the acute danger is an obstruction plus a
fever that equals urocepsis, which is a surgical
emergency. Our final section now moves away from
acute illness and into these chronic functional
issues, urinary incontinence and retention. And
while they aren't typically life -threatening,
they have a profound impact on a patient's quality
of life and dignity. They absolutely do. And
they increase the risk for things like skin breakdown
and infection. So let's start with the two most
common types of incontinence. OK, we need to
understand stress and urge incontinence. Stress
incontinence is that involuntary leakage of urine
when there's an increase in intra -abdominal
pressure. So coughing, laughing, sneezing, exercising.
And what causes that? It's caused by weakened
pelvic floor muscles or a damaged urethral sphincter.
It's really common after childbirth or with aging
and menopause. Okay, and urge incontinence is
different. It's more about the bladder muscle
itself. Correct. Urge incontinence or overactive
bladder is that sudden, strong, compelling desire
to void that's really difficult to put off. It's
caused by involuntary contractions of the detrusor
muscle in the bladder wall. It's like the bladder
is sending faulty signals to the brain. And then
in stark contrast to that, urinary retention,
not being able to empty the bladder. What defines
clinically significant retention? It's usually
defined by a post -void residual or PVR of greater
than 200 milliliters after the patient tries
to void. It's often caused by an obstruction
like BPH or by impaired neurological signaling.
And acute retention, where they can't go at all,
is extremely painful and has to be relieved immediately.
OK, let's look at the pharmacology, specifically
for managing that overactive bladder with urge
incontinence. The primary drug class here is
anticholinergics, like oxybutynin or tolturidin.
These drugs work by blocking parasympathetic
nerve impulses, which relaxes that detrusor muscle,
increases the bladder's capacity, and reduces
the frequency of those involuntary contractions.
And what's the critical nursing alert for these?
drugs, especially in the elderly. Anticholinergics
come with those classic systemic side effects.
You can remember it as the four cants. Can't
see blurred vision, can't spit dry mouth, can't
stool constipation, and most critically for us,
can't pee urinary retention. So you have to monitor
for retention very closely. Very closely, especially
in men who already have BPH. And you help them
manage the annoying side effects like dry mouth
with hard candy or sips of water. The sources
are really clear that the cornerstone of treatment
for all types of incontinence isn't drugs, it's
behavioral therapy. What are the first -line
nursing interventions? Behavioral therapies are
absolutely the foundation. The first one is pelvic
floor muscle training or Kegel exercises. This
is essential for stress incontinence. And it's
more than just telling them to do it, right?
Oh, yeah. We have to teach them how to identify
and contract the right muscles, the ones they
use to stop the flow of urine or gas. And we
have to emphasize they need to do them regularly,
multiple times a day, to see results. What else?
The other big one is timed voiding or bladder
retraining. This involves setting a strict voiding
schedule maybe every two hours at first, and
then gradually increasing that interval to train
the bladder to hold more. And, of course, managing
fluid and diet by reducing bladder irritants
like caffeine and alcohol. And this management
is all tied to maintaining the patient's dignity.
Absolutely. Beyond the behavioral stuff, we prioritize
meticulous skin care to prevent incontinence
-associated dermatitis. Managing this while maintaining
the patient's self -worth is just a core part
of compassionate nursing. Let's pivot to retention,
which often means catheterization, putting us
right back on high alert for CTI Joe. What's
the nursing priority when an indwelling catheter
is needed? Well, the immediate priority is to
relieve that acute retention. But once that's
done, the overarching priority shifts to CITI
prevention and figuring out the underlying cause.
Can you detail the strict protocols for CITI
prevention we have to follow? Of course. The
sources highlight several evidence -based rules.
One, insertion has to be done with strict sterile
technique. No exceptions. And maintenance. Maintain
a closed drainage system at all times. The bag
is always, always positioned below the level
of the bladder to prevent backflow, and the tubing
has to be free of any kinks or loops. Securement
is also important. Yes, you have to secure the
catheter to the patient's leg to prevent movement
and urethral trauma, and you perform daily perineal
care with soap and water. And the most important
part. The most important role for the nurse is
removal advocacy. We have to constantly assess
if that catheter is still medically necessary
and advocate for its prompt removal as soon as
it's not. Every single day that catheter stays
in, the risk of CIUTI goes up exponentially.
Let's do a quick review summary for these functional
problems. Okay. First -line treatment for UI
behavioral therapies like Kegel exercises and
timed voiding. Anti -cholinergics. They're used
to treat urge incontinence, but you're on high
alert for those side effects. constipation, dry
mouth, blurred vision, and retention. And the
priority for retention. Relieve the acute retention,
address the underlying cause like BPH, and then
strictly adhere to all the CIU -TI prevention
protocols, especially advocating for prompt removal
of the catheter. We have completed a really comprehensive
high -yield deep dive into these renal and urologic
priorities. We successfully navigated those three
critical challenges. Fluid balance, pain management,
and sepsis risk. I think we did. To synthesize,
you know, we detailed the aggressive steps you
have to take to fight sepsis and pilonephritis,
where that CVA tenderness is your call to action.
We explored the huge fluid shifts in APSGN and
nephrotic syndrome, emphasizing that HTN control
and meticulous skin care are just so critical.
And we focused on the acute pain management for
kidney stones, really hitting on NSAIs and that
non -negotiable need to strain all the urine.
Finally, we looked at the functional disorders
reinforcing the power of behavioral modification,
those Kegels, and timed voiding as the first
line of defense. So as you integrate all of this
information, what's the single most important
conceptual link you should take away from this
whole review? Well, we've seen almost every single
intervention we talked about, from preventing
UTIs, to avoiding another kidney stone, to managing
incontinence. It's all heavily dependent on consistent,
proactive patient behaviors. It's about hydration,
adherence, and hygiene. It goes about empowerment.
It's all about empowerment. If you can apply
the concept that the nurse's role isn't just
to fix the acute problem, but to empower the
patient through knowledge about their daily habits,
whether that's front -to -back wiping, sticking
to a low oxalate diet, or just drinking their
two liters of water. Then you'll understand the
most essential and I think the most testable
component of nursing care for this whole population.
Prevention and education as treatment. That is
fantastic advice. You've really distilled the
critical need to know from all the noise. Thank
you for sharing your sources and helping everyone
prepare for success. My pleasure. We'll catch
you on the next Deep Dive.