Chapter 8: Care of Patients With Cancer

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Usually, when we look at the human body, there's this really incredible, almost comforting expectation of order, you know?

Oh, absolutely.

It's like a highly synchronized orchestra or something.

Right, exactly.

Every single cell in your body has its own sheet of music, and it plays its specific part at the exact right time.

And then when the song is over, it just quietly steps off the stage to make room for the next one.

Yeah, we really like that idea.

We like knowing our bodies are following the rules.

It's biological choreography, billions of these microscopic events happening every single second.

Right.

But then, and this is why we're here today, you step into the world of oncology.

Yeah, that changes everything.

It really does.

Suddenly you realize the orchestra has been completely hijacked.

When sheet music is just gone.

Gone.

You're looking at a cellular landscape that has just abandoned all the rules and is like operating in this state of absolute ruthless rebellion.

It is the absolute definition of biological chaos.

And as a nurse, stepping into that chaos is probably one of the most profound challenges you're ever going to face.

So true.

And that brings us to why we are here.

Welcome to the deep dive.

If you're listening to this, you know you are stepping right into that challenge.

You're likely a nursing student, right?

Yeah.

Gearing up to master this incredibly complex,

often really intimidating world of oncology.

Exactly.

So consider this dedicated one -on -one tutoring session.

We are sitting right here with you and we're going to unpack chapter eight, care of patients with cancer.

And our mission today, you know, it isn't just to recite a list of symptoms or like have you memorized some chart?

No, definitely not.

We want to translate all that dense pathophysiology, the staging systems, the care plans into real world practical knowledge.

Because when you step up to the bedside of a patient with cancer, you can't just be a task doer.

You know, you can't just hang a bag of chemo because an order tells you to.

Right.

You need to understand the why behind it all.

Why are there white blood cells plummeting?

Why does this cancer spread to the bone specifically?

Exactly.

That why is the entire foundation of your clinical reasoning.

So let's unpack this.

To really understand oncology nursing today,

we kind of have to completely reframe how we think about the disease.

Yeah.

Historically, if a patient heard the C word, it was just synonymous with a terminal diagnosis.

It's but here's where it gets incredibly hopeful.

That is no longer the clinical reality for the majority of patients.

Which is huge.

I mean, that is a massive paradigm shift.

It really is.

It represents one of the most profound shifts in modern medicine.

Today, because of, well,

massive leaps and diagnostics and targeted therapies, cancer is increasingly managed as a chronic disease.

A chronic disease.

Wow.

Yeah.

We're now looking at an overall survival rate of about 68%.

Wait, really?

68%.

So like almost seven out of 10 patients are living five years or much longer after their initial diagnosis.

Yes.

They're managing this over years, sometimes decades.

That's incredible.

It is.

They experience periods of exacerbation where the disease flares up and then periods of remission where it's undetectable.

It's starting to mirror how we manage heart failure or diabetes.

That is just such a critical concept for you to grasp as a nursing student.

You aren't just preparing patients for the end of life anymore.

You're helping them navigate a chronic illness.

Exactly.

But we do have to be realistic.

Even with those survival rates, the sheer volume of people affected is staggering.

Yeah.

The text gives the statistics from 2023 and we're talking about roughly 1 .9 million new cancer cases diagnosed in the U .S.

in a single year.

And tragically, about 609 ,820 cancer deaths.

Right.

And those numbers are exactly why every single nurse will pair for patients with cancer.

It doesn't matter if you're in the ER, labor and delivery, or a community clinic.

It touches literally every specialty.

And when we look at those 1 .9 million new cases, there are four main culprits leading the pack.

The big four.

That's the prostate, the breast, the lung and bronchus, and the colon and rectum.

Right.

Now, breast and prostate cancers have very high incidence rates, meaning a lot of people get diagnosed.

But you have to pay attention to the mortality statistics.

Yeah.

Incidence versus mortality.

Exactly.

Lung cancer remains the undisputed leading cause of cancer mortality for both men and women.

It is by far the most lethal.

I feel like a lot of people assume breast or prostate cancer causes the most deaths just because we hear about them so much in awareness campaigns.

Right.

Yeah.

It's a very common misconception.

But lung cancer outpaces significantly.

We also have to look at the demographics.

The data in the text clearly shows us that disparities exist.

And as a nurse, you have to know these.

You do because they directly inform how you approach screening and education.

The epidemiological data shows that when you combine all cancers, incidence rates are highest among black men and white women.

And knowing that isn't just about passing a test.

It's the first step in recognizing who is at the highest risk in your specific community, you know?

Absolutely.

It lets you advocate for early screening where it's needed the absolute most.

Okay.

So we have this massive macro level view of millions of people, but to understand how to fight it, we need to zoom way in down to the microscopic level.

Down to the cells.

Yeah.

What exactly is going wrong inside the body to cause all this?

Well, that brings us to the fundamental path of physiology.

And to understand a rogue malignant cell, you first have to understand a normal law -abiding cell.

Right.

Because normal cells have rules.

They don't just divide whenever they feel like it.

Exactly.

They only reproduce for very specific reasons, like to replace damaged cells or cells that have naturally died.

And they do that through mitosis, right?

That highly controlled step -by -step division.

Yes.

So, you know, if you scrape your knee, your normal skin cells recognize the damage.

They use mitosis to match the whole, and then crucially, they stop.

That stopping part is so important.

It is everything.

Normal cells have a built -in rule called contact inhibition.

Oh, I love the analogy for this.

It's like walking into a crowded room.

If you bump into someone, you stop moving forward.

Perfect analogy.

Normal cells do the exact same thing.

Once they touch their neighboring cells, a signal goes to the nucleus that says, we're done.

Stop dividing.

They also stay in their assigned seats.

Like, normal skin cells don't suddenly pack up and move to the liver.

Right.

They stay put.

And perhaps most importantly, they come with an expiration date.

They aren't immortal.

They have a self -destruct button.

They do.

When a cell gets too old or damaged, it undergoes apoptosis.

Apoptosis.

Definitely highlight that word in your notes.

Program cell death.

It's a biological sacrifice, really.

The cell realizes its defective, breaks down its own DNA, and lets the immune system clear it away quietly.

But cancer cells, they're the ultimate rule -breakers.

They completely reject the social contract.

They really do.

It starts with damage to the genetic blueprint, the DNA.

That mutation transforms a normal cell into a malignant one.

And they don't have that self -destruct button anymore, do they?

Nope.

They completely ignore the signals for apoptosis.

And they ignore contact inhibition, too.

They just bump into other cells and keep right on dividing.

Continuously and periodically.

It's like a rogue assembly line in a factory.

The normal workers clock in, do their job, and go home.

The cancer cells.

They murder the floor manager, never stop working, build defective products, and hoard all the electricity so the rest of the factory shuts down.

That analogy perfectly captures the metabolic theft of cancer.

Because they're multiplying in this frenzy, they have to go somewhere.

So they pile up.

And that pile is the tumor.

Yes.

Clinically, we call it a neoplasm.

Or a tumor.

And these rapidly dividing cells demand massive amounts of nutrients.

They physically divert the blood supply away from healthy cells.

Literally starving the healthy tissue.

The text actually references figure 8 .2 to show this visually.

If you look at normal skeletal muscle cells under a microscope, what are you seeing?

Normal muscle cells are beautifully uniform.

They're elongated.

Their nuclei are neatly arranged.

They look like a

They're well differentiated.

Exactly.

A pathologist looks at them and immediately knows those are healthy muscle cells.

They have an identity.

But if you look at a rhabdomyosarcoma, a malignant tumor from that same muscle tissue, it's just pure chaos.

Visual chaos.

The cells are wildly different shapes and sizes.

The nuclei are massive and dark.

They're completely disorganized.

They're undifferentiated.

They forgot who they are and what their job is.

Exactly.

So once this rogue mass forms, the primary tumor, how does it actually kill a patient?

Right.

Because a lump sitting in a muscle isn't usually what ends a life.

How does it spread?

That is the most dangerous capability of a malignant cell.

Metastasis.

The movement of cancer cells from the primary site to a completely different part of the body.

Normal cells stay put.

Cancer cells are insidious travelers.

They basically hijack the body's highway systems.

The bloodstream in the lymphatic system.

Right.

As the primary tumor grows, pressure builds.

Eventually a small cluster or even just one rogue cell breaks off.

It invades a blood vessel or lymphatic capillary.

And once it's in there, it just hitches a ride.

It flows through the circulation until the vessel narrows into a tiny capillary bed in a distant organ like the lungs or the liver.

And it gets stuck.

Yeah.

It gets wedged in there, slips through the vessel wall into the new tissue and starts the whole chaotic division process all over again.

Creating a secondary tumor.

But blood and lymph aren't the only ways it spreads, right?

There's direct transplantation.

Yes.

Surgical seeding.

This is critical if you ever work in an OR.

Malignant cells can be physically transplanted during a biopsy or surgery.

So if the surgeon's scalpel touches the tumor, the cells stick to it.

And if they use that same scalpel on healthy tissue nearby, they literally plant the cancer cells in a new location.

That is terrifying.

It's why surgical oncology requires such meticulous technique.

Changing instruments, changing gloves mid surgery.

What about shedding into a body cavity?

The peritoneal space.

Yeah.

That's the third pathway.

Think of your abdominal cavity.

If a tumor on the colon breaks through the outer layer, it can just drop cancer cells right into the open fluid.

Like seeds falling off a dandelion.

Exactly.

And they float until they land on another organ, like an ovary, and take root.

Now, what's really important for clinical assessments is that these travidin cells don't just land randomly.

Table 8 .1 in the text lays out specific predictable pathways.

Right.

Breast cancer, for example, most commonly metastasizes to the bone, lungs, liver, and brain.

So if you have a breast cancer survivor in your clinic and she complains of sudden severe pain in her ribs, your nursing brain needs to immediately flag that as a potential cue for bone metastasis.

You can't just write it off as a pulled muscle.

What about prostate cancer?

Where does that go?

Prostate cancer notoriously spreads to the bone, specifically the pelvis, spine, and femurs.

So severe lower back pain is a massive red flag.

Colorectal cancer.

Because of how blood drains from the GI tract directly into the portal vein, colorectal cancer very frequently metastasizes to the liver.

The liver acts like a massive net.

And melanoma.

Highly aggressive.

It frequently targets the GI tract, lungs, and brain.

This spread is what defines the prognosis.

The clinical terminology here is important.

If biopsy says in situ, what does that mean?

Best case scenario.

In situ literally means in its original place.

The cells haven't broken through the basement membrane.

Easily cured.

But if it's regional?

That means it's spread to nearby tissues or lymph nodes, but not distant organs yet.

And advanced is the most severe.

Metastasize throughout the body.

And clinically, why this matters is that most patients don't die from the primary tumor.

They die from the metastatic disease destroying vital organs like the liver or lungs.

So if it's this destructive, what triggers that initial DNA mutation?

What flips the switch?

The triggers are diverse.

Genetics, chemicals, viruses.

But they all cause physical or chemical defects in the DNA.

Let's start with genetics.

Okay, genes.

Every human has normal genes that regulate cell growth.

But when they mutate, they become oncogenes.

Right.

Think of an oncogene like the gas pedal in your car getting permanently stuck to the floor.

Divide, divide, divide with no way to stop.

Exactly.

And on the flip side, we have tumor suppressor genes.

Those are the brakes.

So if a cell grows too fast, the suppressor genes pump the brakes.

But if you inherit a defective one?

You lose your braking system.

A prime example is the BRCA1 and BRCA2 mutations.

Inheriting those increases the lifetime risk for breast and ovarian cancer significantly.

Another big one is Lynch syndrome, right?

Hereditary non -polyposis colorectal cancer.

Yes.

HNPCC.

If a patient says their dad and sister had colon cancer before 50, alarm bells should ring.

Because with Lynch syndrome, you have an 80 % lifetime risk of developing colon cancer.

And an 80 % risk for endometrial cancer in females.

That's why we use mathematical tools like the Gale model or the Claus model to calculate risk based on family history.

But genetics only account for about 5 to 10 % of all cancers.

Right.

Most require mutations from external exposures.

Chemical carcinogens like benzene and older gasoline link to leukemia.

And infections.

This blew my mind.

You can catch a cancer from a virus.

It used to sound like science fiction, but oncoviruses are very real.

They splice their mutated genetic material right into healthy human DNA.

Hacking the cell's operating system.

HPV is the most prevalent.

It causes almost all cervical cancers plus oral and anal cancers.

Then there's hepatitis B and C, causing liver cancer due to chronic inflammation.

And the Epstein -Barr virus, the one that causes mono, is strongly linked to Burkitt lymphoma.

We have to mention HIV too.

HIV doesn't mutate genes directly, right?

No, it's indirect.

It decimates the immune system's T cells.

So when a cell naturally mutates, the body has no defense sources to destroy it.

Which is why Kaposi sarcoma is seen almost exclusively in severely immunocompromised patients.

Like those with advanced AIDS.

Exactly.

It's not just viruses either.

H.

pylori bacteria inflames the stomach lining, leading to gastric cancer.

And even parasites.

Like that blood fluke in freshwater Cystosoma hematobium.

It lays eggs in the bladder wall, causes massive inflammation, and leads to bladder cancer.

The common denominator is chronic, relentless inflammation, forcing cells to rapidly divide to repair damage, increasing the odds of a copying error in the DNA.

What about intrinsic factors, like age?

76 % of cancers occur in people over 55.

That's due to declining immune surveillance.

As you age, your internal security guards get slower.

Mutated cells slip past undetected.

There's a cruel irony the text mentions.

How can immunosuppressive drugs given for a kidney transplant, or even chemo itself, cause cancer?

Because turning off the immune system to save a transplanted kidney also turns off anti -cancer surveillance.

And older kelo drugs are so toxic, they can cause secondary leukemias years later.

Let's talk about obesity and diabetes.

The text says 15 -20 % of cancer deaths are associated with obesity, and it increases breast cancer risk by 30%.

How?

Fat tissue isn't just passive storage.

It's an active endocrine organ.

Obesity causes high glucose, high insulin, and adipose tissue physically produces estrogen.

So high insulin and high estrogen act like fertilizer for pre -cancer cells.

Exactly.

Same with type 2 diabetes.

The inflammation and insulin resistance basically beg cells to mutate.

Okay, so a patient has been exposed, cells mutated, a tumor formed, how do we name it?

The text gives four main buckets.

Based on tissue origin, first bucket, sarcomas, originating in active tissues like bone or muscle.

Osteosarcoma, rebdomoiosarcoma.

Second bucket,

carcinomas.

Epithelial tissues, the linings, skin, lungs, GI tract.

Basal cell carcinoma is the most common globally.

Third, leukemias and lymphomas.

The blood forming and lymphatic systems, these are liquid tumors.

And fourth, melanomas.

Pigment cells, highly aggressive and prone to early metastasis.

Once we name it, we have to stage it.

The TNM staging system, what does TNM stand for?

T is primary tumor, its size and local invasion.

N is regional nodes, has it spread to lymph nodes.

M is metastasis, has it spread to distant organs.

So if a chart says T1 and 0, M, 0.

Best news, small tumor, zero lymph nodes spread, zero distant metastasis, highly localized.

But T3, N2, M1.

Severe, large tumor deeply invading, T3, moderate lymph node spread, N2, and definitively metastasized to distant organs, M1.

That correlates with stage 4, right?

Yes.

Stage 0 is in situ.

Stage 1 is early local.

Stages 2 and 3 are larger with node involvement.

Stage 4 is advanced metastatic disease.

And staging dictates the entire treatment plan.

You don't use a brutal stage 4 chemo protocol for stage 0 tumor.

Exactly.

Before we stage it, though, we have to find it.

Detection and screening.

Let's go through the Soshin acronym for the seven warning signs.

Number one, unusual bleeding or discharge.

Tumors build fragile blood vessels, so they bleed easily into stool or from the uterus.

Number two, a sore that does not heal.

Normal repair mechanisms are broken.

Three, change in bowel or bladder habits.

Mechanical obstruction from a tumor blocking the colon or prostate.

Four, a lump.

Five, a nagging cough.

A tumor irritating the lung airway or pressing on vocal cords.

Six, change in a mole.

Seven, difficulty swallowing.

Again, mechanical.

A tumor narrowing the esophagus.

Screening guidelines are huge for exams.

Breast cancer.

Mammograms.

Opportunity starts at 40.

Strong recommendation from 45 to 54.

Cervical.

Pap smear and HPV testing starting at 25.

Colorectal.

Starts at 45.

FOBT at home or colonoscopy every 10 years.

Lung cancer.

Targeted.

Low dose CT for ages 55, 74 with a heavy smoking history.

Frost date.

Discussion about PSA and DRE starting at age 50.

And all these start around 45, because of that declining immune surveillance we talked about.

Exactly.

Now diagnostics.

Cytology, like a pap smear, scrapes cells to look at under a microscope.

And the FOBT for colon screening looks for occult blood.

But we need to educate patients that positive occult blood doesn't guarantee cancer.

Right.

It could be hemorrhoids or an ulcer.

They need a colonoscopy to be sure.

The gold standard for diagnosis is a biopsy.

You need tissue.

Fine needle aspiration.

Brush biopsy.

Excisional biopsy.

And the frozen section in the OR.

This is so intense.

The patient is asleep.

The surgeon removed the lump.

And they need to know if the margins are clear right then.

The tissue goes to pathology.

They freeze it, slice it, and call the OR in 15 minutes.

If there are cancer cells at the edge, the surgeon cuts out more tissue immediately.

Yes.

We also use imaging like 3D mammography, ultrasound, and PT scans where radioactive glucose lights up the energy hoarding cancer cells.

And tumor markers like PSA, CA125, CEA.

But the text warns they aren't for diagnosis, right?

Correct.

They track response to therapy.

If CA125 drops from 500 to 15 after chemo, it worked.

If it spikes to 200 a year later, it's an early warning of relapse.

Okay.

So the diagnosis is delivered.

The patient has cancer.

This is where clinical reasoning kicks in.

The nursing process.

Always start with assessment.

Ask, what has your doctor told you?

Establish what they actually understand.

Because they might be in shock and missed everything after the word cancer.

Exactly.

They then assess ADLs, nutrition, psychosocial status.

Establish a baseline.

Let's apply this to CarePlan 8 .1.

Mr.

Pol,

he has leukemia, receiving his third round of chemo.

His platelets are 185 ,000.

He has leukocytosis, painful mouth sores, anorexia, nausea, 15 -pound weight loss, and hair loss.

Problem number one, risk for infection.

This is the most critical.

Because Keno is cytotoxic.

It kills fast -growing cells, including the healthy cells in the bone marrow that make white blood cells.

It suppresses the bone marrow, causing neutropenia.

Yes.

We monitor his absolute neutrophil count, or ANC.

If it drops below 500, he has virtually zero immune defense.

A normal gut bacteria could cause fatal sepsis.

So we implement protective isolation.

Everyone wears a mask, no fresh flowers or unpeeled fruits because they carry bacteria and fungus.

And the drug nufogen.

It stimulates the bone marrow to rapidly produce healthy white blood cells.

Problem number two, risk for injury related to bleeding.

His platelets are dropping.

Thrombocytopenia.

He could hemorrhage.

So strict bleeding precautions.

No IM injections.

Hold firm pressure on blood draws for 5 -10 minutes.

Stool softener so he doesn't strain and tear rectal vessels.

Yeah.

And no rectal temps.

Ultra soft toothbrush.

No flossing.

Problem three, altered nutrition.

He's wasting away.

Give antibiotics 30 -45 minutes before meals and chemo.

Treat the mycositis with non -irritating saline rinses every two hours.

Keep the room odor -free.

Small, frequent, calorie -dense meals.

Problem four, body image and anxiety.

You sit with him, make eye contact, encourage him to express his fears.

No toxic positivity.

Connect him with a chaplain or social worker.

Build a support net.

The think critically scenario here is crucial.

You arrive for your shift with a scratchy throat assigned to a severely neutropenic patient.

What do you do?

You absolutely refuse the assignment.

A minor cold for you is a fatal pneumonia for a patient with an ANC under 500.

Advocate for his safety over your work ethic.

Such a vital point.

Now, treatments.

Neoadjuvant versus adjudant chemotherapy.

Timeline.

Neoadjuvant is before surgery to shrink a large tumor.

Adjuvant is after surgery to mop up microscopic cells that escape.

They use combination chemotherapy, different drugs attacking different phases of cell division.

And we have to watch for extravasation.

If vesicant chemo leaks out of the IV into the tissue.

It causes severe necrosis, eats the skin and muscle.

That's why only certified RNs administer it and check blood return constantly.

How does the patient survive this poison?

Normal cells have DNA repair mechanisms.

Cancer cells don't.

The chemo damages both, but normal cells hit pause, repair, and recover.

Cancer cells just die.

But that collateral damage causes dysjucia taste alterations.

Yes, a metallic taste.

Meat tastes like tinfoil.

We suggest plastic silverware and switching to poultry or dairy.

And cancer -related fatigue, CRF.

It affects up to 99 % of patients.

It's paralyzing exhaustion that sleep doesn't fix.

You have to help them pace activities.

And pain.

The main rule here is relentless advocacy.

If their opioid isn't working, you don't just say too bad.

You call the provider, ask for breakthrough meds, nerve blocks, palliative radiation.

You never stop trying.

We also have to be vigilant for oncologic emergencies,

like febrile neutropenia.

If an ANSI under 500 patient spikes a 100 .4 fever, it's an emergency.

Blood cultures and IV antibiotics immediately to prevent septic shock.

Spinal cord compression, SCC.

A metastatic tumor in the vertebra collapses the bone and crushes the spinal cord.

Signs are new back pain, sudden leg weakness, or loss of bowel bladder control.

Call a rapid response.

They need high -dose steroids and emergency radiation or surgery to save their nerve function.

Superior vena cava syndrome, SBC syndrome.

A tumor in the chest compresses the superior vena cava, blocking blood draining from the upper body.

So you see sudden severe swelling of the face, neck, and arms, distended neck veins, shortness of breath, stridor.

Set them up.

Give steroids, diuretics, oxygen, and emergency radiation.

Care settings change as the disease progresses.

Acute care is the hospital for major surgeries and emergencies.

Then acute rehab to rebuild strength or long -term care if they can't recover independence.

But mostly it's home care, managing oral chemo side effects in the living room.

Eventually, if curative treatment isn't viable, they transition to palliative care.

And we must explain that this isn't giving up.

It's a shift to aggressive symptom management.

Right.

They might still get surgery, but strictly to relieve a bowel obstruction, not to cure the cancer.

Quality of life is the goal.

If the disease progresses and becomes futile, we transition to hospice care.

All curative efforts stop.

The focus is 100 % on comfort, dignity, and managing anticipatory grieving with the team, including chaplains and social workers.

The nurse's role here is sacred, ensuring their final wishes are honored perfectly.

It requires immense emotional resilience.

We've covered a massive amount of ground today.

From a single mutating cell, metastasis, staging, diagnostic, cytotoxic treatments, to the final compassionate moments of hospice.

The key takeaway is understanding the why, why the DNA mutates, why the bone marrow fails.

That unlocks the how for your interventions.

It's all about clinical reasoning.

And for our final thought, cancer is ruthlessly adaptable.

It mutates, finds new pathways, resists drugs.

It's a shapeshifter.

So as a nurse, your practice must be just as adaptable.

Evolve your care plans daily, adjust your communication, outmaneuver the disease's toll on your patients.

It will challenge you every shift, but that's what makes oncology nursing so rewarding.

Thank you so much for joining us.

From the Last Minute Lecture Team, congratulations on tackling Chapter 8.

You've got this.