Chapter 14: Depressive Disorders – Causes & Care

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Welcome to the Deep Dive.

Today, we're really getting into some core academic stuff.

You gave us Chapter 14 from Varkarolis's of Psychiatric Mental Health Nursing, our goal.

Basically, create the ultimate clinical summary, pull out those key psychiatric, biological, and therapeutic concepts you absolutely need.

Exactly.

We're tackling the whole spectrum of depressive disorders and the main thread connecting all of them.

It's these shared symptoms,

sadness, feeling empty, irritability, sometimes physical issues too, and problems with thinking.

It all really impacts a person's ability to just function day to day.

It's definitely not just feeling blue.

It's much deeper than that.

Absolutely.

It's about a breakdown in coping.

We're aiming for a clear, structured way for you to grasp all this complexity.

Let's unpack the spectrum.

We should probably start with the diagnoses that aren't major depressive disorder or MDD.

The chapter mentions disruptive mood, dysregulation disorder, DMDD.

What's the backstory there?

Why was that even created?

Ah, DMDD.

Well, that's a really important one, historically speaking.

It was basically introduced to try and stop the overdiagnosis of bipolar disorder in kids and teens.

Oh, right, because a lot of those kids weren't actually bipolar.

Exactly.

We found many young people initially diagnosed with bipolar disorder were down the line actually presenting more like MDD or an anxiety disorder.

DMDD provides a more accurate picture for some of those kids.

Gotcha.

It helps avoid maybe lifelong medication for something that wasn't the right fit.

Who does DMDD typically apply to?

It's for ages six to 18, but the symptoms usually have to start before age 10.

The key feature, constant, really severe irritability and anger, like pretty much all the time.

And that shows up as?

Frequent, intense temper tantrums.

We're talking verbal outbursts or behavioral blowups that are just totally out of proportion to whatever triggered them.

And this needs to happen at least three times a week, and you need to see it in at least two different places like at home and at school or with friends.

Wow, that sounds incredibly difficult for the child and everyone around them.

How do you even approach treating that?

Yeah, it's tough.

Treatment usually starts with focusing on the symptoms and the problems they cause.

So things like cognitive behavioral therapy, CBT, and really importantly, parent training.

Medication isn't the first step.

But sometimes it's needed.

Sometimes, yes.

If the irritability is really severe, you might use low doses of antidepressants or sometimes even generation antipsychotics like risperidone or aripiprazole just to target that specific symptom.

But again, psychosocial interventions come first.

Okay.

Moving along the spectrum,

persistent depressive disorder, PDD.

Now that used to be called dysthymia, right?

The name sounds like it's about time.

It is, exactly.

PDD or dysthymia is basically a chronic, low -level depression.

It has to last for at least two years in adults or one year in kids and adolescents.

So not usually the acute crisis kind of depression.

Generally, no.

The symptoms aren't typically severe enough to land someone in the hospital.

You'll see that depressed mood, plus at least two other things like changes in appetite or sleep, low energy, poor self -esteem, trouble concentrating, or that feeling of hopelessness.

And here's something the chapter highlights that's, well, really crucial for nurses assessing these patients because it's so chronic, often starting young.

They feel like they've always felt this way.

That's what you'll hear.

Yeah.

And that chronic low mood just becomes their baseline, their normal.

It does.

And that's a real challenge clinically because they might not even recognize it as an illness.

It makes getting them motivated for treatment pretty difficult sometimes.

They're just trying to get by with very little energy.

Okay.

We should also quickly touch on premenstrual dysphoric disorder, PMDD.

Very specific timing with this one.

Right.

PMDD is this cluster of pretty severe mood and physical symptoms.

Think intense mood swings,

anxiety,

feeling totally overwhelmed, plus physical stuff like bloating, breast tenderness.

And the key is when it happens.

Exactly.

It reliably pops up in that last week before menstruation starts and then poof, it disappears or gets much better once the period begins.

Treatment.

Often lifestyle changes help exercise, diet changes, sleep hygiene.

But SSRIs like fluoxetine or sertraling are actually FDA approved and often really effective for the mood symptoms.

Good to know.

And just to round out this part of the spectrum, the chapter mentions depression can also be triggered by other things, right?

Definitely.

You've got substance or medication -induced depressive disorder that usually gets better within weeks once the substance is stopped.

And then there's depressive disorder due to another medical condition.

Think things like strokes, Parkinson's, Cushing's disease, hypothyroidism.

Those can all manifest with depressive symptoms.

Okay.

That covers the wider spectrum.

Let's really zero in now on the classic presentation.

Major depressive disorder, MDD.

What are the absolute must -haves for that diagnosis according to the DSM -5?

Alright, MDD.

The core is a persistently depressed mood that lasts for a minimum of two weeks.

Okay?

But that's not enough.

To get the diagnosis of a major depressive episode, you need five or more specific symptoms present during that two -week period.

Five or more.

And there's a critical requirement in there, isn't there?

Yes.

At least one of those five must be either one, depressed mood, or two, what we call anhedonia.

That's a marked loss of interest or pleasure in pretty much all activities.

Anhedonia.

That inability to enjoy things you used to love.

It's such a stark symptom.

What other kinds of symptoms make up that list of five or more?

It's a mix of physical and cognitive stuff.

Significant weight changes like losing or gaining 5 % of body weight in a month without trying.

Sleep problems, either insomnia or sleeping way too much.

Constant fatigue or loss of energy.

Feelings of worthlessness or excessive guilt.

Trouble thinking, concentrating, or making decisions.

And crucially, recurrent thoughts of death or suicidal ideation.

And it's worth remembering for kids and adolescents that mood might show up more as irritability than sadness, right?

Absolutely.

That's a key point for younger populations.

Okay.

Epidemiology.

Who's most affected?

Well, we see the highest rates in young adults, sort of that 18 to 25 age group.

And consistently, prevalence is higher in females than males.

What about older adults?

Is depression just part of getting older?

No,

absolutely not.

That's a really important myth to bust.

Depression in older adults is common, but it is not a normal part of aging, and it needs treatment.

Sometimes you see something called pseudo dementia.

Ah, right.

Where the depression makes their thinking so slow, it looks like a neurocognitive disorder.

Exactly.

Severe cognitive slowing.

Looks like dementia.

And this is key.

It's reversible if you treat the underlying depression,

unlike true dementia.

Also worth noting, anxiety is incredibly common alongside MDD.

About 70 % of people with MDD also have significant anxiety symptoms.

Okay, let's get into the why.

What does the biology tell us?

How strong is that genetic link?

It's pretty strong.

If you look at identical twins, the concordance rate, meaning if one twin has MDD, the other does too, is almost 50%.

So genetics definitely plays a significant role.

And biochemically, what's happening in the brain?

The focus has traditionally been on key neurotransmitters, specifically the model means.

Serotonin, that's 5 -HT, is huge.

It helps regulate sleep, appetite, libido.

So when serotonin pathways are dysregulated, you see problems in those areas.

Makes sense.

Then there's norepinephrine.

That's involved in attention, motivation, behavior.

A deficiency there can lead to apathy, fatigue, that psychomotor slowing we sometimes see.

The chapter also briefly touches on glutamate, and importantly, the link between chronic stress, inflammation, and reduced neurogenesis.

Neurogenesis, the brain's ability to grow new neurons.

Right.

Chronic stress seems to put the brakes on that.

And this all ties nicely into the diathesis stress model.

Okay, break that down for us.

Diathesis stress.

So the diathesis is your underlying vulnerability.

That could be your genetics, your biochemical makeup.

The stress part is, well, life events, environmental stressors, trauma, loss.

The model says it's the interaction between that vulnerability and those stressors that actually triggers the depressive episode.

So you might have the genetic predisposition, but you need that stressful trigger to actually develop the illness.

Often, yes.

And things like early life trauma can actually sort of prime the stress circuits in the brain, making them reactive later in life.

Fascinating.

So that's the biological side.

What about the psychological perspective?

Beck's cognitive theory comes up a lot.

It does.

And it's really fundamental for understanding therapies like CBT.

Beck basically argued that depression isn't just caused by negative events, but it's maintained by negative automatic ways of thinking.

The way people interpret things.

Exactly.

He described the cognitive triad.

Three core negative beliefs.

First, a negative view of oneself.

I'm worthless.

I'm a failure.

Second, a pessimistic view of the world.

Everything is terrible.

Nothing ever goes right.

And the third?

The third is the belief that negative things will just keep happening in the future.

It's hopeless.

Things will never get better.

It becomes this self -perpetuating cycle of negative thoughts feeding negative feelings.

Okay.

That gives us a good theoretical grounding.

Let's translate this now into nursing practice.

When you're assessing a patient who might be depressed, what's the absolute first priority?

Safety.

Always.

Always safety.

And in depression, that means immediately assessing for suicidality.

Right.

Looking for any suicidal ideation.

Which isn't just one thing, is it?

It's a range.

Exactly.

It can range from a sort of vague passive thoughts like, I wish I wouldn't wake up, all the way to having a very specific active plan with the means to carry it out.

If there's a plan and intent, that's a psychiatric emergency requiring immediate intervention.

So how do you actually ask about that?

It can feel difficult.

It can, but it's non -negotiable.

You need to be direct, but you can build up to it.

Start maybe more generally.

Tell me what things have been like for you lately, or sometimes when people feel this down, they have thoughts about, but you must get to the direct questions.

Like what specifically?

Things like, have you been having any thoughts about ending your life?

If yes, do you have a plan for how you would do that?

And do you have access to the things you would need to carry out that plan?

You have to ask correctly.

Okay, absolutely critical.

Beyond immediate suicide risk, what are the other key things you're looking for in your assessment?

Things you would observe or the patient might report?

Well, appearance can tell you a lot.

You might see neglected grooming, maybe slumped posture, poor eye contact.

Behaviorally, look for inertia.

Energia, that profound lack of energy.

Yeah, an abnormal lack of energy.

Yeah.

And this can show up in two kind of opposite ways.

One is psychomotor retardation.

Everything is slowed way down.

Movement, speech, thinking.

They might barely move, take forever to answer a question.

Like moving through molasses.

Exactly.

Or you might see the opposite, psychomotor agitation.

They can't sit still, pacing, fidgeting, wringing their hands.

It's this restless, anxious energy.

And then there are those physical symptoms, the vegetative signs.

Right.

Those are the fundamental physical processes needed to sustain life.

We already mentioned appetite changes, significant weight loss or gain.

Sleep disturbances are classic,

especially waking up really early in the morning and not being able to get back to sleep, though some people sleep excessively.

And usually a decrease in libido, in sexual interest.

Okay.

Can you clarify for listeners the difference between mood and affect?

We hear those terms a lot.

Sure.

Think of mood as the patient's sustained emotional state.

What they report feeling over time, like I've felt depressed for weeks.

It's subjective.

Affect, on the other hand, is the outward expression of emotion that you, the nurse, observe.

It's objective.

So what you see on their face and their tone.

Exactly.

In depression, affect is often described as constricted, limited range, blunted, even more reduced or flat, like almost no visible emotional expression at all.

And those feelings we talked about, worthlessness, guilt, hopelessness, especially hopelessness, those are really strongly linked to suicide risk.

When you have a patient who is severely withdrawn, maybe barely speaking, communication becomes really challenging, but also super important.

Any key tips from the chapter?

Definitely.

Keep it simple.

Yeah.

Use short, concrete sentences.

Don't bombard them with questions.

Critically, allow silence.

Give them plenty of time to process and respond because remember, their thinking might be slowed.

And what not to do.

Oh, definitely avoid platitudes.

Saying things like, cheer up or things will get better, can actually make them feel worse, like you don't understand, or they're failing even more.

So what can you say if they're silent?

Use the technique of making observations.

Just state the obvious factual things you see.

I noticed you changed your shirt today, or you finished your breakfast.

It acknowledges them, connects them to reality, but doesn't demand a complex emotional response.

Simple, concrete, reality -based.

Got it.

And in terms of the nursing process, risk for suicide is obviously the top diagnosis.

Outcomes should always be patient -centered.

Absolutely.

Guided by the recovery model, meaning goals are developed with the patient, focusing on their hopes and strengths, not just symptom reduction.

Okay, great.

Let's switch gears to treatment.

Pharmacotherapy is a cornerstone.

What's the main principle behind how these meds work?

Basically, they aim to correct those neurotransmitter imbalances we talked about, primarily serotonin and norepinephrine.

But the crucial thing to tell patients, and for you to remember, is that they don't work overnight.

It usually takes one to three weeks, sometimes longer, to really start feeling a therapeutic effect.

Patience is key.

What's the first -line choice, usually?

Typically, it's the SSRI's selective serotonin reuptake inhibitors.

Think fluoxetine, sertraline, citalopram.

They're first -line, mainly because they have a generally better side -effect profile than older drugs.

They don't usually cause those annoying anti -colonogic effects like dry mouth, blurred vision, constipation.

Safer overall, but not without risks.

There's a serious one we need to highlight.

Serotonin syndrome.

Yes.

Absolutely critical to know about.

This is a potentially life -threatening condition caused by too much serotonin activity, maybe from taking too high a dose or combining serotonergic drugs.

What does it look like?

What are the warning signs?

You're looking for a cluster of symptoms, mental status changes like confusion, agitation, maybe delirium, autonomic hyperactivity, things like fever, sweating, high blood pressure, fast heart rate,

and neuromuscular hyperactivity tremors, muscle rigidity, twitching, which we call myoclonus.

And if you suspect it?

Stop the suspected offending drug immediately.

That's the first step.

Then supportive care.

It's an emergency.

Okay.

SSRI's first line.

What if they don't work or aren't tolerated?

What's often second line?

Then you might move to the tricyclic antidepressants, the TCA's.

These are older drugs like amitripline, nortitripline.

They are effective, but they come with more baggage.

Like those anti -colonogic side effects?

Yes.

Dry mouth, blurred vision, constipation, urinary retention are common.

But the biggest concern with TCA is the really critical warning is their lethality and overtoses.

They can cause serious cardiac conduction problems, basically.

Fatal heart rhythm disturbances.

So for any patient who might be impulsive or has a significant suicide risk,

prescribing TCA's is extremely risky.

Usually only give them a small supply at a time.

Wow.

Okay.

High alert for TCA's.

Then there's a third line, the MAOIs, monamine oxidase inhibitors.

Right.

MAOIs are generally reserved for treatment resistant depression because they require significant dietary restrictions and have potentially dangerous interactions.

This is the one with the cheese reaction, right?

Hypertensive crisis.

Exactly.

MAOIs work by blocking an enzyme that breaks down neurotransmitters like norepinephrine and serotonin.

But that enzyme also breaks down tiramide, which is found in certain foods.

What kinds of foods?

Things that are aged, fermented, or cured.

Aged cheeses, cured meats like salami or pepperoni, soy sauce, sauerkraut, fava beans.

The list is pretty long.

If a patient on an MAOI eats these foods, they can't break down the tiramide.

And that causes...

A massive surge of norepinephrine leading to a hypertensive crisis.

Extremely high blood pressure, severe headache, sweating,

nausea, vomiting.

It can lead to stroke or even death.

Patient education about the diet is absolutely non -negotiable.

They need to know to seek immediate medical help if they get a severe headache.

Okay, so SSRIs, TCA's, MAOIs, each with their own safety profiles.

The chapter also mentions some newer, more novel treatments.

Yes, briefly.

There's esketamine, which is a nasal spray derived from ketamine.

It works differently on the NMDA receptor system.

And it's used for treatment -resistant depression.

But because it can cause dissociation and sedation, it has to be administered in a certified clinic.

And patients need to be monitored for two hours afterwards.

And the other one, for postpartum depression.

That's Brexanolone.

It's specifically for postpartum depression.

And it's given as a continuous IV infusion over 60 hours.

Requires careful monitoring too, including continuous pulse oximetry because of the risk of excessive sedation.

Interesting stuff.

You mentioned genetics earlier with the diethesis stress model.

Is there a connection between genetics and how people respond to these meds?

Increasingly, yes.

We're learning more about pharmacogenetics.

For instance, many antidepressants are metabolized by enzymes called CYP450 enzymes.

People have genetic variations in these enzymes.

Some are poor metabolizers, meaning they break down the drug very slowly.

So they might need a lower dose to avoid side effects or toxicity?

Exactly.

Others might be ultra rapid metabolizers and need a higher dose to get any effect.

While routine genetic testing isn't standard practice everywhere yet, it's definitely a growing area that could help personalize medication selection and dosing in the future.

That's really fascinating.

Okay, beyond medications, what about brain stimulation therapies?

ECT comes to mind immediately, especially for severe cases.

Electroconvulsive therapy.

ECT is actually one of the most effective treatments we have, particularly for severe treatment -resistant depression, psychotic depression, or when there's acute imminent suicide risk.

It can work much faster than medications.

How does it actually work?

People have misconceptions.

Right.

It's done under general anesthesia with a muscle relaxant.

An electrical current is passed through the brain to induce a brief, controlled seizure, typically lasting 30 to 60 seconds or more.

The seizure seems to cause changes in brain chemistry that alleviate depression.

What about side effects?

Memory loss is often mentioned.

The most common side effects are temporary confusion immediately after the procedure and retrograde amnesia, difficulty remembering events from the time leading up to and including the ECT treatments.

Some people report persistent memory issues, but for most, it resolves.

Are there less invasive stimulation options?

Yes.

There's repetitive transcranial magnetic stimulation or RTMS.

This uses magnetic pulses generated by a coil placed on the scalp to stimulate specific areas of the cerebral cortex involved in mood regulation.

How does that compare to ECT?

It's non -invasive, doesn't require anesthesia, and it's done as an outpatient procedure, usually daily for several weeks.

Side effects are generally mild, like headache or scalp tingling.

The main contraindications having any metal implants in the head near the stimulation site, like cochlear implants.

And one more, vagus nerve stimulation.

VNS, yes.

This involves surgically implanting a small device, kind of like a pacemaker, in the chest wall.

A wire runs under the skin connecting the device to the vagus nerve in the neck.

The device sends intermittent electrical pulses to the nerve, which then travels up to the brain.

And side effects for VNS?

The most common one is voice alteration hoarseness.

Or a change in voice quality when the stimulator cycles on, because the vagus nerve runs near the vocal cords, usually mild.

All right, so meds, stimulation therapies, what else is in the toolbox?

Don't forget other important modalities.

Light therapy using a special light box is actually first -line treatment for seasonal affective disorder, or SAD.

Exercise is huge.

It's proven to boost serotonin and dopamine, improve sleep, and enhance self -concept.

It should be part of basically every treatment plan.

And therapy, of course.

Absolutely.

Psychotherapies like cognitive behavioral therapy, CVT, which directly targets those negative thought patterns we discussed from Beck's theory, and interpersonal therapy, IPT, which focuses on relationship issues that might contribute to depression, are highly recommended, especially for preventing relapse during the maintenance phase.

Okay, that's a comprehensive look.

Let's try to wrap this up.

What are the absolute key takeaways listeners should pull from this chapter?

All right, big picture.

One, depressive disorders aren't monolithic.

They exist on a spectrum thing DMDD, PDD, MDD, but they all impair function.

Two, for MDD, remember the criteria.

Five or more symptoms for at least two weeks, and one must be depressed mood or anhedonia.

Three, assessment is paramount.

Prioritize suicide risk immediately, and always assess for those vegetative signs.

Four, treatment options are broad, from meds to therapy to stimulation, but safety is non -negotiable, especially knowing the risks like serotonin syndrome with SSRIs and hypertensive crisis with MAOIs.

Excellent summary.

Now for that final thought to leave our listeners with, we talked about the diathesis stress model, that mix of genetic vulnerability and life events, and we touched on pharmacogenetics, like those CYP450 enzymes affecting how people metabolize drugs.

So here's something to ponder.

Given how much trial and error can be involved in finding the right antidepressant and knowing the serious risks of some drugs, how might psychiatric practice change if your teen genetic testing before prescribing became the norm?

Could understanding someone's specific metabolic profile significantly improve safety and speed up the path to finding effective treatment right from the start?

It's a really compelling question about where the field is heading.

Definitely something to think about.

Well thank you for joining us on this deep dive into a really foundational chapter of psychiatric nursing.

We hope breaking it down like this helps you feel more confident with this material.

Until next time.