Chapter 72: Other Psychiatric Disorders

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Usually when we talk about a medical diagnosis, there's, you know, this expectation of precision, like engineering.

Right.

Like you break your arm, the x -ray shows that jagged white line, and the provider just points and says, yep, there it is.

Broken or not broken.

It's clean.

And it's comforting, honestly, because we really like things to be visible and easily categorized.

We do.

But then you step into the world of psychiatric disorders and specifically eating disorders and sleep -wake disorders.

Oh, yeah.

That's a whole different ballgame.

Suddenly that x -ray machine is just completely useless.

We're looking at a diagnostic landscape that is honestly incredibly murky.

It is the absolute definition of diagnostic muddy waters.

And as an advanced practice nurse, you are standing on the front lines in primary care.

Right.

You really have to spot these issues before they become fatal.

So today we are doing a deep dive into the hidden overlaps between eating disorders and sleep -wake disorders.

We want to understand what's actually happening to the body.

So if you are listening, consider this your one -on -one clinical tutoring session.

We are mastering Chapter 72, Other Psychiatric Disorders, from your primary care text.

I love that.

Yeah.

The physical, psychological, and systemic overlap between these conditions is just massive.

So we need to understand the foundational science before we even think about assessing a patient.

Like, what are these diseases and what is driving them?

Well, let's start with how the DSM -5 -TR categorizes the main eating disorders.

Anorexia nervosa, or AN, is fundamentally a restrictive illness.

Okay, so restricting intake.

Exactly.

The individual fails to maintain an expected body weight and experiences the severe disturbance regarding their body shape.

But the presentation isn't identical for everyone.

Right, because there are subtypes.

Yeah.

AN actually breaks down into two subtypes.

Right.

You have a purely restrictive type and then a binge -eating, purging subtype.

Wait, hold on.

If an anorexia patient is binging and purging, how do you distinguish them from a patient with bulimia nervosa?

That sounds like the exact same behavior.

That is such a great distinction to make.

It comes up all the time.

The primary clinical divider is body weight.

Oh really?

Bulimia nervosa is characterized by binge -eating, followed by compensatory mechanisms like self -induced vomiting or excessive exercise.

But these patients generally maintain a weight that is normal or above normal.

I see.

Anorexia nervosa, on the other hand, strictly requires the patient to be at a significantly low body weight.

That makes perfect sense.

And then we have binge -eating disorder, or BIBI, which involves recurrent binge -eating episodes causing high levels of distress, but crucially without those compensatory purging mechanisms.

No purging in BIBI.

We also need to factor in avoidant restrictive food intake disorder, or ARFD, and then the catch -all category, OSFED,

other specified feeding or eating disorder for those who have severe symptoms but, you know, just don't quite meet the rigid criteria of the others.

The epidemiology here completely shatters a lot of dangerous clinical assumptions.

Oh, so?

Well, historically, there's this provider bias to picture eating disorders exclusively affecting young, thin, white females.

Right, that's the stereotype.

Exactly.

And while females do predominate overall,

ARFAD and BIDI actually see a much higher percentage of males.

Wow, okay.

Furthermore, BED usually presents later, in early adulthood, around age 25, whereas anorexia and bulenia typically peak earlier, in the mid -to -late teens.

We also really have to talk about the sheer lethality of these disorders.

Anorexia nervosa carries a suicide risk that is 31 times higher than age -matched peers.

31 times.

That is just staggering.

It is.

One in five individuals who die because of AN die by suicide.

That number is chilling.

Like, this isn't just about weight loss, this is a severe psychiatric emergency.

And the pathophysiology explains some of that severity.

We see a really complex interplay between genetics and the environment.

Like personality traits.

Yes.

Restrictive disorders like AN are heavily linked to personality traits like neuroticism, perfectionism, and negative emotionality.

It's this intense need for control.

That makes sense.

Conversely, the binge and purge disorders are biologically linked to impulsivity and negative urgency.

Think of ARA or D though.

It's completely different.

It really is.

It's less like a body image issue and more like an intense sensory phobia or a trauma response.

That's a great way to put it.

Imagine a child who had a terrifying choking incident and now their nervous system is just absolutely terrified to swallow solid food.

Or someone with such an extreme sensory aversion to the texture of food that they literally cannot eat it.

Exactly.

They aren't trying to conform to a thin ideal, they are just avoiding the food itself.

Which of course still leads to severe life -threatening nutritional deficits.

And those nutritional deficits manifest vividly in the exam room.

When we look at Table 72 .1, the clinical presentation and physical science, I mean every single organ system is affected.

Every single one.

When the body is starved, it enters a state of physiological panic.

Cardiovascularly we see profound bradycardia.

Because the body is literally consuming its own cardiac muscle for energy, the heart rate drops because the heart itself is being starved.

Exactly.

It's breaking down muscle tissue.

We also see hypotension and a dangerously prolonged QT interval on the ECG.

Why the prolonged QT?

That happens because electrolyte imbalances, especially low potassium, from purging or pour intake delay, the electrical reset of the heart,

which can directly trigger sudden cardiac death.

Wow.

And what about the GI tract?

Gastrointestinally, the system just slows way down to extract every possible nutrient.

This leads to delayed gastric emptying and severe constipation.

There are also telltale physical signs you have to actively hunt for during your physical exam.

Oh, absolutely.

You're looking for Russell sign, which are these abrasions or calluses on the knuckles from repeated self -induced vomiting.

Right.

From the teeth scraping the skin.

Exactly.

You might also see lanugo, which is that fine downy hair the body grows.

Since it has consumed all its insulating fat, the body desperately tries to grow hair to prevent hypothermia.

It's a survival mechanism.

Yeah.

You also want to check for parotid gland swelling.

That gives the cheeks a puffy appearance because the salivary glands are chronically inflamed from the acid of vomiting.

To capture all this, your assessment components, laid out in box 72 .2, must be meticulous.

Meticulous is the word.

You must take orthostatic vital signs.

You are checking for a pulse increase of more than 20 beats per minute or a blood pressure drop of 20 millimeters of mercury when the patient moves from lying to standing.

And what does that tell us?

It reveals severe autonomic dysfunction and fluid volume deficit.

You also need a 24 -hour dietary recall and a full comprehensive lab workup.

So CBC, electrolytes.

Whip or thyroid function tests and definitely that ECG.

You can also utilize screening tools, right?

Like the SGAF questionnaire or the ET26 to help identify potential cases in primary care.

Yes.

Those are excellent.

But let's pause here because there's a massive misconception when it comes to prioritizing safety.

Oh, this is so important.

Right.

If a patient comes in and their absolute weight or BMI falls in the normal range, but they've been rapidly losing weight,

a provider might just brush it off.

Why can't we just rely on BMI to decide if someone is sick enough to hospitalize?

That oversight literally costs lives.

Rapid weight loss and starvation behaviors damage organ systems regardless of the patient's starting weight.

Regardless of the starting weight.

Exactly.

A patient might have a statistically normal BMI, but be suffering from severe hypokalemia that could trigger a lethal arrhythmia that very afternoon.

So we have box 72 .1, the criteria for medical hospitalization, and these are based on hard physiological limits.

Yes, hard numbers.

You hospitalize if their BMI is less than or equal to 75 % of the median for their age and height.

You hospitalize if their resting heart rate is below 50 beats per minute or if their blood pressure is less than 90 over 45.

Very clear cutoffs.

Severe electrolyte balances,

a prolonged QT on their ECG, or acute food refusal for 24 hours all mandate immediate medical hospitalization.

Your goal in primary care is to stabilize their failing organs so they can eventually be transferred to psychiatric care.

Right.

And once they are medically stable, we move into diagnostic reasoning.

Synthesizing this data to make a definitive diagnosis requires ruling out medical mimics first.

Like what?

Hyperthyroidism, GI malignancies, or conditions like Prader -Willi syndrome, which causes uncontrollable

hyperphagia.

All of those need to be off the table.

Okay, that makes sense.

You also have to rule out psychiatric mimics like schizophrenia, where a patient might refuse food due to paranoia or severe substance use disorders.

Once those are ruled out, it basically comes down to splitting clinical hairs.

We established earlier that anorexia nervosa and bulimia nervosa cannot be diagnosed concurrently.

Correct.

The weight criterion makes them mutually exclusive.

But we also need to clearly define what a binge actually is for the BN and BED diagnoses.

I mean, a binge isn't just having three massive helpings at Thanksgiving.

No, not at all.

The sheer volume of food matters.

But the defining diagnostic hallmark is the profound loss of control.

The loss of control.

Yes.

The patient feels like they are physically and psychologically incapable of stopping.

And to meet the severity markers for a formal diagnosis, bulimia nervosa and binge eating disorder require these behaviors to occur at least weekly for a continuous three -month period.

So where does atypical anorexia fit into this?

We mentioned OSFED earlier, the other specified feeding or eating disorder category.

What makes atypical AN different from regular AM?

It goes right back to our discussion on BMI.

Atypical AN features all the intense fears of gaining weight, the severe restrictive behaviors and the profound body image distortion seen in classic anorexia.

But the weight is different.

Exactly.

The only difference is that the patient's weight falls within or above the normal weight range.

But make no mistake, their organ systems are still failing and their psychiatric distress is just as lethal.

Okay, with the diagnosis locked in, we have to look at evidence -based management.

As an advanced practice nurse, you are coordinating a multidisciplinary treatment plan.

First, you determine the level of care.

Why?

Intensive outpatient, or IOP,

involve therapy a few days a week.

Partial hospitalization, PHP, is more robust, usually Monday through Friday for most of the day.

And then there's residential.

Yes.

Residential care means the patient lives at an unlocked facility 247 for extended psychological rehabilitation.

And, inpatient, as we discussed, is strictly for acute medical or psychiatric stabilization.

Now, for prescribers, the pharmacological management of eating disorders is highly nuanced.

Medications are largely adjunctive.

Not the main event.

Right.

For Blemian rosa, floxatine is the only FDA -approved medication.

It is remarkably effective at reducing the frequency of binge eating and purging episodes.

For binge eating disorder, lisaxamphetamine is the first FDA -approved drug, helping to curb that impulsive drive.

But prescribing for anorexia and rosa is a completely different landscape, isn't it?

It is deeply frustrating clinically.

SSRIs are generally ineffective in patients with severe anorexia.

Wait, really?

Why?

Think about the biochemistry.

Serotonin is synthesized from tryptophan, which is an amino acid we get from dietary protein.

Oh, wow.

If a patient is starving, they simply don't have the building blocks to make serotonin.

And SSRI cannot inhibit the reuptake of a neurotransmitter that isn't there.

That is wild, but it makes total biological sense.

So what do you use?

Often, providers turn to olanzapine, a second -generation antipsychotic used off -label.

It helps promote weight gain and, crucially, reduces the rigid, obsessional thinking around food.

Good to know.

Are there any absolute no -go's?

Yes.

One absolute contraindication to remember, tricyclic antidepressants, or TCAs, they cause significant weight gain, making them a disastrous choice for a patient who is already terrified of gaining weight.

Oh, yeah, that would backfire horribly.

And for ARFID, just as a side note, there are currently no FDA -approved medications at all.

That puts a huge emphasis on non -pharmacological interventions.

Cognitive behavioral therapy, CBT, is first line for adults with BN, BE, and ARIFID.

But for adolescents with anorexia, family -based therapy, or FBT,

is the gold standard.

And this isn't just like family counseling.

No, it's very intensive.

Right.

It is a highly structured intervention where the parents initially take complete, systematic control over meal serving and supervision.

They sit at the table and ensure every single bite is consumed until the adolescent's brain is nourished enough to gradually resume control.

It really highlights how severe the cognitive impairment of starvation actually is.

The adolescent literally cannot make rational choices about food, so the parents must function as their external prefrontal cortex.

Before we transition, I have a practical clinical question for you.

If a patient with an eating disorder hasn't had a period in months due to severe malnutrition,

my instinct as a provider might be to prescribe oral contraceptives to induce a cycle and protect her bone health.

Should I do that?

Firmly no.

No.

Unless she specifically requires it for pregnancy prevention, you never prescribe oral contraceptives just to induce a bleed.

Why is that?

Spontaneous resumption of menses is the most crucial, objective, physiological marker of recovery and weight restoration.

If you artificially induce bleeding with hormones,

you completely mask that vital clinical sign, and you falsely reassure both the patient and the treatment team.

That is a massive clinical pearl.

Thank you for that.

Now, the bridge connecting the first half of Chapter 72 to the second half is homeostasis.

Yes, the 24 -hour cycle.

Exactly.

Mental health, physical recovery, and hormone regulation rely entirely on the 24 -hour circadian rhythm.

If the circadian pacemaker is misaligned, everything else just crumbles.

Understanding the pathophysiology of sleep architecture is essential here.

Normal sleep continuously alternates between non -rapid eye movement NREM and rapid eye movement REM cycles.

And those occur pretty predictably, right?

Yes.

These cycles occur roughly every 90 to 100 minutes.

NREM is broken into four stages, with stages three and four being your deep, restorative, slow -wave sleep.

I always think of normal sleep architecture like a washing machine.

Okay.

I like that.

You have the soak, the wash, the rinse, the spin.

If you keep opening the lid and interrupting the cycle, the brain never gets that deep clean of slow -wave and REM sleep.

And that lack of a deep clean leads directly to severe cognitive impairment, mood disturbances, and profound fatigue.

Which perfectly leads us to the diagnostic criteria for insomnia disorder.

We are looking for specific symptoms.

Difficulty falling asleep, difficulty staying asleep, or early morning awakening.

And how frequently.

Occurring at least three nights per week for at least three months.

Crucially, it must cause significant daytime distress or impairment.

The assessment phase here requires hunting for the sleep thief.

The patient needs to keep a detailed sleep diary for two to four weeks to uncover underlying medical or psychiatric triggers.

That sleep diary is non -negotiable.

Right.

Is it G or E that worsens when they lie down?

Is it chronic joint pain?

Or is it a psychiatric cause like generalized anxiety or depression keeping their nervous system in overdrive?

Once you identify insomnia, the first line management is entirely non -pharmacological.

It's CBTI or cognitive behavioral therapy for insomnia.

What does that actually look like for the patient?

This involves sleep restriction therapy, where you deliberately limit the patient's time in bed to their actual sleep time to consolidate their rest.

It also involves strict stimulus control, teaching the brain that the bed is exclusively for sleep and sex.

So that means enforcing strict sleep hygiene, outlined in box 72 .7, keeping the room dark, maintaining a regular rise time seven days a week, regardless of how poorly they slept.

Consistency is key.

And implementing the 20 -minute rule.

If they are awake in bed for 20 minutes, they must get up, leave the room, and do a quiet non -stimulating activity until they feel sleepy enough to try again.

You cannot force sleep.

You really can't.

But when lifestyle modifications fail, prescribers must turn to the pharmacological guidelines in drug chart 72 .1.

And you have to navigate these drug classes with extreme caution.

For sure.

Let's look at the benzodiazepines first.

We know these carry heavy risks for older adults.

Fallers, confusion, rebound insomnia.

But if a provider must use one, the prescribing guidelines differentiate them by their metabolic pathways.

Tamazepam is an intermediate acting option with no active metabolites.

It does its job and leaves the system, making it a safer choice for older adults.

Comparatively safer, yes.

Conversely, flirzipam is long -acting with active metabolites that accumulate in the body, causing dangerous morning grogginess and a massive fall risk.

You avoid flirzipam in the elderly.

Definitely.

Then we have the benzodiazepine receptor agonists, commonly known as the Z drugs.

Their utility depends entirely on their half -life.

How so?

Well, zeleplon has a very short half -life of about one hour.

It is fantastic if the patient simply has trouble initiating sleep, but it won't help them stay asleep.

Right, they'll just wake up at 2 a .m.

Exactly.

Azopaclone, on the other hand, has a longer half -life of around 6 hours.

It is excellent for sleep maintenance, but you must strictly advise the patient to dedicate at least 8 solid hours to sleep.

Otherwise, they will experience severe next -day impairment.

The guidelines also highlight alternative mechanisms.

Rymelteon is a melatonin receptor agonist.

It promotes sleep onset by mimicking the body's natural hormone without the risk of withdrawal or rebound insomnia.

Which is great.

Yeah.

And suvarexant is an orexin receptor antagonist.

It essentially turns off the brain's wakefulness pathway, and it works much faster if taken on an empty stomach.

However, the safety warnings on these medications cannot be overstated.

Both the Z drugs and suvarexant carry a significant black box level risk for complex sleep -related behaviors.

We're talking about sleepwalking.

Far more extreme than just walking.

Patients have driven cars, cooked entire meals on a hot stove, binged on food, and made coherent phone calls while completely neurologically asleep, with absolutely no memory of it the next morning.

That is terrifying.

You must comprehensively educate your patients about this risk before they take that first pill.

Now, we know depression is the most common psychiatric comorbidity with chronic insomnia.

If a patient presents with both, does a provider treat the insomnia first so they have the energy to fight the depression or tackle the depression to fix the sleep?

You target them concurrently.

That yields the best clinical results.

Okay, both at once.

Yes.

In advanced practice, you often utilize an antidepressant that possesses sedating properties like mirtazapine or trazodone to effectively treat the mood disorder and the sleep disturbance simultaneously.

Let's finish up with restless leg syndrome, or RLS.

This often gets confused with insomnia because it ruins sleep, but it is distinctly different.

RLS is a neurological sensorimotor condition.

The clinical presentation is an uncontrollable urge to move the legs, usually accompanied by deeply uncomfortable crawling, burning, or tingling sensations.

How does a provider distinguish RLS from just positional discomfort or, say, a severe muscle cramp?

A muscle cramp is a sudden localized painful spasm.

RLS is a systemic sensory discomfort that demands motor activity for relief.

Okay, so movement is the key.

Yes.

The defining diagnostic trait is the absolute urge to move the legs to relieve that strange crawling sensation.

It dramatically worsens at night or when the patient is at rest, which destroys their ability to initiate the sleep cycle.

But the sensation is temporarily relieved the moment they start walking or stretching.

The pathophysiology is fascinating because it's driven by dopaminergic dysfunction in the brain.

But clinically, it is heavily exacerbated by low iron levels.

Which means your management plan must start with a blood draw.

Check their serum ferritin and iron levels immediately.

Just check the iron.

Absolutely.

If those are low, simply supplementing iron can sometimes resolve the RLS entirely.

And if they need meds?

If pharmacological treatment is required, the FDA -approved first -line medications are dopaminergic agents, primipaxol and ropinerol, typically taken one to three hours before bedtime.

Non -pharmacological management includes warm baths, aggressive massage, and strict adherence to sleep hygiene.

Wow.

We have covered massive ground today.

From the intense pathophysiology and physiological fallout of eating disorders to the precise metabolic management of insomnia and RLS.

It is dense material, no doubt.

But understanding the biological why behind these symptoms and treatments is what separates an adequate prescriber from an excellent advanced practice provider.

Completely agree.

And before we close, I want to leave you with a final thought to mull over.

Let's hear.

Considering the incredibly high rates of comorbid psychiatric disorders we see intertwined with both eating disorders and sleep -wake disorders, could mastering sleep architecture and repairing broken circadian rhythms actually be the untapped key to drastically improving recovery rates in severe eating disorders?

Oh, wow.

If the brain cannot get its deep clean, can it ever truly rewire its rigid, restrictive thought patterns?

It's a physiological connection that warrants deep exploration in your future practice.

Fix the foundational rhythm.

Fix the brain.

Well, you survived Chapter 72.

On behalf of the Last Minute Lecture Team, I want to explicitly thank you for joining us on this deep dive.

Thanks for listening.

We know how intense advanced practice nursing programs are, but you are putting in the vital work and it is going to pay off for your future patients.

We wish you the absolute best of luck on your exams and, more importantly, out there on the front lines in clinical practice, you've got this.

Keep diving deep.