Depressive disorders Flashcards
As opposed to normal sadness, what makes pathological sadness abnormal
Disproportionate to the situation or it’s unrelated to any specific event (just comes out of no where)
Sustained
Impairs function
Causes somatic complaints
Object Loss Theory (theory of what causes MDD)
Problems early in life make the person vulnerable to depression later.
The 1st stage of development is normal, which means they can form a normal relationship.
Then in the 2nd stage though, there’s a traumatic separation (usually from the mother)
Freud’s theory of what causes MDD
Aggression-turned-inward
It starts out the same as object loss theory: the child has a normal 1st stage of development, but then in the 2nd stage, there’s a traumatic separation.
The child is angry about the loss, but afraid to express it. The only safe way to express it is direct it inward. The child tells himself that he deserves the anger because he caused the loss somehow. He also feels guilt about the anger.
The depression comes out as an adult when they expect another loss will happen.
Cognitive Theory of what causes MDD
Things that happen early in life sensitize a person and causes them to respond to future stressors with depression.
Depressed people have a distorted world view, and think bad things will happen to them because there’s something wrong with them.
Learned Helplessness-Hopelessness theory of MDD
By Martin Seligman
It’s like cognitive theory but modified.
They have no control over what happens, so they just give up.
Biological theories of the cause of MDD
It’s possible there is a polygenic single nucleotide polymorphism (SNP) disorder
Having a depressed parent is the single strongest predictor of depression (the kids are 3x more likely to have MDD, and 40% chance of having an episode before age 18)
The earlier the depression starts, the worse the prognosis
Neurovegetative symptoms (sleep, eating, sex, energy) are related to the functioning of
the hypothalamus and pituitary, and the hormones they secrete
A high incidence of postpartum mood disturbances is suggestive of
endocrine dysfunction
Deregulation of the hypothalamic-pituitary-adrenal axis (theory of what causes depression)
HPA controls the physiological response to stress and consists of feedback pathways between the hypothalamus, pituitary gland, and adrenal glands.
MDD is caused by an abnormal response to stress.
When stressed, the hypothalamus releases corticotropin-releasing hormone, which stimulates the pituitary to release adrenocorticotropic hormone. This then stimulates the adrenals to release cortisol.
Hyperactivity of the HPA (and maybe elevated cortisol) is found in people with MDD.
Overtime, cortisol can actually damage the nervous system, including changing the size of the brain.
MDD can also be associated with proinflammatory cytokine activation
(fyi, this theory was why they used to do the dexamethasone test, but not anymore because it’s too nonspecific)
Neurotransmitter theory of MDD
besides 5HT, DA, and NE, this theory says MDD might be related to:
- low levels of endogenous catecholamines in specific brain areas
- low tyrptophan
- low level of the serotonin metabolite 5HTIAA
- receptor sensitivity is too high in certain areas (a stronger response from transmitters is needed)
- not enough receptors
- hypometabolism in certain brain areas
Structural brain changes theory of MDD
MDD people can have hypovolemic hippocampus and hypovolemic prefrontal cortex-limbic striatal regions
Also MDD is very common in people who had brain damage, from trauma or stroke.
Chronobiological theory of MDD
messed up circadian rhythms produces symptoms that are like MDD.
Statistics of MDD
5% of the population in the U.S.
It’s the leading cause of disability
Only 50% of MDD people get treatment
Over the life time, women have a 25% chance, men have a 12% chance
MDD is the greatest source of morbidity for women (more than any other illness)
15% of people with MDD die of suicide
MDD age of onset
mid 20s
If left untreated, an MDD episode usually lasts
4 months or longer
One year after the MDD diagnosis,
40% will still have enough symptoms to meet the dx
20% of clients don’t meet the dx anymore, but still have symptoms
40% have no symptoms
People with a first episode of MDD have a __% chance of another episode
60%
2 episodes = 70% chance of a 3rd
3 episodes = 80% change of a 4th
MDD risk factors
Female
Unmarried
EPDS
Edinburgh postnatal depression scale
MDD diurnal variation
low in the morning, better later on
MDD, the sleep disturbance is typically
middle or terminal insomnia
Weight changes in MDD
5% change (gain or lose).
Sometimes there’s craving for specific foods, like carbs
Bereavement
MDD symptoms that start within 2 months of the loss, and only last for 2 months
MDD assessment: Memory
impaired recent and short term
General guidelines for med treatment for MDD
Treat for a minimum or 6 to 12 months
If they have more than 2 episodes of MDD, continue the meds indefinitely
Not all symptoms will respond to medication
Stopping abruptly can cause rebound depression
TCA mechanism
elevate 5HT and NE
MAOI mechanism
elevate 5HT and NE
Citalopram
20 to 40 mg daily
Sedation, agitation, yawning, weight gain
Pregnancy category, Lactation L2
Warning about prolonged QTc interval in doses above 40 (or above 20 in older adults) and in those susceptible to prolonged QTc
Escitalopram
10 to 20 mg daily
Somnolence
Pregnancy C, Lactation L2
Fluoxetine
20 to 80 mg daily.
There’s a liquid form
Insomnia
Pregnancy C, Lactation L2
Fluvoxamine
SSRI
100 to 300 mg daily
Sedation, agitation
Doses above 150mg should be given BID
Pregnancy C, Lactation L2
Paroxetine
20 to 60 mg daily
Somnolence
Pregnancy category D!, Lactation L2
Discontinuation syndrome is a big problem
Sertraline
50 to 200mg daily
Somnolence
Pregnancy C, Lactation L2
Vilazodone
SPARI (serotonin paritial agonist reuptake inhibitor)
20 to 40 mg daily
Dry mouth
Pregnancy C, Lactation category is not established but we do know it’s excreted in the breast milk
Amitriptyline
50 to 300mg
Comes in IM form too
TCA
Used for chronic pain and insomnia
Pregnancy C, L2
Clomipramine
100 to 250
TCA
Approved for OCD
Seizures can occur if the dose goes over 250
Pregnancy C, L2
Desipramine
100 to 300 mg
TCA
Also used for ADHD in adults (and in kids off label)
Pregnancy C, L2
Doxepin
100 to 300 mg
TCA
Also used for insomnia
Pregnancy C, L5 (avoid!)
Imipramine
100 to 300
TCA
Also comes in IM
Used for enuresis and separation anxiety
Pregnancy D, L2
Nortriptyline
50 to 150 mg
TCA
Also used for enuresis and ADHD
Pregnancy D, L2
Protriptyline
15 to 60mg daily
TCA
Pregnancy C, L is unknown
Trimipramine
100 to 300 mg daily
TCA
Pregnancy C, L is unknown
SSRI pregnancy and lactation categories
Everything is Pregnancy C and L2 except:
Paroxetine is Pregnancy D
Pregnancy and lactation for TCAs
Most are Pregnancy C and L2
Imipramine and nortriptyline are Pregnancy D
Doxepine is L5
Protriptyline and trimipramine are L unknown
SARIs
Serotonin agonist and reuptake inhibitors
Trazadone and Nefazodone
Isocarboxazid
20 to 60 mg daily
MAOI
Also used for panic disorder, phobic disorders, and selective mutism
give BID or TID
Pregnancy C, L unknown
Phenelzine
45 to 90 mg daily
MAOI
Also used for panic disorder, phobic disorders, and selective mutism
give BID or TID
Pregnancy C, L unknown
Tranylcypromine
30 to 60 mg daily
MAOI
Also used for panic disorder, phobic disorders, and selective mutism
give BID or TID
Pregnancy C, L unknown
Selegiline
6 to 12mg daily
No dietary restrictions with the 6 mg dose, but 6 mg might not be high enough to be therapeutic
Pregnancy C, L4 (Avoid!)
SSRIs are first line for
MDD with mild to moderate symptoms
Side effects that are common to most TCAs
Anticholinergic: Dry mouth, blurred vision, constipation, memory impaired (from muscarinic receptor blockade)
Antiadrenergic: Orthostatic hypotension (from alpha 1 blockade)
Antihistaminergic: Sedation, weight gain
EKG changes (not safe if they have another cardiac disease)
Can induce hypomania in susceptible patients
TCA considerations
You can monitor blood levels (especially with nortriptyline)
They’re cheap
The anticholinergic effects can actually be helpful if they have bowel irritability
Don’t stop suddenly or you’ll have discontinuation syndrome
Let an SSRI washout for 2 weeks (5 with fluoxetine) before starting an TCA (although you can use both at the same time with caution)
MAOIs and hypertensive crisis
Hypertensive crisis happens when taken with foods with tyramine (a precursor for NE)
In addition to tyramine, other things can cause HTN: Meperidine Decongestants TCAs 2nd gens St John's Wort L-tryptophan Stimulants/sympathomimetics Asthma meds
Symptoms of a HTN crisis
Sudden explosive headache, usually occipital
Facial flushing
Pupils dilate
Fever
Treatment of HTN crisis from an MAOI
Give phentolamine (binds with NE receptors, blocks NE)
Stabilize the fever
Symptoms of serotonin syndrome
Agitation, restless Tachy and HTN Headache Sweating, shivering, goose bumps Myoclinic jerking and loss of coordination Confusion, fever, seizures, unconsciousness Altered sensorium Hyperreflexia Hyperthermia Chills Insomnia Autonomic instability
Treatment of serotonin syndrome
If it’s mild, you might carefully use benzos.
If it’s more severe, you’ll use cyproheptadine, anticonvulsants, and autonomic support.
Treatment of serotonin syndrome
If it’s mild, you might carefully use benzos.
If it’s more severe, you’ll use cyproheptadine, anticonvulsants, and autonomic support.
MAOI side effects
Insomnia
Weight gain
Anticholinergic effects
Sexual side effects
Venlafaxine
75 to 375 mg daily for immediate release
75 to 225 mg daily for XR
Needs to be above 150mg to be therapeutic
Sweating
Dizziness
Can raise BP
For the immediate release, give BID or TID
Pregnancy C
L3
Don’t stop suddenly (discontinuation syndrome)
Duloxetine
30 to 120mg
Dizziness
Can elevate BP
Can elevate LFTs
Don’t stop suddenly (discontinuation syndrome)
Pregnancy C, L3
Vortioxetine
20mg daily
Serotonin 3 and 7 antagonist, and serotonin 1A agonist
Dizziness
Pregnancy C, L is unknown
Levomilnacipran
40 to 120
SNRI
Constipation Sweating Palpitations Urinary hesitancy HTN or hypotension Decreased appetite
Pregnancy C, L is unknown
ECT theories of how it works
Do 6 to 12 treatments
Possibly increases DA, NE, 5HT
Possibly releases hormones like prolactin, TSH, pituitary, endorphins, and adrenocorticotropic hormones
Possibly has an anticonvulsant effect
Reasons for choosing ECT
Patient preference
Need for a quick response because the illness is severe
MDD with psychotic features
Treatment resistance
Possible contraindications for ECT
Cardiac disease Pulmonary disease Brain injury Brain tumor Anesthesia complications
ECT adverse effects
Cardiovascular effects
Systemic effects (headaches, muscle aches, drowsiness)
Cognitive effect
Burpropion
contraindicated in eating disorders
Pregnancy C, L3
With SR (not so much XL), use with caution with caffeine and panic disorder
Mirtazapine
alpha 2 and 5HT 2 antagonist
15 to 45
Increased cholesterol
The higher the dose, the less sedating
Pregnancy C, L3
Trazadone
Serotonin antagonist and reuptake inhibitor (SARI)
200 to 600 (but as a hypnotic it’s given at 50 to 200mg)
At the dose needed to have an antidepressant effect, it’s usually too sedating
Hypotension
Prolonged QTc
Pregnancy B, L2
Nefazodone
Serotonin antagonist and reuptake inhibitor (SARI)
300 to 600mg daily
Drowsiness
Very important to monitor LFTs because it can cause liver failure
QHS or BID dosing
Inhibits the P450 3A4
Pregnancy C, L4
TMS
Transcranial magnetic stimulation
The put a small wire in your scalp
Anesthesia is not used
40 minute sessions, 5 times a week, for 6 weeks
There are minimal side effects, but it can cause pain, tingling, twitches in the face, lightheadedness, hearing discomfort from the noise of the procedure. Seizures are rare, but have been reported
Vagal nerve stimulation
Pacemaker-like device placed in the chest.
Anesthesia is required, although it can be done outpatient.
It can cause voice changes, hoarseness, cough, throat/neck pain, chest spasm, dyspnea on exertion, tingling, and dysphagia
It’s intended to be used alongside other treatments
Phototherapy
2,500 to 10,000 lux light for 30 minutes up to 2 hours, 1 or 2 times a day
Brief Therapy (Solution focused therapy)
Focus on the stressor that started everything
Cope with the immediate impacts of MDD
Modify the environment
Risk factors for suicide
45 or older if male 55 or older if female Single/separated White Living alone Psyc illness Physical illness Substance abuse previous attempt Recent loss Male
MDD in children is similar to adults, but certain features tend to be pronounced
Irritability
Somatic complaints
Social withdrawal
Separation anxiety
Some symptoms are less common in children before puberty
Psychosis
Motor retardation
Hypersomnia
Increased appetite
Different medication classes for MDD kids
They respond well to SSRIs, but not TCAs
All antidepressants have a blackbox warning for kids
MDD in older adults
To distinguish between memory symptoms of MDD and symptoms of dementia, check if they had a premorbid cognitive slowing (dementia). With MDD, the cognitive changes will be acute.
Skill deficit is when they can’t perform a skill. Performance deficit is when they have the ability to perform a skill, but don’t have the motivation.
Components of a functional assessment
ADLs- bathing, eating, dressing
IADLs- instrumental activities of daily living, shopping, cooking, driving
Executive functioning- judgement, planning, maintaining a calendar, prioritizing
Some long term effects of SSRIs
Increased blood sugar levels
Hyperlipidemia
Elevated LFTs
SSRI discontinuation syndrome
Flu like Fatigue Myalgia Decreased concentration and memory N/V Paresthesias and "shocks" Irritable/anxious Insomnia Crying randomly Dizziness/vertigo
Risk factors for SSRI discontinuation syndrome
Irregular use pattern
High dose
Long term treatment
History of discontinuation syndrome
How long after remission of MDD should you take meds?
12 months
If you’ve had 3 or more MDD episodes, you need lifelong meds
Persistent depressive disorder (dysthymia)
Doesn’t have psychotic features
Doesn’t have neurovegetative symptoms like sleep and appetite problems
The mood occurs for most of the day, on more days than not
Low self esteem, feeling that you’re incompetent compared to others
Dysthymia in children
It’s equal among boys and girls
Only requires a 1 year history
Mood is often irritable instead of sad
Grief and Bereavement
Develops within 3 months of a stressor
If there are not other significant symptoms, it’s usually classified as adjustment disorder (with depressed mood, with disturbed conduct, etc)
Meds for Grief
Benzos
Nonbenzo hypnotics like zolpidem
TCAs
Antihistamines
Premenstrual dysphoric disorder
Symptoms usually start in the luteal phase, 1 week before the start of menses. The symptoms usually stop a day or two after menses starts
Symptoms may worsen when the patient is perimenopausal
Treatment can be SSRIs, hormonal contraceptives, or both