Psych 1,2 - Depression, bipolar Flashcards
Describe the DSM 5 criteria for MDD, how many must be present for dx, and w/in what time period.
5/9 criteria present at least 2 wks (and represent change from previous functioning). Must include depressed mood and/or anhedonia. Depressed mood + PISS CAGE 1. Psychomotor agitation or retardation 2. Interest 3. Sleep 4. Suicide 5. Concentration 6. Appetite 7. Guilt 8. Energy
Causes significant impairment or distress in social, occupational, or other functioning
To dx MDD, the sx cannot be caused by __________ or __________.
- General medical condition
- Direct physiological effects of a substance/medication
What is the difference b/w mood and affect?
- Mood is what the patient states they are feeling in general
- Affect is what we observe at the moment
Mood:Affect::Climate:Weather
Which sex are more at risk for MDD?
Peak age of onset?
How much genetic risk is there?
Which races are more/less at risk
- Females (2x)
- 20-40 y/o
- Mod genetic risk
- Culture: lower in AA men; Asians; higher in Hispanic females; American Indians
What disease is often found in families w/MDD?
Alcoholism
Besides age and sex, name some other r/f’s for MDD.
- Single, divorced, widowed > married
- Major childhood traumas – loss, neglect, abuse
- Catastrophic events: deaths, losses, medical illness, etc
In MDD, how do the relapsing rates change w/increasing amounts of MDD episodes?
Is MDD chronic or acute in most people?
- 1 episode has 50% relapse rate
- If 2 episodes 70% relapse
- If 3 episodes 90% relapse
*chronic reoccurring illness in most
(Triggers to relapse are less over time)
What are the 3 phases of depression?
Acute, continuation, and maintenance
What are the 5 possible outcomes of tx to MDD?
Response, remission, relapse, recovery, recurrence
- Response: reduced sx
- Remission: no more sx, < 6 months
- Relapse: return of sx w/in 6 months
- Recovery: > 6 months w/o sx
- Recurrence: recovery, but then get sx again
What is the best biological biomarker we have for MDD?
Chronically elevated cortisol
chronic stress. greater neurodegeneration and less neurogenesis.
Just name the 4 major theories of depression.
Monoamine theory
Inflammatory theory
Structural theory
Network hypothesis
What is the monoamine theory of depression?
Low levels of NE, DA, and 5-HT (esp. 5-HT) in the brain.
What is the inflammatory theory of depression?
Low levels of chronic inflammation from either active illness (eg Lupus or CAD) or persistent heightened level of corticosteroids from “stress” produce a toxic inflammatory milieu where neurodegeneration increases and neurogenesis is inhibited. It is thought that IL-6, which interferes with 5-HT metabolism might be the main culprit. The cytokines that are involved also create disruption of other end organs and create higher risk for heart disease as well as Alzheimer’s. Hypersecretion of cortisol can cause acute and more severe depression (Cushing’s disease).
What is the structural theory of depression?
Depression is caused by abnormal changes in brain areas that can be identified premorbidly and are exacerbated in active illness. Atrophy of the prefrontal cortex, amygdala, and hippocampus, and enlargement of the insula and anterior cingulate cortex done via MRI suggest this. Enhancing neurogenesis in those areas that are atrophied (BDNF infusion into the rat hippocampus-quickly alleviated depression) or altering GABA (neuronal excitatory/inhibitory) in the insula are areas of exploration.
What is the network hypothesis of depression?
It is not specifically an altered brain area that causes depression but aberrancies in the tracts between areas. Diffusion tension imagery has revealed white matter abnormalities in the tracts between the medial PFC, amygdala, and hippocampus. Glucose activity is reduced in the hippocampus and dorsolateral PFC and increased in the amygdala, ventral striatum, and subgenual cingulated gyrus (an area that is stimulated in the new technique of deep brain stimulation). Sertoninergic agents reactivate a juvenile like plasticity in the neuronal tracts which if also stimulated by normal external phenomenon or psychotherapy leads to recovery. Depression is therefore a result of miscommunication and misinterpretation of various brain regions involved with
interpreting emotions. (can see abnormalities on PET)
What are some sequelae of untreated/undertreated depression?
- More Major Depressive episodes
- Other Psychiatric co-morbidity (60% of the time something is found)
- Cardiac events-CAD (cytokines – inflammation)
- Neurological events-strokes, seizures, Parksonism, Alzheimers
What are some psychological/other etiologies of depression?
- Aggression turned inward (Abraham)
- Object loss (Freud and Bowlby)
- Cognitive distortions (Beck)
- Self-esteem (Bibring)
- Environmental: poverty, deaths, wars, oppression, learned helplessness, infectious diseases, medical conditions, etc
These can explain why a person feels depressed but does it lead to MDD episode?
In what 3 general areas should you direct your approach towards treating depression?
Biological, psychological, social/environment
List medications that can mimic depression. (8)
Corticosteroids Oral contraceptives Antipsychotics Immunosuppressives Interferons Reserpine Isotretinoin (Accutane) Propranolol/B-Blockers
What infectious diseases can mimic depression? (6)
- Mononucleosis
- Tertiary syphilis
- Toxoplasmosis
- Influenza
- Viral hepatitis
- HIV
What endocrine disorders can mimic depression? (4)
- Hyper/hypoparathryoidism
- Hyper/hypothyroidism
- Hyper/hypoadrenocortical function (Cushing’s and Addison’s)
- Diabetes
What nutrition/metabolic disorders can mimic depression? (3)
- Uremia
- Pellagra
- Anemia
What neurological conditions can mimic depression? (8)
Frontotemporal dementia Parkinson’s Huntington’s Subdural hematoma Temporal lobe epilepsy Strokes MS Head trauma
What general types of neoplasms can mimic depression?
- Abdominal (particular pancreatic)
- Brain tumors
- Lymphomas
(likely due to inflammatory response to these)
Abuse of what substances can mimic depression?
(“Especially”) alcohol, heroin, marijuana or many prescribed psychotropics: benzodiazepines, opiates, antipsychotics
If you see the signs for MDD, is a full medical w/u necessary?
A Medical w/u is always a good first step – hx, PE, labs –even if the sx are quite definitive for MDD. If there is an underlying medical condition it is usually quite obvious from other s/s, but remember to come back to the depression.
“Whenever you hear hoof beats it’s most likely to be horses and not a Zebra”
In DSM 5, there is an attempt to add specifiers to diagnoses (like Major Depression) in order to better qualify them and possibly lead to different treatment – these include:
(just read them over a few times)
W/ anxious distress
W/ mixed features (anxiety and sadness)
W/ melancholic features (mood worse in AM, terminal insomnia, excessive guilt, marked weight loss, total lack of pleasure-anhedonia)
W/ atypical features (wt gain, over sensitive mood reactivity, oversleeping, leaden paralysis)
W/ mood congruent psychotic features- about 10% of episodes-(hallucinations and delusions that have depressive content)
W/ mood in-congruent psychotic features
W/ catatonia
W/ peripartum onset
W/ seasonal pattern (20% of those of us in Chicago’s latitude have an element of this)
Describe the DSM 5 criteria for persistent depressive disorder (formerly “athymia”), how many must be present for dx, and w/in what time period?
2 years of duration; has never been free of symptoms for longer than 2 months.
Depressed mood for most of the day on more days than not (course tends to be nonremitting).
Requires 2 of 6: CHESS A - Concentration (or indecisive) - Hopelessness - Energy (ie fatigue) - Sleep - Self-esteem - Appetite
No signs of other significant mental disorder that would explain symptoms.
Can pts w/persistent depressive disorder have overlying MDD?
Yes
Is PMS a real thing?
Yes, called PMDD: premestrual dysmorphic disorder
