1. Secondary Depression
Etiopathogenesis &
management
Presenter:
Dr Angshuman
Kalita
Chairperson:
Dr Utpal Bora
Asst Professor
Deptt of Psychiatry
Date: 03/09/2014
2. Secondary depression is a depression in an
individual who has one or more pre-existing,
nonaffective psychiatric disorders or an
incapacitating or life-threatening medical
illness which precedes and parallels the
symptoms of depression.
Journal of Affective Disorders.1981; 3 :
25-35
3. Primary vs. secondary depression
In secondary, depression
emerges after the
medical illness.
In primary, the depressive
situation is already
established, with the medical
illness superimposed upon it
4. Secondary Depression
• For every 5 patients who are seen with a diagnosis of
depression, approximately 2 should be classified as
secondary
• The symptom picture of secondary depression is almost
indistinguishable from primary depression
5. MDD is estimated to occur in 4% of those with 1
or more medical conditions compared with 2.8%
of those without.
Medical illnesses may exacerbate or cause
depressive signs or symptoms through effect on
mood, neuroendocrine & immune funtion, self-care
abilities & social interaction which are
mediated through the patient’s premorbid
personality, ego defences & coping style
6. Inflammation as a cause of
depression
• Depression has been linked with activation of CMI since the early
1990s linking together the observations of increased HPA axis
activation & increased inflammatory response in depression.
• In recent studies IL 1a levels were found to significantly predict the
development of depressive symptoms at 3 & 6 year follow up
suggesting a causal role of inflammation in development of late life
depression
• Several studies have found increased IL-6 levels to be a strong
predictor of depression. The observation of a relationship between
hippocampal atrophy & high levels of IL-6 suggest an inflammatory
mechanism for hippocampal volume loss in depression
7. • Several studies have suggested that
depressed patients have shorter telomeres
than age matched controls suggesting a
relationship between depression & more
rapid cellular aging
9. Features of Schizophrenia
Positive symptoms
- Delusions
- Hallucinations
- Disorganization
Cognitive deficits
Functional Impairments
Work
Interpersonal relationships
Self-care
Negative symptoms
- emotional range
- expression of
emotion
- motivation/drive
- interests
- social drive
- poverty of speech
Mood symptoms
Disorganization
- speech
- behavior
10. Depressive Symptoms
– Primary to schizophrenia
– “Reactive”
• psychosis is frightening
• reality of illness is demoralizing
– Co-morbid disorder
• major depressive episode
11. 1. Depression in the recovery stage from disturbance
of consciousness
• Disturbance of consciousness caused by head trauma,
encephalitis, or other central nervous system disorders may
lead to depression which can for several weeks or months.
• Symptom Patterns
Depressive mood combined with amnestic symptoms
Marked anxiety and delusion
Irritability and impaired social functioning
Excessive or inappropriate guilt under depressive mood
Hallucination and delusion
JMAJ.2001; 44 : 279–282
12. 2. Depression in Neurological Disease
(a.) Depression in cerebrovascular disorder
• In chronic cerebral vascular insufficiency, affective
symptoms such as affective incontinence, depression,
impatience, irritability, and affective flattening may occur
JMAJ.2001; 44 : 279–282
13. • Studies on depression secondary to focal brain lesions have
indicated that frontal lobe damage, especially in the
dominant hemisphere, is associated with an increased
likelihood of developing depression.
• Robinson et al demonstrated that depression was likely to
occur after a stroke affecting the left hemisphere,
especially in the left frontal area.
• Among the frontal regions, the prefrontal and paralimbic
frontal areas, especially on the left side, have been
repeatedly pointed out to be the most crucial sites.
• Baxter et al demonstrated that depressive patients
(unipolar depression and bipolar depression) had a glucose
hypometabolism in the bilateral anterolateral prefrontal
cortices and that the severity of depression correlated with
a decrease in glucose metabolic rate & decrease in blood
flow in both areas
14. 2. Depression in Neurological Disease
(b.) Depression in Alzheimer’s disease
• It is frequent for affective symptoms such as depressive
mood, decreased spontaneity, affective lability, affective
flattening, and anxiety/impatience to occur as prodromal
symptoms of dementia in the early stage of Alzheimer’s
disease.
• In these cases, anxiety, depressive mood, behavioural
retardation, and inactivity are common, whereas feelings
of guilt, suicidal ideation, and secondary delusion are rare.
JMAJ.2001; 44 : 279–282
16. • Depression may occur at any time during the course
of PD and may occur even before the motor features.
• Depression occurs in 40 to 50% of persons with PD
at some time in their illness, 5-20% moderate to
severe
17. DEPRESSION IN
PARKINSON’S DISEASE
•Characterized by:
Feeling of guilt
Lack of self esteem
Loss of initiative
Helplessness, remorse, sadness
18. Depression in PD: how common is it and what
are the outcomes
• Associated with increased disability
• Associated with impaired quality of life.
• Tends to be under recognized and under treated in
patients with PD
– As many as 40% of depressed patients are
not treated or not referred for treatment
WHY ???
19. Why is Depression in PD under recognized?
• Major depression and Parkinson’s disease share
common symptoms.
• Depression may be confused with other conditions such
as dementia and apathy.
• Patients may be hesitant to bring up depressive
symptoms to their doctor.
20. Depression in PD: symptoms
• Compared to non-PD depressed patients:
– More:
• anguish, anxiety, irritability,
• pessimism regarding the future,
• suicidal ideation
– Less:
• guilt, self blame,
• feelings of failure,
• suicide
• Low incidence of delusion & hallucination
•Lack of diurnal variation
21. What causes depression in PD?
cause of depression in PD is unknown
The loss of mesocortical & mesolimbic dopamine connections to the
frontal lobe & disruption of monoaminergic afferent from the
mesencephalon has been implicated in pathogenesis of depression in PD
on the basis of reduced brain serotonin, nigral & ventral tegmental area
dopamine & locus ceruleus norepinephrine in patients who die from PD
Loss of these brainstem monoaminergic neurons, with degeration of their
respective cortical & subcortical projection, is a plausible mechanism of
depression in this patients
22. 2. Depression in Neurological Disease
(d.) Depression in other neurologic diseases
Following neurodegenerative diseases may be complicated by
depression:
• Huntington’s disease
• Progressive supranuclear palsy,
• Fronto-temporal lobe dementia
• Neurosyphilis, toxic diseases,
• pellagra, folic acid deficiency, and Wernicke’s encephalopathy
JMAJ.2001; 44 : 279–282
23. Depression as a symptom of dementia
• Depression has been noted to occur in patients
with a previously diagnosed dementia or MCI
suggesting that depression could be considered
one of the many “ behavioral & psychological
symptoms of dementia”(BPSD). Depressive
symptoms in patients with dementia have been
linked with frontal & parietal white matter hyper
intensities
24. Depression after traumatic brain injury
Depressive disorders are the most common
neuropsychiatric sequels of traumatic brain injury
Cases in which depressive disorder develop in the
late post injury period , psychological & social
factors appears to be etiologically important
25. Depression in medically ill patients
• Depression in medically ill patients is first &
foremost a phenotype. Many underlying etiologies
may take a final common pathway of producing
such a phenotype, but have divergent implications
for prognosis and management. Thus appropriate
management requires first establishing the most
likely diagnosis that has caused depression
28. • Highest rate of depression is seen those who
are oxygen dependant
29. Etiopathogenesis
Loss of independence
Inability to carry out previous activities,
Social isolation may play a role in the
depression these patients experiences
Many patients have temporary depressive
symptoms during COPD-related exacerbations
that resolve once their respiratory symptoms
improve
30. • Awareness of the effects that medications
used for depression & COPD have on each
illness must be maintained.
– Corticosteroid used in the treatment of COPD
may cause depressive symptoms.
– Oral theophyllines, may disrupt sleep in
depressed patients with COPD
31. • Decreased appetite
• Sleep disturbances
• Lack of energy
• Poor memory & concentration
• Weight loss
• Lack of confidence
• Feelings of hopelessness
It is difficult to decide when these
symptoms are secondary to
depression and when they are
secondary to COPD
Respirology. 2012; 17: 627-38
32. • As symptoms of depression & COPD may
overlap, care must be taken to avoid
mistaking symptoms of worsening COPD
for depression & vice versa, but sustained
depressed mood or anhedonia should not
be attributed to lung disease alone
33. Cognitive behavioral therapy
• Low intensity intervention for mild to
moderate depression
• High intensity intervention in combination
with medication for moderate to severe
depression
Pulmonary Rehabilitation:
• Evidence confirms reduction of depressive
symptoms with this therapy
Pharmacological treatment
• Despite the lack of rigorous evidence,
pharmacological therapy is the most
common treatment of depression in COPD
Respirology. 2012; 17: 627-38
34. SSRIs
considered the
first-line agents
for control of
depression
symptoms in
patients with
COPD
Venlafaxine or mirtazapine are useful for
patients who are non responsive to SSRI
Weight gain was a side-effect with long term use of
Respirology. 2012; 17: 627-38
ADs.
It may be of particular benefit in patients with severe COPD,
low BMI and poor prognosis
36. • Depressed individuals are more likely to have
conventional cardiac risk factors:
– Hypertension, high cholesterol, diabetes,
obesity
– Maladaptive health behaviours like smoking,
unhealthy diet, physical inactivity and medical
non-adherence
• Heart disease can also precipitate depression:
– Post-MI, Acute Coronary Syndrome,
Congestive Heart Failure
Curr Psychiatry Rep. 2010; 12: 255-64
37. • Since the 1970s,studies have delineated a
link between depression & Cardiovascular
disease and mortality.
• Studies also indicate that 16%-18% of
patients after an acute MI are affected by
MDD. A total of one third will experience
depression during the 1st year, especially in
first 6 months
38. • An estimated 15%-23% of those with established
IHD may have MDD & depression in this
population conveys a three to four fold increase in
subsequent CVS morbidity & mortality
• The Rotterdam study found that subjects age 60
years & older with atherosclerosis correlated with
higher depression rating scores
39. • The past decade has provided increasing
evidence for a “vascular depression”. It has
also been described as a depression–executive
dysfunction syndrome
• Characterized by
– psychomotor retardation,
– greater anhedonia,
– impaired verbal fluency & visual naming &
– poor performance on task of initiation &
perseveration
• It is associated with less family history, greater
functional disability & perhaps worse
treatment outcomes
40. Behavioural mechanisms linking depression and heart
disease - I
Mechanism Comment Effect on heart disease
Sleep disturbance Common in depression; may
be exacerbated by heart
disease symptoms
Leads to autonomic
hyperactivity which is linked to
obesity, diabetes,
hypertension, and the
metabolic syndrome
Physical inactivity Common in depression Increases cardiovascular
morbidity and mortality
Cigarette smoking Individuals with depression
are more likely to smoke, and
depressed smokers are less
likely to quit
Increases cardiovascular
morbidity and mortality
From Ziegelstein RC, Elfrey MK. Behavioural and psychological mechanisms linking depression and
heart disease. In: Depression and Heart Disease. Glassman AH, Maj M, Sartorius N (eds). Chichester:
Wiley, 2010.
41. Behavioral mechanisms linking depression and heart disease
- I
Mechanism Comment Effect on heart disease
Poor hygiene Inattentiveness to self care is
more common in depression;
depression is associated with
decreased salivary flow and
cariogenic diet.
Periodontal disease (especially
gingivitis) has been associated
with increased cardiovascular
morbidity and mortality
Adherence to treatment Patients with depression are
less likely to adhere to medical
therapy and risk reducing
behaviors
Poor adherence to medical
therapy is associated with
increased cardiovascular
morbidity and mortality
From Ziegelstein RC, Elfrey MK. Behavioural and psychological mechanisms linking depression and
heart disease. In: Depression and Heart Disease. Glassman AH, Maj M, Sartorius N (eds). Chichester:
Wiley, 2010.
42. Psychological mechanisms linking depression and heart
disease - II
Mechanism Comment Effect on heart disease
Attitudes about treatment Depression may be associated with
negative attitudes toward
treatment. Individuals with
depression may perceive more, and
have greater concern about,
medication side effects
Attitudes about treatment appear
important to therapeutic effect;
even poor adherers to placebo in
cardiovascular disease trials have
increased mortality
Social isolation Depression is associated with less
social support and greater social
isolation
Decreased social support and social
isolation are associated with
increased cardiovascular morbidity
and mortality
From Ziegelstein RC, Elfrey MK. Behavioural and psychological mechanisms linking depression and
heart disease. In: Depression and Heart Disease. Glassman AH, Maj M, Sartorius N (eds). Chichester:
Wiley, 2010.
43. Psychological mechanisms linking depression and heart
disease - II
Mechanism Comment Effect on heart disease
Cardiovascular stress response Some studies show that depression
is associated with heightened, and
some with attenuated,
cardiovascular reactivity to
physiological stress
Autonomic hyperactivity at baseline
and in response to stressors may
increase cardiovascular risk
Self-efficacy Depression is often associated with
low self-efficacy
Low self-efficacy is associated with
greater symptom burden and
physical limitation; worse quality of
life; poor adherence; and possibly
increased cardiovascular morbidity
and mortality
From Ziegelstein RC, Elfrey MK. Behavioural and psychological mechanisms linking depression and
heart disease. In: Depression and Heart Disease. Glassman AH, Maj M, Sartorius N (eds). Chichester:
Wiley, 2010.
44. Biological mechanisms possibly underlying the
association between depression and heart disease
• Autonomic nervous system dysregulation (low heart rate variability is a powerful predictor of
mortality in patients with coronary heart disease; depressed patients have a decreased heart
rate variability than non-depressed controls).
• Blood clotting and endothelial dysfunction (depression is associated with enhanced platelet
activation, increased plasma levels of pro-thrombogenic factors and reduced endothelial
dependent vasodilatation).
• Inflammation
• Neuroendocrine abnormalities (depression is associated with an increased activity of the
hypothalamic-pituitary-adrenal axis, with a consequent overstimulation of the sympathetic
nervous system).
From Monteleone P. The association between depression and heart disease: the role of biological mechanisms. In:
Depression and Heart Disease. Glassman AH, Maj M, Sartorius N (eds). Chichester: Wiley, 2010.
45. • Exact etiopathogenesis remains unclear
• Vascular disease may contribute to
depression by affecting sub cortical
structures involved in mood regulation & the
white matter pathways that connect these
structures to the frontal cortex
• Increased activity by 5-lipoxygenase has
been proposed as a common mechanism for
atherosclerosis & depression
46. Role of genetic factors in explaining the
association between depression and heart
disease
• Twin and family studies provide evidence for a role of genetic pleiotropy in the
association between major depression and coronary heart disease (i.e., genetic
variants influence risk factors that independently increase the risk for both
major depression and coronary heart disease). The actual genetic variants at
the base of this pleiotropy remain to be detected.
From de Geus E. The association between depression and heart disease: the role of genetic factors. In: Depression
and Heart Disease. Glassman AH, Maj M, Sartorius N (eds). Chichester: Wiley, 2010.
47. Antidepressants in post-myocardial (MI)
infarction
• (SSRIs) are safe in the immediate post-MI period and are effective
antidepressants.
• There is strong suggestion that antidepressants in general, and SSRIs in
particular, reduce morbidity and mortality in post-MI depressed patients.
From Glassman AH, Bigger JT. Depression and cardiovascular disease: the safety of antidepressant
drugs and their ability to improve mood and reduce medical morbidity. In: Depression and Heart Disease.
Glassman AH, Maj M, Sartorius N (eds). Chichester: Wiley, 2010.
48. Recognition and management of depression
in post-myocardial infarction (MI) patients
• Post-MI patients should be screened for the presence of depression by a
simple well-validated instrument
• When a patient screens positive for depression, a primary care provider
familiar with managing depression should follow and support him/her,
with the regular supervision by a psychiatrist.
From Glassman AH, Bigger JT. Depression and cardiovascular disease: the safety of
antidepressant drugs and their ability to improve mood and reduce medical morbidity. In:
Depression and Heart Disease. Glassman AH, Maj M, Sartorius N (eds). Chichester: Wiley, 2010.
49. Recommendations for clinicians providing care
for patients with comorbid depression and heart
disease - I
• Sleep. Ask your patients about their sleep habits.
• Physical activity. Strongly encourage your patients to exercise at home and to
become involved (and stay involved) in structured exercise programs.
• Cigarette smoking. Ask every patient whether he/she smokes, and counsel about
smoking cessation if appropriate.
From Ziegelstein RC, Elfrey MK. Behavioural and psychological mechanisms linking
depression and heart disease. In: Depression and Heart Disease. Glassman AH, Maj M, Sartorius N
(eds). Chichester: Wiley, 2010.
50. Recommendations for clinicians providing care
for patients with comorbid depression and heart
disease - II
• Medication adherence. Specifically address the issue of medication adherence
with every patient and try to decrease barriers to adherence.
• Attitudes and beliefs about cardiac treatment regimens. Discuss the importance
of each medication, what the goals of treatment are, and how the patient’s
particular health goals are more likely to be achieved by adhering to a particular
medical treatment.
From Ziegelstein RC, Elfrey MK. Behavioural and psychological mechanisms linking
depression and heart disease. In: Depression and Heart Disease. Glassman AH, Maj M, Sartorius N
(eds). Chichester: Wiley, 2010.
51. Recommendations for clinicians providing care
for patients with comorbid depression and heart
disease - III
• Social isolation. Encourage patients to socialize with family and friends,
encourage the patient to participate in group activities that may be
appropriate and desirable
• Self-efficacy. If the patient’s confidence is low, consider specific
counseling that might enhance self-efficacy.
From Ziegelstein RC, Elfrey MK. Behavioural and psychological mechanisms linking
depression and heart disease. In: Depression and Heart Disease. Glassman AH, Maj M, Sartorius N
(eds). Chichester: Wiley, 2010.
52. HYPERTENSIO
N
• SNRIs increase BP mildly. it is
because of Drug-drug interactions
between antihypertensive
medications and ADs
Hypertension induced due to treatment with SNRI may
respond by lowering the dose.
59. DIABETES
• Strict monitoring of blood glucose
is required
• Use of TCAs may be associated
with worsened glycemic control
SSRIs preferable to TCAs in patients with diabetes.
ADs and psychotherapy may be used in combination to
reduce depressive symptoms and to attain glycemic control.
Diabetes Research and Clinical Practice. 2010; 87: 302-312
61. Hypothyroidism and Depression
• Depressive symptoms are common in
hypothyroidism
• Many hypothyroid patients fulfill DSM-5 or
ICD10 criteria for a depressive disorder
• Depressed patients may be more likely
than normal individuals to be hypothyroid
• All depressed patients should be evaluated
for thyroid dysfunction
61
63. Thyroxine in Depression
1. Thyroxin therapy is recommended for
patients with depression who have
persistently elevated serum TSH
2. Antidepressants may be less effective if
thyroid function not normalized
63
64. • More than 70% of men older than 70 years
have free testosterone levels consistent with
hypogonadism. Decreased levels of
testosterone in men are associated with
depression, fatigue, hot flushes, sweating, &
weight gain
65. DEPRESSION & CHRONIC RENAL
DISEASE
Depression is the most common psychiatric
disorder found in patients with ESRD
A study of patients with CKD stages 2 to
5,with a mean age of 64.5 years,
demonstrated a prevalence of major
depression to be 21%, with no significant
variation between stages
Suicide rates may be 15 times higher than in
general population
66. The diagnosis of depression in pateints with
CKD can be complicated, as many of the
symptoms seen in CKD such as
1)poor concentration
2)anergia
3)loss of appetite,
4)disturbed sleep
5)decreased libido are also seen in
depression
67. The diagnosis of depression in patients with
CKD may be better indicated by
Feeling of helplessness, hopelessness,
worthlessness
Suicidal thoughts
68. Exact etiopathogenesis is unknown
Hyper secretion of proinflammatory cytokines in CKD
may play a role via malfunction of noradrenergic &
serotonergic neurotransmission in the brain
Endocrine abnormalities such as hyperparathyroidism
Functional decline
Diminished independence,
changes in roles & responsibilities
Limitations imposed by dialysis
69. • The effect of depression itself may have a
negative impact on the course of CKD; e.g.
decreased oral intake related to depression
may worsen the anemia & malnutrition is
common in patients receiving hemodialysis
70. Depression & gastrointestinal disease
• There is a close relationship between gut & the
brain, resulting in frequently co-occuring GI
disorders & psychiatric disorders
• Clinical epidemiologic studies have shown that
approximately 50% of patients with “functional”
disorders have co morbid mood or anxiety
disorders
• The onset of depression & anxiety tend to occur
at approximately the same time as the onset of
IBS, suggesting a potentially common etiologic
pathway
71. Depression tend to be seen in patients with
more chronic, unremitting illness
The presence of depression predicts a poorer
prognosis
In PUD loss of appetite & weight loss are
common & can be a result of a number of
conditions , including depression
72. HCV infection provides an excellent example of the 2-
way street between medical & psychiatric illness
Patients with HCV are at greater risk for depression
On the one hand, infection with HCV can contribute to
depression via multiple mechanisms. Psychologically, it
may be depressing to learn that you are infected with
the virus & therefore are at risk for complications from
HCV
It is typical for patients with HCV to worry that they
may have inadvertently infected someone else,
including family members, leading to a depressed
mood
Furthermore, there is increasing evidence that HCV
may directly cause brain changes & may cross the
blood-brain barrier, suggesting that the virus may
directly contribute to depressed states
77. HIV/AIDS
• TCAs as effective as SSRIs, but
limited to second-line and third-line
treatment, due to their
adverse effect profile
• No data yet available for SNRIs
SSRIs preferable to TCAs.
In small and large group trials, SSRIs have shown a significant
reduction in depression scores and symptoms in patients with
HIV.
The major drawback is drug interactions in use with
antiretrovirals.
Ann Pharmacother. 2013; 47: 75-89
78. Anti-depressant Antiretroviral Mechanism Potential Effect
Fluoxetine Protease
inhibitors
Fluoxetine
metabolized by
CYP2D6, 2C9, 2C19,
3A4
Increased
Fluoxetine levels,
potential for
serotonin syndrome
Paroxetine Fosamprenavir/
ritonavir
Protein binding
displacement
Inhibition of CYP2D6
Decreased
paroxetine levels
Increased ritonavir
levels
Sertraline Protease
inhibitors
Inhibition of
CYP3A4, 2D6
Increased sertraline
levels
Increased ritonavir
levels
Citalopram Protease
Citalopram Protease
inhibitors
inhibitors
Inhibition of CYP3A4 Likely no effect
Inhibition of CYP3A4 Likely no effect
Escitalopram Protease
Escitalopram Protease
inhibitors
inhibitors
Inhibition of CYP3A4 No effect
Inhibition of CYP3A4 No effect
“Citalopram and Escitalopram may be more optimal
choices in the context of drug interactions when
Tricyclic
antidepressants
Protease
inhibitors
Inhibition of
CYP3A4, 2D6
Increased tricyclic
antidepressant
levels
administering with antiretrovirals”
Venlafaxine Protease
inhibitors
Inhibition of
CYP3A4, 2D6
Increased
venlafaxine levels
Ann Pharmacother. 2013; 47: 75-89
Bupropion ritonavir Induction of CYP2B6 Decreased
80. Oropharyngeal: 22 – 57%
Pancreatic: 33 – 50%
Breast Cancer: 1.5 – 46%
Lung Cancer: 11 – 44%
Less high prevalence for:
Colon: 13 – 25%
Gynaecological: 12 – 23%
Lymphoma: 8 – 19%
Results from an 8-
year follow-up
study among
10,000 patients:
Co-existence of
cancer and
depression is
associated with
an increased risk
of death
- 2006
J Natl Cancer Inst Monogr 2004;32:57–71
Clinical Practice and Epidemiology in Mental Health. 2007; 3(2): 1-9
81. • Many symptoms overlap: fatigue,
weight loss, loss of appetite, and sleep
disruption
• Certain cancer treatment might lead to
depressive symptoms
Fatigue is associated with chemotherapy and
depression, but both present differently in a cancer
patient.
Fatigue in depression includes an emotional
component: demoralized feelings.
Fatigue due to chemotherapy does not involve an
emotional component.
Clinical Practice and Epidemiology in Mental Health. 2007;
3(2): 1-9
82. Research provides only a modest evidence for
benefits of pharmacological treatments
SSRIs have been observed to improve the QOL of the patients.
Support Care Cancer. 2007; 15: 123–136
83. CANCER
SSRIs or TCAs:
Medication should be tailored to each patient based on
characteristics of each drug.
Based on evidence and clinical expert opinion, combined
treatments most effective
85. • When important medical treatments are the
etiology of depressive symptoms, the medical
team should discuss with the patient the risk
& benefit of continuing the offending
treatment protocol. Adjunctive antidepressant
pharmacotherapy may help when medical
treatments cannot be discontinued
86. When “depression” is not depression
at all
I. Hypoactive delirium- it is a common mimic of depression in
medically ill patients, as its presenting symptoms- behavioral
withdrawal, sleep disturbance, affective flattening & amotivation-overlap
closely with a depression
II. Dementia- it can cause a patient to appear amotivated,
withdrawn ,affectively blunted
III. Substance intoxication- it can produce a behavioral syndrome that
appears consistent with a depressive episode, including suicidal
ideation & dramatic emotional posturing
IV. Pain- itself can produce the symptoms of depression when it is
untreated or inadequately managed
87. Important aspects of managing depression
• Assessment for suicidal thoughts or plan
• Assessment for psychosis – hallucinations or delusions
• Assessment for substances that may cause depressive symptoms such
as sedatives, narcotic pain meds, or alcohol
• Association of other conditions that may cause depression or have
symptoms in common with depression such as dementia, thyroid
problems, or diabetes
• Prior history of depression and response to treatment
88. Special consideration when treating
depression in medically ill patients
I. Biological interventions:
A)medications: drugs should be chosen to take
advantage of beneficial side effects while avoiding
undesirable once & minimizing polypharmacy
B)A common consultation question regards alternate
routes of antidepressant administration for patients
unable to take pills because of swallowing difficulties,
malabsorption, GI obstruction, or NPO status for
surgery or other concerns. Unfortunately , most FDA
approved antidepressants are available in oral form
only
89. Suggested medications for depression
co morbid with prominent physical
symptoms
Insomnia- 1st choice -mirtazapine
2nd choice TCAs
Neuropathic pain/migraine-TCA or duloxetine
Functional abdominal pain-SSRI or TCA
Fatigue- bupropion
stimulants( methylphenidate,
amphetamines
90. C) ECT: it can be used safely & successfully. Its advantage
is that it acts quickly. ECT can be considered for
patients with treatment resistant depression,
unremitting suicidality, intolerance to oral medication
or NMS
D)TMS: It has shown promise in improving depressive
symptoms in patients with various neurological
disorders including Parkinson's disease, epilepsy,
stroke & has been used safely in pregnant patients
E) Ketamine: emerging data suggests IV Ketamine can be
used in rapidly ameliorating treatment resistant
depression in emergency rooms
91. precautions
a) Medically ill patients may be particularly vulnerable to adverse
effects of antidepressant medication
b) Hepatic & renal impairment can affect the metabolism &
elimination of antidepressant
c) For patients with cardiac disease or those on medications that
leads to QTc prolongation, it is important to be sensitive to the
potential for further QTc prolongation with many antidepressants
d) In case TCAs the cumulative anticholinergic burden of medications
should be considered, particularly when the patient is susceptible
to delirium
e) Serotonin syndrome- in medically ill patients the constellation of
symptoms may go unrecognized or misidentified as sepsis or
anxiety
92. Psychotherapeutic interventions:
Supportive psychotherapy & problem-solving
approaches are useful in depressed medically ill
patients
IPT can be readily used in depressed medically ill
patients, with a focus on role transition & role
disputes that invariably accompany chronic illness
CBT can help patients recognize thought
distortions that accompany illness & can also
encourage behavioral activation in these patients
93. • Psychosocial intervention: higher depression
risk among family caregivers of medically ill
patients is clearly established. In these cases
psychosocial intervention may help
94. Depression is not only highly
prevalent in chronic illness, but
also complicates the underlying
cause.
Depression increases the risk of
mortality in chronic illnesses.
Depression is associated with
poor treatment adherence.
Self-management is often
difficult due to cognitive ill-effects
of depression
Comorbid depression in chronic
illnesses is often
misdiagnosed/underdiagnosed
95. • Depression associated with medical illness is
probably best addressed from a preventive
perspective. In some cases, treatment of a
medical disorders relieves depressive
symptoms as well
96. References
1. Depression, Psychiatric Clinics of North America, 2012
March,vol35 no.1
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