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Secondary Depression 
Etiopathogenesis & 
management 
Presenter: 
Dr Angshuman 
Kalita 
Chairperson: 
Dr Utpal Bora 
Asst Professor 
Deptt of Psychiatry 
Date: 03/09/2014
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
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
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
 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
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
• Several studies have suggested that 
depressed patients have shorter telomeres 
than age matched controls suggesting a 
relationship between depression & more 
rapid cellular aging
Schizophrenia and depression
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
Depressive Symptoms 
– Primary to schizophrenia 
– “Reactive” 
• psychosis is frightening 
• reality of illness is demoralizing 
– Co-morbid disorder 
• major depressive episode
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
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
• 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
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
Depression and Parkinson’s Disease
• 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
DEPRESSION IN 
PARKINSON’S DISEASE 
•Characterized by: 
Feeling of guilt 
Lack of self esteem 
Loss of initiative 
Helplessness, remorse, sadness
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 ???
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.
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
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
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
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
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
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
Secondary  depression: etiopathogenesis & management
Respirology. 2012; 17: 627-38
• Highest rate of depression is seen those who 
are oxygen dependant
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
• 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
• 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
• 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
 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
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
Secondary  depression: etiopathogenesis & management
• 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
• 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
• 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
• 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
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.
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.
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.
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.
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.
• 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
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.
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.
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.
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.
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.
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.
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.
DEPRESSION 
DUE TO 
DIABETES
Diabetes Research and Clinical Practice. 2010; 87: 302-312 
Indian J Med Res. 2010; 132: 195-200
Diabetes Research and Clinical Practice. 2010; 87: 302-312
Diabetes Research and Clinical Practice. 2010; 87: 302-312
Effect of depression on all-cause 
mortality in patients 
with diabetes 
Diabetes Research and Clinical Practice. 2010; 87: 302-312
Diabetes Research and Clinical Practice. 2010; 87: 302-312
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
DEPRESSION & ENDOCRINE 
DISORDERS
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
Hypothyroidism and Depression 
Depression 
62 
Hypothyroidism 
Sleep decrease 
Suicidal ideation 
Weight change 
Delusions 
Constipation 
Decreased Conc. 
Decreased libido 
Depressed mood 
Diminished interest 
Weight increase 
Fatigue 
Bradycardia 
Cardiac and lipid 
Abnormalities 
Cold intolerance 
Hair and skin changes 
Delayed reflexes 
Goiter
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
• 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
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
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
The diagnosis of depression in patients with 
CKD may be better indicated by 
Feeling of helplessness, hopelessness, 
worthlessness 
Suicidal thoughts
 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
• 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
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
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
 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
Secondary  depression: etiopathogenesis & management
Neurobehavioral HIV Medicine. 2010; 2: 73-83 
Ann Pharmacother. 2013; 47: 75-89
Neurobehavioral HIV Medicine. 2010; 2: 73-83
Neurobehavioral HIV Medicine. 2010; 2: 73-83
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
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
DEPRESSION 
DUE TO 
CANCER
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
• 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
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
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
Classes of drugs that may cause depressive symptoms 
Drug class examples 
ACEI Captopril, enalapril, lisinopril 
antibiotics Ciprofloxacin ,cycloserine, dapsone,metronidazole, trimethoprim-sulfamethoxazole, 
amphotericine B, ethionamide 
anticholinergics Dicyclomine, scopolamine 
antivirals Acyclovir, efavirenz, interferon alfa, nevirapine 
barbiturates Phenobarbital, secobarbital 
Beta-blockers 
BZDs Alprazolam, chlordiazepoxide,clonazepam,diazepam,lorazepam,temazepam,trizolam 
CCBs Diltiazem,nifedipine,verapamil 
corticosteroids Prednisolone,cortisone,ACTH 
Dermatologics Finasteride, isotretinoin 
Endocrine modifiers Estrogen,leuorolide 
H2 antihistamines Cimetidine,famotidine,nizatidine,ranitidine 
NSAIDs Ibuprofen,indomethacin,naproxen,meloxicam 
opiods Codeine,meperidine,morphine,oxycodone 
Antineoplastic drugs Procarbazine,vincristine,vinblastine,aspraginase 
Parkinson drugs Amantadine,levodopa,pramipexole,ropinirole 
statins
• 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
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
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
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
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
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
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
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
• Psychosocial intervention: higher depression 
risk among family caregivers of medically ill 
patients is clearly established. In these cases 
psychosocial intervention may help
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
• 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
References 
1. Depression, Psychiatric Clinics of North America, 2012 
March,vol35 no.1 
2. Late life Depression, Psychiatric Clinics of North 
America,2013,Dec, vol36 no.4 
3. Neuropsychiatry of Traumatic Brain Injury, Psychiatric Clinics of 
North America,2014 March, vol 37 no 1. 
4. Frontal lobe dysfunction in secondary depression-journal of 
neuropsychiatry & clinical neurosciences, vol6,no 4,1994 
5. Post stroke depression-epidemiology, pathophysiology& biological 
treatment-biological psychiatry vol52,issue 3. aug 2002, 
6. Frontal lobe hypo metabolism & depression in Alzheimer's 
disease-neurology,feb 1998,vol 50 ,no2 
7. Prevalence, etiology & treatment of depression in Parkinson 
disease-biological psychiatry vol 54 aug 2003
Thank you!

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Secondary depression: etiopathogenesis & management

  • 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.
  • 53. DEPRESSION DUE TO DIABETES
  • 54. Diabetes Research and Clinical Practice. 2010; 87: 302-312 Indian J Med Res. 2010; 132: 195-200
  • 55. Diabetes Research and Clinical Practice. 2010; 87: 302-312
  • 56. Diabetes Research and Clinical Practice. 2010; 87: 302-312
  • 57. Effect of depression on all-cause mortality in patients with diabetes Diabetes Research and Clinical Practice. 2010; 87: 302-312
  • 58. Diabetes Research and Clinical Practice. 2010; 87: 302-312
  • 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
  • 62. Hypothyroidism and Depression Depression 62 Hypothyroidism Sleep decrease Suicidal ideation Weight change Delusions Constipation Decreased Conc. Decreased libido Depressed mood Diminished interest Weight increase Fatigue Bradycardia Cardiac and lipid Abnormalities Cold intolerance Hair and skin changes Delayed reflexes Goiter
  • 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
  • 74. Neurobehavioral HIV Medicine. 2010; 2: 73-83 Ann Pharmacother. 2013; 47: 75-89
  • 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
  • 84. Classes of drugs that may cause depressive symptoms Drug class examples ACEI Captopril, enalapril, lisinopril antibiotics Ciprofloxacin ,cycloserine, dapsone,metronidazole, trimethoprim-sulfamethoxazole, amphotericine B, ethionamide anticholinergics Dicyclomine, scopolamine antivirals Acyclovir, efavirenz, interferon alfa, nevirapine barbiturates Phenobarbital, secobarbital Beta-blockers BZDs Alprazolam, chlordiazepoxide,clonazepam,diazepam,lorazepam,temazepam,trizolam CCBs Diltiazem,nifedipine,verapamil corticosteroids Prednisolone,cortisone,ACTH Dermatologics Finasteride, isotretinoin Endocrine modifiers Estrogen,leuorolide H2 antihistamines Cimetidine,famotidine,nizatidine,ranitidine NSAIDs Ibuprofen,indomethacin,naproxen,meloxicam opiods Codeine,meperidine,morphine,oxycodone Antineoplastic drugs Procarbazine,vincristine,vinblastine,aspraginase Parkinson drugs Amantadine,levodopa,pramipexole,ropinirole statins
  • 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 2. Late life Depression, Psychiatric Clinics of North America,2013,Dec, vol36 no.4 3. Neuropsychiatry of Traumatic Brain Injury, Psychiatric Clinics of North America,2014 March, vol 37 no 1. 4. Frontal lobe dysfunction in secondary depression-journal of neuropsychiatry & clinical neurosciences, vol6,no 4,1994 5. Post stroke depression-epidemiology, pathophysiology& biological treatment-biological psychiatry vol52,issue 3. aug 2002, 6. Frontal lobe hypo metabolism & depression in Alzheimer's disease-neurology,feb 1998,vol 50 ,no2 7. Prevalence, etiology & treatment of depression in Parkinson disease-biological psychiatry vol 54 aug 2003