Depression-

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Depression-:

Depression-

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may be described as feeling sad, blue, unhappy, miserable, or down in the dumps. Most of us feel this way at one time or another for short periods. True clinical depression is a mood disorder in which feelings of sadness, loss, anger, or frustration interfere with everyday life for weeks or longer.

Incidence/risk factor:

Incidence/risk factor Lifetime prevalence Major-17% Minor-17% Women : Men ratio is 2:1(19 million ) 25% of drug and alcohol problems related to depression 30-40% of depressed individuals have sudden bouts of anger Only 20% of depressed receiving adequate Tx .

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Depression can effect anyone but there is a significantly higher rate of depression among women than men. 17 million Americans develop depression each year. 8.6% of adults over 18 have a mental health problem for at least 2 weeks a year.

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2% of Children get depressed 6-8% of Teenagers 1999 survey- reported that1 of every 10 American high school students reported making a suicide attempt the year before. Teenage boys are more likely than girls to kill themselves. Look for a change in behavior or performance in school

Major depression in women:

Major depression in women Twice as many woman as men During extreme hormonal shifts Early puberty 22% incidence in ages 20-45 Perimenopausal symptom Pregnancy –especially around wk 32 Post partum ; 2wks- 3 months

Major depression in men:

Major depression in men Commonly occurs with attempts to self-medicate with alcohol, drugs, food, gambling or sex; Men often do not experience these behaviors as signs of depression and have more reluctance to ask for professional help. Depression may be precipitated by loss of ability to function in an impt or especially valued area of life.

Aetiology-:

Aetiology- Genetics : Family history could increase likelihood six-fold Biological Factors: Neurotransmitters- Serotonin, Nor-epinephrine, Dopamine Sleep disorders Light deprivation Reproductive Hormones: Sudden fluctuations of estrogen & progesterone

Biological factors-:

Biological factors- the monoamine neurotransmitters norepinephrine , dopamine, serotonin, and histamine were the main focus of theories and research about the etiology of these disorders. A progressive shift has occurred from focusing on disturbances of single neurotransmitter systems in favor of studying neurobehavioral systems, neural circuits, and more intricate neuroregulatory mechanisms. The monoaminergic systems, thus, are now viewed as broader, neuromodulary systems, and disturbances are as likely to be secondary or epiphenomenal effects as they are directly or causally related to etiology and pathogenesis

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Norepinephrine The correlation suggested by basic science studies between the downregulation or decreased sensitivity of β-adrenergic receptors and clinical antidepressant responses is probably the single most compelling piece of data indicating a direct role for the noradrenergic system in depression. Other evidence has also implicated the presynaptic β 2 -receptors in depression, because activation of these receptors results in a decrease of the amount of norepinephrine released. Presynaptic β 2 -receptors are also located on serotonergic neurons and regulate the amount of serotonin released. The clinical effectiveness of antidepressant drugs with noradrenergic effectsfor example, venlafaxine ( Effexor ) further supports a role for norepinephrine in the pathophysiology of at least some of the symptoms of depression.

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Serotonin With the huge effect that the selective serotonin reuptake inhibitors (SSRIs) for example, fluoxetine (Prozac) have made on the treatment of depression, serotonin has become the biogenic amine neurotransmitter most commonly associated with depression. The identification of multiple serotonin receptor subtypes has also increased the excitement within the research community about the development of even more specific treatments for depression. Besides that SSRIs and other serotonergic antidepressants are effective in the treatment of depression, other data indicate that serotonin is involved in the pathophysiology of depression. Depletion of serotonin may precipitate depression, and some patients with suicidal impulses have low cerebrospinal fluid (CSF) concentrations of serotonin metabolites and low concentrations of serotonin uptake sites on platelets.

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Dopamine Although norepinephrine and serotonin are the biogenic amines most often associated with the pathophysiology of depression, dopamine has also been theorized to play a role. The data suggest that dopamine activity may be reduced in depression and increased in mania. The discovery of new subtypes of the dopamine receptors and an increased understanding of the presynaptic and postsynaptic regulation of dopamine function have further enriched research into the relation between dopamine and mood disorders. Drugs that reduce dopamine concentrations for example, reserpine ( Serpasil )”and diseases that reduce dopamine concentrations (e.g., Parkinson's disease) are associated with depressive symptoms. In contrast, drugs that increase dopamine concentrations, such as tyrosine, amphetamine, and bupropion ( Wellbutrin ), reduce the symptoms of depression. Two recent theories about dopamine and depression are that the mesolimbic dopamine pathway may be dysfunctional in depression and that the dopamine D 1 receptor may be hypoactive in depression.

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Alcohol or drug abuse Certain medical conditions, including underactive thyroid, cancer, or long-term pain Certain medications such as steroids Sleeping problems Stressful life events, such as: Breaking up with a boyfriend or girlfriend Failing a class Death or illness of someone close to you Divorce Childhood abuse or neglect Job loss Social isolation (common in the elderly)

pathogenesis/pathophysiology:

pathogenesis/ pathophysiology Acetylcholine ( ACh ) is found in neurons that are distributed diffusely throughout the cerebral cortex. Cholinergic neurons have reciprocal or interactive relationships with all three monoamine systems. Abnormal levels of choline , which is a precursor to ACh , have been found at autopsy in the brains of some depressed patients, perhaps reflecting abnormalities in cell phospholipid composition. Cholinergic agonist and antagonist drugs have differential clinical effects on depression and mania. Agonists can produce lethargy, anergia , and psychomotor retardation in healthy subjects, can exacerbate symptoms in depression, and can reduce symptoms in mania. These effects generally are not sufficiently robust to have clinical applications, and adverse effects are problematic. In an animal model of depression, strains of mice that are super- or subsensitive to cholinergic agonists have been found susceptible or more resistant to developing learned helplessness . Cholinergic agonists can induce changes in hypothalamic-pituitary adrenal (HPA) activity and sleep that mimic those associated with severe depression. Some patients with mood disorders in remission, as well as their never-ill first-degree relatives, have a trait-like increase in sensitivity to cholinergic agonists.

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γ-Aminobutyric acid (GABA) has an inhibitory effect on ascending monoamine pathways, particularly the mesocortical and mesolimbic systems. Reductions of GABA have been observed in plasma, CSF, and brain GABA levels in depression. Animal studies have also found that chronic stress can reduce and eventually can deplete GABA levels. By contrast, GABA receptors are upregulated by antidepressants, and some GABAergic medications have weak antidepressant effects. The amino acids glutamate and glycine are the major excitatory and inhibitory neurotransmitters in the CNS. Glutamate and glycine bind to sites associated with the N-methyl-D- aspartate (NMDA) receptor, and an excess of glutamatergic stimulation can cause neurotoxic effects. Importantly, a high concentration of NMDA receptors exists in the hippocampus. Glutamate, thus, may work in conjunction with hypercortisolemia to mediate the deleterious neurocognitive effects of severe recurrent depression. Emerging evidence suggests that drugs that antagonize NMDA receptors have antidepressant effects.

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Second Messengers and Intracellular Cascades The binding of a neurotransmitter and a postsynaptic receptor triggers a cascade of membrane-bound and intracellular processes mediated by second messenger systems. Receptors on cell membranes interact with the intracellular environment via guanine nucleotide-binding proteins (G proteins). The G proteins, in turn, connect to various intracellular enzymes (e.g., adenylate cyclase , phospholipase C, and phosphodiesterase ) that regulate utilization of energy and formation of second messengers, such as cyclic nucleotide (e.g., cyclic adenosine monophosphate [ cAMP ] and cyclic guanosine monophosphate [ cGMP ]), as well as phosphatidylinositols (e.g., inositol triphosphate and diacylglycerol ) and calcium- calmodulin . Second messengers regulate the function of neuronal membrane ion channels. Increasing evidence also indicates that mood-stabilizing drugs act on G proteins or other second messengers.

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Growth Hormone Growth hormone (GH) is secreted from the anterior pituitary after stimulation by NE and Dopamine (DA). Secretion is inhibited by somatostatin , a hypothalamic neuropeptide , and CRH. Decreased CSF somatostatin levels have been reported in depression, and increased levels have been observed in mania.

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Prolactin Prolactin is released from the pituitary by serotonin stimulation and inhibited by DA. Most studies have not found significant abnormalities of basal or circadian prolactin secretion in depression, although a blunted prolactin response to various serotonin agonists has been described. This response is uncommon among premenopausal women, suggesting that estrogen has a moderating effect.

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Immunological Disturbance Depressive disorders are associated with several immunological abnormalities, including decreased lymphocyte proliferation in response to mitogens and other forms of impaired cellular immunity. These lymphocytes produce neuromodulators , such as corticotropin -releasing factor (CRF), and cytokines, peptides known as interleukins. There appears to be an association with clinical severity, hypercortisolism , and immune dysfunction, and the cytokine interleukin-1 may induce gene activity for glucocorticoid synthesis.

CLINICAL FEATURES:

CLINICAL FEATURES Depression can change or distort the way you see yourself, your life, and those around you. People who have depression usually see everything with a more negative attitude. They cannot imagine that any problem or situation can be solved in a positive way. Symptoms of depression can include: Agitation, restlessness, and irritability Becoming withdrawn or isolated Difficulty concentrating Dramatic change in appetite, often with weight gain or loss Fatigue and lack of energy Feelings of hopelessness and helplessness Feelings of worthlessness, self-hate, and guilt Loss of interest or pleasure in activities that were once enjoyed Thoughts of death or suicide Trouble sleeping or too much sleeping Depression can appear as anger and discouragement, rather than feelings of sadness. If depression is very severe, there may also be psychotic symptoms, such as hallucinations and delusions

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Neurological Conditions The most common neurological problems that manifest depressive symptoms are Parkinson's disease, dementing illnesses (including dementia of the Alzheimer's type), epilepsy, cerebrovascular diseases, and tumors . About 50 to 75 percent of all patients with Parkinson's disease have marked symptoms of depressive disorder that do not correlate with the patient's physical disability, age, or duration of illness but do correlate with the presence of abnormalities found on neuropsychological tests. The symptoms of depressive disorder can be masked by the almost identical motor symptoms of Parkinson's disease. Depressive symptoms often respond to antidepressant drugs or ECT. The interictal changes associated with temporal lobe epilepsy can mimic a depressive disorder, especially if the epileptic focus is on the right side. Depression is a common complicating feature of cerebrovascular diseases, particularly in the 2 years after the episode. Depression is more common in anterior brain lesions than in posterior brain lesions and, in both cases, often responds to antidepressant medications. Tumors of the diencephalic and temporal regions are particularly likely to be associated with depressive disorder symptoms.

DIFFERENTIAL DIAGNOSIS:

DIFFERENTIAL DIAGNOSIS Medical- Mononucleosis Thyroid disorder such as hypothyroidism Adrenal disorder HIV

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Psychiatric- Anxiety disorders Generalized anxiety disorder Mixed anxiety-depressive disorder Panic disorder Posttraumatic stress disorder Obsessive compulsive disorder pseudodementia

Investigation-:

Investigation- Structural and Functional Brain Imaging Computed axial tomography (CAT) and magnetic resonance imaging (MRI) scans have permitted sensitive, noninvasive methods to assess the living brain, including cortical and subcortical tracts, as well as white matter lesions. The most consistent abnormality observed in the depressive disorders is increased frequency of abnormal hyperintensities in subcortical regions, such as periventricular regions, the basal ganglia, and the thalamus. More common in bipolar I disorder and among the elderly, these hyperintensities appear to reflect the deleterious neurodegenerative effects of recurrent affective episodes. Ventricular enlargement, cortical atrophy, and sulcal widening also have been reported in some studies. Some depressed patients also may have reduced hippocampal or caudate nucleus volumes, or both, suggesting more focal defects in relevant neurobehavioral systems. Diffuse and focal areas of atrophy have been associated with increased illness severity, bipolarity, and increased cortisol levels.

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The most widely replicated positron emission tomography (PET) finding in depression is decreased anterior brain metabolism, which is generally more pronounced on the left side. From a different vantage point, depression may be associated with a relative increase in nondominant hemispheric activity. Furthermore, a reversal of hypofrontality occurs after shifts from depression into hypomania, such that greater left hemisphere reductions are seen in depression compared with greater right hemisphere reductions in mania. Other studies have observed more specific reductions of reduced cerebral blood flow or metabolism, or both, in the dopaminergically innervated tracts of the mesocortical and mesolimbic systems in depression. Again, evidence suggests that antidepressants at least partially normalize these changes.

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DSM-IV-TR Criteria for Major Depressive Episode Five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure. Note: Do not include symptoms that are clearly due to a general medical condition, or mood-incongruent delusions or hallucinations. depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad or empty) or observation made by others (e.g., appears tearful). Note: In children and adolescents, can be irritable mood markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account or observation made by others) significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body weight in a month), or decrease or increase in appetite nearly every day. Note: In children, consider failure to make expected weight gains. insomnia or hypersomnia nearly every day psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of restlessness or being slowed down) fatigue or loss of energy nearly every day feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick) diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others) recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide The symptoms do not meet criteria for a mixed episode. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. The symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., hypothyroidism). The symptoms are not better accounted for by bereavement, i.e., after the loss of a loved one, the symptoms persist for longer than 2 months or are characterized by marked functional impairment, morbid preoccupation with worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation

Treatment-:

Treatment- general, treatments for depression include: Medications called antidepressants Talk therapy, called psychotherapy If you have mild depression, you may only need one of these treatments. People with more severe depression usually need a combination of both treatments. It takes time to feel better, but there are usually day-to-day improvements. If you are suicidal or extremely depressed and cannot function you may need to be treated in a psychiatric hospital. MEDICATIONS FOR DEPRESSION Drugs used to treat depression are called antidepressants. Common types of antidepressants include: Selective serotonin re-uptake inhibitors (SSRIs), including fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), fluvoxamine ( Luvox ), citalopram ( Celexa ), and escitalopram ( Lexapro ). Serotonin norepinephrine reuptake inhibitors (SNRIs), including desvenlafaxine ( Pristiq ), venlafaxine ( Effexor ), and duloxetine ( Cymbalta ).

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Other medicines used to treat depression include: Tricyclic antidepressants Bupropion ( Wellbutrin ) Monoamine oxidase inhibitors If you have delusions or hallucinations, your doctor may prescribe additional medications. WARNING: Children, adolescents, and young adults should be watched more closely for suicidal behavior , especially during the first few months after starting medications. If you do not feel better with antidepressants and talk therapy, you may have treatment-resistant depression. Your doctor will often prescribe higher (but still safe) doses of an antidepressant, or a combination of medications. Lithium (or other mood stabilizers) and thyroid hormone supplements also may be added to help the antidepressants work better.

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TALK THERAPY Talk therapy is counseling to talk about your feelings and thoughts, and help you learn how to deal with them. Types of talk therapy include: Cognitive behavioral therapy teaches you how to fight off negative thoughts. You will learn how to become more aware of your symptoms and how to spot things that make your depression worse. You'll also be taught problem-solving skills. Psychotherapy can help you understand the issues that may be behind your thoughts and feelings. Joining a support group of people who are sharing problems like yours can also help. Ask your therapist or doctor for a recommendation.

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OTHER TREATMENTS FOR DEPRESSION Electroconvulsive therapy (ECT) is the single most effective treatment for severe depression and it is generally safe. ECT may improve mood in people with severe depression or suicidal thoughts who don't get better with other treatments. It may also help treat depression in those who have psychotic symptoms. Transcranial magnetic stimulation (TMS) uses pulses of energy to stimulate nerve cells in the brain that are believe to affect mood. There is some research to suggest that it can help relieve depression. Light therapy may relieve depression symptoms in the winter time. However, it is usually not considered a first-line treatment

prognosis:

prognosis Expectations (prognosis) Some people with major depression may feel better after taking antidepressants for a few weeks. However, many people need to take the medicine for 4 - 9 months to fully feel better and prevent the depression from returning. People who have repeated episodes of depression may need quick and ongoing treatment to prevent more severe, long-term depression. Sometimes people will need to stay on medications for long periods of time.

Prevention-:

Prevention- Do not drink alcohol or use illegal drugs. These substances can make depression worse and might lead to thoughts of suicide. Take your medication exactly as your doctor instructed. Ask your doctor about the possible side effects and what you should do if you have any. Learn to recognize the early signs that your depression is getting worse. The following tips might help you feel better: Get more exercise Maintain good sleep habits Seek out activities that bring you pleasure Volunteer or get involved in group activities Talk to someone you trust about how you are feeling Try to be around people who are caring and positive

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References Fava M, Cassano P. Mood disorders: Major depressive disorder and dysthymic disorder. In: Stern TA, Rosenbaum JF, Fava M, Biederman J, Rauch SL, eds. Massachusetts General Hospital Comprehensive Clinical Psychiatry . 1st ed. Philadelphia, Pa: Mosby Elsevier; 2008:chap 29. American Psychiatric Association. Practice guidelines for the treatment of patients with major depressive disorder. 2nd ed. September 2007. Accessed January 22, 2010. Little A. Treatment-resistant depression. Am Fam Physician . 2009;80:167-172