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{{DrugProjectFormSinglePage
__NOTOC__
|authorTag={{Alonso}}
{{CMG}}; {{AE}} {{Alonso}}
|genericName=Dopamine
|aOrAn=a
|drugClass=Adrenergic receptor agonist
|indicationType=treatment
|indication=hemodynamic imbalances present in the [[shock]] syndrome due to [[myocardial infarctions]], [[trauma]], endotoxic [[septicemia]], [[open heart surgery]], [[renal failure]], and chronic cardiac decompensation as in [[congestive heart failure]]
|hasBlackBoxWarning=Yes
|adverseReactions=[[chest pain]], [[hypertension]], [[palpitations]], [[tachyarrhythmia]], injection site reaction, [[piloerection]], [[nausea]], [[vomiting]], [[headache]], [[mydriasis]], [[anxiety]], [[oliguria]], [[dyspnea]]
|blackBoxWarningTitle=IMPORTANT
|blackBoxWarningBody=<i><span style="color:#FF0000;">Antidote for Peripheral Ischemia:</span></i> To prevent sloughing and necrosis in ischemic areas, the area should be infiltrated as soon as possible with 10 to 15 mL of saline solution containing 5 to 10 mg of phentolamine, an adrenergic blocking agent. A syringe with a fine hypodermic needle should be used, and the solution liberally infiltrated throughout the ischemic area. Sympathetic blockade with phentolamine causes immediate and conspicuous local hyperemic changes if the area is infiltrated within 12 hours. Therefore, phentolamine should be given as soon as possible after the extravasation is noted.
|fdaLIADAdult======Condition 1=====


* Dosing Information
Infobox goes here


:* (Dosage)
<nowiki>{{SI}}</nowiki>


=====Condition 2=====
'''''Synonyms and keywords:'''''


* Dosing Information
== Overview ==
'''Body dysmorphic disorder (BDD)''' is a mental disorder that involves a disturbed [[body image]]. It is generally diagnosed in those who are extremely critical of their physique or self-image, despite the fact there may be no noticeable disfigurement or defect.


:* (Dosage)
Most people wish they could change or improve some aspect of their physical appearance, but people suffering from BDD, generally considered of normal appearance, believe that they are so unspeakably hideous that they are unable to interact with others or function normally for fear of ridicule and humiliation at their appearance. They tend to be very secretive and reluctant to seek help because they are afraid others will think them vanity|vain or they may feel too embarrassed to do so.
|offLabelAdultGuideSupport======Condition 1=====


* Developed by: (Organisation)
Ironically, BDD is often misunderstood as a vanity driven obsession, whereas it is quite the opposite; people with BDD believe themselves to be irrevocably ugly or defective.


* Class of Recommendation: (Class) (Link)
BDD combines obsessive and compulsive aspects, which links it to the [[Obsessive-Compulsive Disorder|OCD]] spectrum disorders among psychologists. People with BDD may engage in compulsive mirror checking behaviors or mirror avoidance, typically think about their appearance for more than one hour a day, and in severe cases may drop all social contact and responsibilities as they become homebound. The disorder is linked to an unusually high [[suicide]] rate among all mental disorders.


* Strength of Evidence: (Category A/B/C) (Link)
A German study has shown that 1-2% of the population meet all the diagnostic criteria of BDD, with a larger percentage showing milder symptoms of the disorder (''Psychological Medicine'', vol 36, p 877). Chronically low self-esteem is characteristic of those with BDD due to the value of oneself being so closely linked with their perceived appearance. The prevalence of BDD is equal in men and women, and causes chronic social [[anxiety]] for those suffering from the disorder[http://www.lipo.com/Health_Articles/Lifestyle_Articles/When_the_mirror_lies_-_Body_dysmorphic_disorder_(dysmorphophobia)_on_the_rise_and_taking_lives./].


* Dosing Information/Recommendation
Phillips & Menard (2006) found the completed suicide rate in patients with BDD to be 45 times higher than in the general US population. This rate is more than double that of those with [[Clinical depression]] and three times as high as those with [[bipolar disorder]]<ref>http://ajp.psychiatryonline.org/cgi/content/full/163/7/1280</ref>. There has also been a suggested link between undiagnosed BDD and a higher than average suicide rate among people who have undergone cosmetic surgery<ref>http://www.newscientist.com/channel/health/mg19225745.200-cosmetic-surgery-special-when-looks-can-kill.html</ref>.


:* (Dosage)
==Historical Perspective==
BDD was first documented in 1886 by the researcher Morselli, who called the condition simply "'''Dysmorphophobia'''". BDD was first recorded/formally recognized in 1997 as a disorder in the [[Diagnostic and Statistical Manual of Mental Disorders|DSM]]; however, in 1987 it was first truly recognized by the [[American Psychiatric Association]].


=====Condition 2=====
In his practice, [[Sigmund Freud|Freud]] eventually had a patient who would today be diagnosed with the disorder; Russian [[aristocrat]] [[Sergei Pankejeff]], nicknamed "The Wolf Man" by Freud himself in order to protect Pankejeff's identity, had a preoccupation with his nose to an extent that greatly limited his functioning.


* Developed by: (Organisation)
==Classification==


* Class of Recommendation: (Class) (Link)
==Pathophysiology==
BDD usually develops in adolescence, a time when people are generally most sensitive about their appearance. However, many patients suffer for years before seeking help. When they do seek help through mental health professionals, patients often complain of other symptoms such as depression, social anxiety or obsessive compulsive disorder, but do not reveal their real concern over body image. Most patients cannot be convinced that they have a distorted view of their body image, due to the very limited knowledge of the disorder as compared to OCD or others.


* Strength of Evidence: (Category A/B/C) (Link)
An absolute cause of body dysmorphic disorder is unknown. However research shows that a number of factors may be involved and that they can occur in combination, including:


* Dosing Information/Recommendation
'''A chemical imbalance in the brain.''' An insufficient level of [[serotonin]], one of the brain's [[neurotransmitter]]s involved in mood and pain, may contribute to body dysmorphic disorder. Although such an imbalance in the brain is unexplained, it may be hereditary.
'''Obsessive-compulsive disorder.''' BDD often occurs with OCD, where the patient uncontrollably practices ritual behaviors that may literally take over their life. A history of, or [[gene]]tic predisposition to, OCD may make people more susceptible to BDD.


:* (Dosage)
'''Generalized anxiety disorder.''' Body dysmorphic disorder may co-exist with generalized anxiety disorder. This condition involves excessive worrying that disrupts the patient's daily life, often causing exaggerated or unrealistic anxiety about life circumstances, such as a perceived flaw or defect in appearance, as in BDD.
|offLabelAdultNoGuideSupport======Condition 1=====


* Dosing Information
==Causes==


:* (Dosage)
==Differentiating type page name here from other Diseases==


=====Condition 2=====
== Epidemiology and Demographics ==
''According to Dr Katharine Phillips (2004) :''


* Dosing Information
Although large [[epidemiology|epidemiologic]] surveys of BDD's prevalence have not been done, studies to date indicate that BDD is relatively common in both nonclinical and clinical settings (Phillips & Castle, 2002). Studies in community samples have reported current rates of 0.7% and 1.1%, and studies in nonclinical student samples have reported rates of 2.2%, 4%, and 13% (Phillips & Castle, 2002). A study in a general inpatient setting found that 13% of patients had BDD (Grant, Won Kim, Crow, 2001). Studies in outpatient settings have reported rates of 8%-37% in patients with OCD, 11%-13% in social phobia, 26% in trichotillomania, 8% in major depression, and 14%-42% in atypical major depression (Phillips & Castle, 2002). In one study of atypical depression, BDD was more than twice as common as OCD (Phillips, Nierenberg, Brendel et al 1996), and in another (Perugi, Akiskal, Lattanzi et al, 1998) it was more common than many other disorders, including OCD, social phobia, simple phobia, generalized anxiety disorder, [[bulimia nervosa]], and substance abuse or dependence. In a [[dermatology]] setting, 12% of patients screened positive for BDD, and in [[cosmetic surgery]] settings, rates of 6%-15% have been reported (Phillips & Castle, 2002).


:* (Dosage)
BDD is underdiagnosed, however. Two studies of inpatients (Phillips, McElroy, Keck et al, 1993, and Grant, Won Kim, Crow, 2001), as well as studies in general outpatients (Zimmerman & Mattia, 1998) and depressed outpatients (Phillips, Nierenberg, Brendel et al 1996), systematically assessed a series of patients for the presence of BDD and then determined whether clinicians had made the diagnosis in the clinical record. All four studies found that BDD was missed by the clinician in every case in which it was present. Thus, underdiagnosis of BDD appears common.


=====Condition 3=====
== Risk Factors ==


* Dosing Information
== Screening ==


:* (Dosage)
== Natural History, Complications, and Prognosis==
|fdaLIADPed======Condition 1=====


* Dosing Information
== Diagnosis ==


:* (Dosage)
=== Symptoms ===
*Compulsive mirror checking, glancing in reflective doors, windows and other reflective surfaces.
*Alternatively, an inability to look at one's own reflection or photographs of oneself; often the removal of mirrors from the home.
*Compulsive skin-touching, especially to measure or feel the perceived defect.
*Reassurance-seeking from loved ones.
*Social withdrawal and co-morbid depression.
*Obsessive viewing of favorite celebrities or models the person suffering from BDD may wish to resemble.
*Excessive grooming behaviors: combing hair, plucking eyebrows, shaving, etc.
*Obsession with [[plastic surgery]] or multiple plastic surgeries with little satisfactory results for the patient.
*In obscure cases patients have performed plastic surgery on themselves, including [[liposuction]] and various implants with disastrous results.


=====Condition 2=====
===Location of imagined defects===
In research carried out by Dr. Katharine Philips, involving over 500 patients, the percentage of patients concerned with the most common locations were as follows:
{{col-begin}}
{{col-break}}
*skin (73%)
*hair (56%)
*nose (37%)
*weight (22%)
*stomach (22%)
*breasts/chest/nipples (21%)
*eyes (20%)
*thighs (20%)
*teeth (20%)
*legs (overall) (18%)
*body build / bone structure (16%)
*ugly face (general) (14%)
*lips (12%)
*buttocks (12%)
*chin (11%)
*fingers
*eyebrows (11%)


* Dosing Information
''source: '''The Broken Mirror''', Katharine A Philips, Oxford University Press, 2005 ed, p56 ''


:* (Dosage)
People with BDD often have more than one area of concern.
|offLabelPedGuideSupport======Condition 1=====


* Developed by: (Organisation)
==The Disabling Effects of BDD==
BDD can be anywhere from slightly to severely debilitating. It can make normal employment or family life impossible. Those who are in regular employment or who have family responsibilities would almost certainly find life more productive and satisfying if they did not have the symptoms. The partners of sufferers of BDD may also become involved and suffer greatly, sometimes losing their loved one to [[suicide]].


* Class of Recommendation: (Class) (Link)
==Prognosis==
Many individuals with BDD have repeatedly sought treatment from dermatologists or cosmetic surgeons with little satisfaction before finally accepting psychiatric or psychological help. Treatment can improve the outcome of the illness for most people. Other patients may function reasonably well for a time and then relapse, while others may remain chronically ill. Research on outcome without therapy is not known but it is thought the symptoms persist unless treated.


* Strength of Evidence: (Category A/B/C) (Link)
== Treatment ==
Typically the [[psychodynamic]] approach to therapy does not seem to be effective in battling BDD while in some patients it may even be countereffective.


* Dosing Information/Recommendation
CBT ([[Cognitive Behavioral Therapy]]) coupled with [[exposure therapy]] has been shown effective in the treatment of BDD. Low levels or insufficient use of serotonin in the brain has been implicated with the disorder and so [[SSRI]] drugs are commonly used, and with some success, in the treatment of Body Dysmorphic Disorder. Drug treatment will sometimes also include the use of an [[anxiolytic]].


:* (Dosage)
BDD tends to be chronic; current information suggests that symptoms do not subside, but rather worsen through time. Indeed in most patients, the symptoms and concerns diversify and social contacts may further deteriorate. As so, treatment should be initiated as early as possible following the diagnoses.


=====Condition 2=====
==References==
{{reflist|2}}


* Developed by: (Organisation)
{{WikiDoc Help Menu}}
{{WikiDoc Sources}}


* Class of Recommendation: (Class) (Link)
[[Category:Disease]]
 
[[Category:FLK]]
* Strength of Evidence: (Category A/B/C) (Link)
 
* Dosing Information/Recommendation
 
:* (Dosage)
|offLabelPedNoGuideSupport======Condition 1=====
 
* Dosing Information
 
:* (Dosage)
 
=====Condition 2=====
 
* Dosing Information
 
:* (Dosage)
 
=====Condition 3=====
 
* Dosing Information
 
:* (Dosage)
|contraindications=* Patients with [[pheochromocytoma]].
* Uncorrected [[tachyarrhythmias]] or [[ventricular fibrillation]].
|warnings=* Do no add dopamine to any alkaline diluent solution, since the drug is inactivated in alkaline solution.
* Patients who have been treated with [[monoamine oxidase]] ([[MAO]]) inhibitors prior to the administration of dopamine will require substantially reduced dosage. * Contains sodium metabisulfite, a sulfite that may cause allergic-type reactions including anaphylactic symptoms and life-threatening or less severe [[asthmatic]] episodes in certain susceptible people. The overall prevalence of sulfite sensitivity in the general population is unknown, and probably low. Sulfite sensitivity is seen more frequently in [[asthmatic]] than in non[[asthmatic]] people.
 
====Precautions====
* '''Careful monitoring required:''' Close monitoring of the following indices-urine flow, [[cardiac output]]and [[blood pressure]] during dopamine infusion is necessary as in the case of any adrenergic agent.
* '''Avoid hypovolemia:''' Prior to treatment with dopamine, [[hypovolemia]] should be fully corrected, if possible with either whole blood or plasma as indicated. Monitoring of central venous pressure of left ventricular filling pressure may be helpful in detecting and treating [[hypovolemia]].
* '''Hypoxia, Hypercapnia, Acidosis:''' These conditions which may also reduce the effectiveness and/or increase the incidence of adverse effects of dopamine, must be identified and corrected prior to, or concurrently with administration of dopamine HCl.
* '''Ventricular Arrhythmias:''' If an increased number of ectopic beats are observed, the dose should be reduced if possible.
* '''Decreased Pulse Pressure:''' If a disproportionate rise in the [[diastolic pressure]] (i.e., a marked decrease in the [[pulse pressure]]) is observed in patients receiving dopamine, the infusion rate should be decreased and the patient observed carefully for further evidence of predominant vasoconstrictor activity, unless such an effect is desired.
* '''Hypotension:''' At lower infusion rates, if [[hypotension]] occurs, the infusion rate should be rapidly increased until adequate [[blood pressure]] is obtained. If [[hypotension]] persists, dopamine HCl should be discontinued and a more potent vasoconstrictor agent such as [[norepinephrine]] should be administered.
* '''Extravasation:''' Dopamine should be infused into a large vein whenever possible to prevent the possibility of extravasation into tissue adjacent to the infusion site. Extravasation may cause [[necrosis]] and sloughing of surrounding tissue. Large veins of the actecubital fossa are preferred to veins in the dorsum of the hand or ankle. Less suitable infusion sites should be used only if the patient’s condition requires immediate attention. The physician should switch to more suitable sites as rapidly as possible. The infusion site should be continuously monitored for free flow.
* '''Occlusive vascular disease:''' Patients with a history of occlusive vascular disease (for example, atheroscierosis, arterial embolism, and [[Raynaud's phenomenon|Raynaud’s disease]], cold injury, diabetic endarteritis, and Buergers disease) should be closely monitored for any changes in color or temperature of the skin in the extremities. If a change in skin color or temperature occurs and is thought to be the result of compromised circulation to the extremities, the benefits of continued dopamine infusion should be weighed against the risk of possible [[necrosis]]. This condition may be reversed by either decreasing or discontinuing the rate of infusion.
'''Weaning:''' When discontinuing the infusion, it may be necessary to gradually decrease the dose of dopamine HCl while expanding blood volume with IV fluids, since sudden cessation may result in marked [[hypotension]].
|clinicalTrials=======Central Nervous System======
 
: (list/description of adverse reactions)
 
======Cardiovascular======
 
: (list/description of adverse reactions)
 
======Respiratory======
 
: (list/description of adverse reactions)
 
======Gastrointestinal======
 
: (list/description of adverse reactions)
 
======Hypersensitive Reactions======
 
: (list/description of adverse reactions)
 
======Miscellaneous======
 
: (list/description of adverse reactions)
 
=====Condition 2=====
 
======Central Nervous System======
 
: (list/description of adverse reactions)
 
======Cardiovascular======
 
: (list/description of adverse reactions)
 
======Respiratory======
 
: (list/description of adverse reactions)
 
======Gastrointestinal======
 
: (list/description of adverse reactions)
 
======Hypersensitive Reactions======
 
: (list/description of adverse reactions)
 
======Miscellaneous======
 
: (list/description of adverse reactions)
|postmarketing=(Description)
|drugInteractions=* Cyclopropane or halogenated hydrocarbon anesthetics increase cardiac autonomic irritability and may sensitize the [[myocardium]] to the action of certain intravenously administered [[catecholamines]], such as dopamine. The interaction appears to be related both to pressor activity and to the beta adrenergic stimulating properties of these [[catecholamines]], and may produce [[ventricular arrhythmias]].  Therefore, '''extreme caution''' should be exercised when administering dopamine HCl to patients receiving cyclopropane or halogenated hydrocarbon anesthetics. Results of studies in animals indicate that dopamine induced ventricular arrhythmias during anesthesia can be reversed by propranolol.
* Because dopamine is metabolized by [[monoamine oxidase]] ([[MAO]]), inhibition of this enzyme prolongs and potentiates the effect of dopamine. Patients who have been treated with MAO inhibitors within two to three weeks prior to the administration of dopamine should receive initial doses of dopamine HCl not greater than one-tenth (1/10) of the usual dose.
* Concurrent administration of low-dose dopamine HCl and [[diuretic]] agents may produce an additive or potentiating effect on urine flow.
* [[Tricyclic antidepressants]] may potentiate the cardiovascular effects of adrenergic agents.
* Cardiac effects of dopamine are antagonized by [[beta-blockers]], such as [[propranolol]] and [[metoprolol]]. The peripheral vasoconstriction caused by high doses of dopamine HCl is antagonized by [[alpha-blockers]]. Dopamine-induced renal and mesenteric vasodilation is not antagonized by either alpha- or beta-adrenergic blocking agents.
* Butyrophenones (such as [[haloperidol]]) and [[phenothiazines]] can suppress the dopaminergic renal and mesenteric vasodilation induced with low-dose dopamine infusion.
* The concomitant use of [[vasopressors]], vasoconstricting agents (such as [[ergonovine]]) and some oxytocic drugs may result in severe [[hypertension]].
* Administration of [[phenytoin]] to patients receiving dopamine HCl has been reported to lead to [[hypotension]] and [[bradycardia]]. It is suggested that in patients receiving dopamine HCl, alternatives to [[phenytoin]] should be considered if anticonvulsant therapy is needed.
|FDAPregCat=C
|useInPregnancyFDA=[[Teratogenicity]] studies in rats and rabbits at dopamine hydrochloride dosages up to 6 mg/kg/day intravenously during organogenesis produced no detectable [[teratogenic]] or embryotoxic effects, although maternal toxicity consisting of mortalities, decrease body weight gain, and pharmacotoxic signs were observed in rats. In a published study, dopamine hydrochloride administered at 10 mg/kg subcutaneously for 30 days, markedly prolonged metestrus and increased mean pituitary and ovary weights in female rats. Similar administration to pregnant rats throughout gestation or for 5 days starting on gestation day 10 or 15 resulted in decreased body weight gains, increased mortalities and slight increases in cataract formation among the offspring. There are no adequate and well-controlled studies in pregnant women, and it is not known if dopamine hydrochloride crosses the placental barrier. Dopamine hydrochloride should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
|useInLaborDelivery=In obstetrics, if vasopressor drugs are used to correct [[hypotension]] or are added to a local anesthetic solution the interaction with some oxytocic drugs may cause severe [[hypertension]].
|useInNursing=It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when dopamine is administered to a nursing mother.
|useInPed=Safety and effectiveness in children have not been established. Dopamine HCl has been used in a limited number of pediatric patients, but such use has been inadequate to fully define proper dosage and limitations for use. Peripheral [[gangrene]] has been reported in neonates and children.
|administration=Intravenous
|monitoring=Close monitoring of the following indices-urine flow, [[cardiac output]] and [[blood pressure]] during dopamine infusion is necessary as in the case of any adrenergic agent.
|IVCompat======Cardiovascular System=====
* [[Ventricular arrhythmia]] (at very high doses)
* Ectopic beats
* [[Tachycardia]]
* [[Angina]]l pain
* [[Palpitation]]
* Cardiac conduction abnormalities
* Widened QRS complex
* [[Bradycardia]]
* [[Hypotension]]
* [[Hypertension]]
* [[Vasoconstriction]]
 
=====Respiratory System=====
* [[Dyspnea]]
 
=====Gastrointestinal System=====
* [[Nausea]]
* [[Vomiting]]
 
=====Metabolic/Nutritional System=====
* [[Azotemia]]
 
=====Central Nervous System=====
* [[Headache]]
* [[Anxiety]]
 
=====Dermatological System=====
* [[Piloerection]]
 
=====Other=====
* [[Gangrene]] of the extremities has occurred when moderate to high doses were administered for prolonged periods or in patients with occlusive vascular disease receiving low doses of dopamine HCl.
* A few cases of peripheral [[cyanosis]] have been reported.
|overdose=In case of accidental overdosage, as evidenced by excessive [[blood pressure]] elevation, reduce rate of administration or temporarily discontinue dopamine until patient’s condition stabilizes. Since the duration of action of dopamine is quite short, no additional remedial measures are usually necessary. If these measures fail to stabilize the patient’s condition, use of the short-acting [[alpha-blocker]], [[phentolamine]], should be considered.
|drugBox={{Drugbox2
| Watchedfields = changed
| drug_name = Dopamine
| verifiedrevid = 595793408
| image =DopamineStructure.png
| width=200px
| alt =
| width2=180px
| alt2 =
| IUPAC_name=4-(2-Aminoethyl)benzene-1,2-diol
| synonyms=2-(3,4-Dihydroxyphenyl)ethylamine;  3,4-Dihydroxyphenethylamine;  3-hydroxytyramine; DA; Intropin; Revivan; Oxytyramine
 
<!--Clinical data-->
| tradename =
| Drugs.com =
| pregnancy_US =
| legal_AU =
| legal_CA =
| legal_UK =
| legal_US =
| licence_US = Dopamine
| legal_status = Rx-only
| dependency_liability =
| routes_of_administration= [[Intravenous]] Injection
 
<!--Pharmacokinetic data-->
| bioavailability =
| protein_bound =
| metabolism = [[aldehyde dehydrogenase|ALDH]], [[Dopamine beta hydroxylase|DBH]], [[Monoamine oxidase A|MAO-A]], [[Monoamine oxidase B|MAO-B]], [[catechol-O-methyl transferase|COMT]]
| elimination_half-life =
| excretion = Renal
 
<!--Identifiers-->
| UNII_Ref = {{fdacite|correct|FDA}}
| UNII = VTD58H1Z2X
| InChI = 1/C8H11NO2/c9-4-3-6-1-2-7(10)8(11)5-6/h1-2,5,10-11H,3-4,9H2
| InChIKey = VYFYYTLLBUKUHU-UHFFFAOYAA
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C8H11NO2/c9-4-3-6-1-2-7(10)8(11)5-6/h1-2,5,10-11H,3-4,9H2
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = VYFYYTLLBUKUHU-UHFFFAOYSA-N
| CAS_number_Ref = {{cascite|correct|??}}
| CAS_number =51-61-6
| CASNo_Ref = {{cascite|correct|CAS}}
| CAS_supplemental ={{CAS|62-31-7}} (hydrochloride)
| PubChem=681
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 59
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 661
| KEGG_Ref = {{keggcite|correct|kegg}}
| KEGG = D07870
| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
| DrugBank = DB00988
| IUPHAR_ligand = 940
| ChEBI_Ref = {{ebicite|correct|EBI}}
| ChEBI = 18243
| SMILES = c1cc(c(cc1CCN)O)O
| ATC_prefix = C01
| ATC_suffix = CA04
 
<!--Chemical data-->
| C=8 | H=11 | N=1 | O=2
| molecular_weight = 153.18 g/mol
| density = 1.26
| boiling_point =
| boiling_notes = decomposes
| melting_point = 128
| melting_notes =
| solubility = <!--60.0 g/100 ml-->
}}
|mechAction=Dopamine is a natural catecholamine formed by the decarboxylation of 3,4-dihydroxyphenylalanine (DOPA). It is a precursor to norepinephrine in noradrenergic nerves and is also a neurotransmitter in certain areas of the central nervous system, especially in the nigrostriatal tract, and in a few peripheral sympathetic nerves.
 
Dopamine produces positive chronotropic and inotropic effects on the myocardium, resulting in increased heart rate and cardiac contractility. This is accomplished directly by exerting an agonist action on beta-adrenoceptors and indirectly by causing release of norepinephrine from storage sites in sympathetic nerve endings.
|structure=Dopamine hydrochloride injection is a clear, practically colorless, aqueous, additive solution for intravenous infusion after dilution. Each mL contains either 40 mg, 80 mg, or 160 mg dopamine HCl, USP (equivalent to 32.3 mg, 64.6 mg and 129.2 mg dopamine base respectively) in Water for Injection, USP, containing 9 mg sodium metabisulfite as an antioxidant. The pH range (2.5 to 5.0) may be adjusted with citric acid and/or sodium citrate. The solution is sterile and nonpyrogenic. Dopamine HCl, a naturally occurring catecholamine, is an inotropic vasopressor agent. Its chemical name is 3,4 dihydroxyphenethylamine hydrochloride and its chemical structure is:
 
[[File:DopamineStructure.png|600px|thumbnail|left|This image of the FDA label is provided by the National Library of Medicine.]]
{{clr}}
 
Dopamine HCl is sensitive to alkalis, iron salts and oxidizing agents. dopamine must be diluted in an appropriate, sterile parenteral solution before intravenous administration.
|PD=The predominant effects of dopamine are dose-related, although actual response of an individual patient will largely depend on the clinical status of the patient at the time the drug is administered. At low rates of infusion (0.5-2 mcg/kg/min) dopamine causes vasodilation that is presumed to be due to a specific agonist action on dopamine receptors (distinct from alpha and beta adrenoceptors) in the renal, mesenteric, coronary, and intracerebral vascular beds. At these dopamine receptors, [[haloperidol]] is an antagonist. The vasodilation in these vascular beds is accompanied by increased glomerular filtration rate, renal blood flow, sodium excretion, and urine flow. [[Hypotension]] sometimes occurs. An increase in urinary output produced by dopamine is usually not associated with a decrease in osmolarity of the urine.
 
At intermediate rates of infusion (2-10 mcg/kg/min) dopamine acts to stimulate the beta1- adrenoceptors, resulting in improved [[myocardial contractility]], increased SA rate and enhanced impulse conduction in the heart. There is little, if any, stimulation of the beta2-adrenoceptors (peripheral vasodilation). Dopamine causes less increase in myocardial oxygen consumption than [[isoproterenol]], and its use is not usually associated with a [[tachyarrhythmia]]. Clinical studies indicate that it usually increases [[systolic pressure]] and [[pulse pressure]] with either no effect or a slight increase in [[diastolic pressure]]. Blood flow to the peripheral vascular beds may decrease while mesenteric flow increases due to increased cardiac output. At low and intermediate doses, total peripheral resistance (which would be raised by alpha activity) is usually unchanged.
 
At higher rates of infusion (10-20 mcg/kg/min) there is some effect on alpha-adrenoceptors, with consequent vasoconstrictor effects and a rise in [[blood pressure]]. The vasoconstrictor effects are first seen in the skeletal muscle vascular beds, but with increasing doses they are also evident in the renal and mesenteric vessels. At very high rates of infusion (above 20 mcg/kg/min), stimulation of alpha-adrenoceptors predominates and vasoconstriction may compromise the circulation of the limbs and override the dopaminergic effects of dopamine, reversing renal dilation and natriuresis.
|PK=Dopamine’s onset of action occurs within five minutes of intravenous administration, and with dopamine’s plasma half-life of about two minutes, the duration of action is less than ten minutes. If [[monoamine oxidase]] ([[MAO]]) inhibitors are present, however, the duration may increase to one hour. The drug is widely distributed in the body but does not cross the [[blood-brain barrier]] to a significant extent. [[Dopamine]] is metabolized in the [[liver]], [[kidney]], and plasma by [[MAO]] and catechol-O-methyltransferase to the inactive compounds homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid. About 25% of the dose is taken up into specialized neurosecretory vesicles (the adrenergic nerve terminals), where it is hydroxylated to form norepinephrine. It has been reported that about 80% of the drug is excreted in the urine within 24 hours, primarily as HVA and its sulfate and glucuronide conjugates and as 3,4-dihydroxyphenylacetic acid. A very small portion is excreted unchanged.
|nonClinToxic=Long-term animal studies have not been performed to evaluate carcinogenic potential of dopamine hydrochloride.
 
Dopamine hydrochloride at doses approaching maximal solubility shows no clear genotoxic potential in the Ames test. Although there was a reproducible dose-dependent increase in the number of revertant colonies with strains TA100 and TA98, both with and without metabolic activation, the small increase was considered inconclusive evidence of mutagenicity. In the L5178Y TK+/− mouse lymphoma assay, dopamine hydrochloride at the highest concentrations used of 750 mcg/mL without metabolic activation, and 3000 mcg/mL with activation, was toxic and associated with increases in mutant frequencies when compared to untreated and solvent controls; at the lower concentrations no increases over controls were noted.
 
No clear evidence of clastogenic potential was reported in the in vivo mouse or male rat [[bone marrow]] micronucleus test when the animals were treated intravenously with up to 224 mg/kg and 30 mg/kg of dopamine hydrochloride, respectively.
|clinicalStudies======Poor Perfusion of Vital Organs=====
 
Clinical studies have shown that when dopamine is administered before urine flow has diminished to levels approximating 0.3 mL/minute, prognosis is more favorable.  Nevertheless, in a number of [[oliguric]] or [[anuric]] patients, administration of dopamine resulted in an increase in urine flow which in some cases reached normal levels. Dopamine may also increase urine flow in patients whose output is within normal limits and thus may be of value in reducing the degree of preexisting fluid accumulation. It should be noted that at doses above those optimal for the individual patient urine flow may decrease, necessitating reduction of dosage. Concurrent administration of dopamine and [[diuretic]] agents may produce an additive or potentiating effect.
|howSupplied=* Packages of 25 vials: 200 mg/5 mL Vial (40 mg/mL) (NDC 0517-1805-25) (color-coded WHITE)
* Packages of 25 vials: 400 mg/5 mL Vial (80 mg/mL) (NDC 0517-1905-25)(color-coded GREEN)
* Packages of 25 vials: 800 mg/5 mL Vial (160 mg/mL) (NDC 0517-1305-25) (color-coded YELLOW)
 
|storage=* Store at 20° to 25°C (68° to 77°F); excursions permitted to 15° to 30°C (59° to 86°F).
* Avoid contact with alkalis (including sodium bicarbonate), oxidizing agents or iron salts.
|fdaPatientInfo=There is limited information regarding Patient Counseling Information of aminocaproic acid in the drug label.
|alcohol=Alcohol-SandboxAlonso interaction has not been established. Talk to your doctor about the effects of taking alcohol with this medication.
|brandNames=* Intropin
|lookAlike=* Dopamine - [[Dobutamine]]
|nlmPatientInfo=(Link to patient information page)
|drugShortage=Drug Shortage
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Latest revision as of 01:53, 14 October 2014

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Alonso Alvarado, M.D. [2]

Infobox goes here

{{SI}}

Synonyms and keywords:

Overview

Body dysmorphic disorder (BDD) is a mental disorder that involves a disturbed body image. It is generally diagnosed in those who are extremely critical of their physique or self-image, despite the fact there may be no noticeable disfigurement or defect.

Most people wish they could change or improve some aspect of their physical appearance, but people suffering from BDD, generally considered of normal appearance, believe that they are so unspeakably hideous that they are unable to interact with others or function normally for fear of ridicule and humiliation at their appearance. They tend to be very secretive and reluctant to seek help because they are afraid others will think them vanity|vain or they may feel too embarrassed to do so.

Ironically, BDD is often misunderstood as a vanity driven obsession, whereas it is quite the opposite; people with BDD believe themselves to be irrevocably ugly or defective.

BDD combines obsessive and compulsive aspects, which links it to the OCD spectrum disorders among psychologists. People with BDD may engage in compulsive mirror checking behaviors or mirror avoidance, typically think about their appearance for more than one hour a day, and in severe cases may drop all social contact and responsibilities as they become homebound. The disorder is linked to an unusually high suicide rate among all mental disorders.

A German study has shown that 1-2% of the population meet all the diagnostic criteria of BDD, with a larger percentage showing milder symptoms of the disorder (Psychological Medicine, vol 36, p 877). Chronically low self-esteem is characteristic of those with BDD due to the value of oneself being so closely linked with their perceived appearance. The prevalence of BDD is equal in men and women, and causes chronic social anxiety for those suffering from the disorder[3].

Phillips & Menard (2006) found the completed suicide rate in patients with BDD to be 45 times higher than in the general US population. This rate is more than double that of those with Clinical depression and three times as high as those with bipolar disorder[1]. There has also been a suggested link between undiagnosed BDD and a higher than average suicide rate among people who have undergone cosmetic surgery[2].

Historical Perspective

BDD was first documented in 1886 by the researcher Morselli, who called the condition simply "Dysmorphophobia". BDD was first recorded/formally recognized in 1997 as a disorder in the DSM; however, in 1987 it was first truly recognized by the American Psychiatric Association.

In his practice, Freud eventually had a patient who would today be diagnosed with the disorder; Russian aristocrat Sergei Pankejeff, nicknamed "The Wolf Man" by Freud himself in order to protect Pankejeff's identity, had a preoccupation with his nose to an extent that greatly limited his functioning.

Classification

Pathophysiology

BDD usually develops in adolescence, a time when people are generally most sensitive about their appearance. However, many patients suffer for years before seeking help. When they do seek help through mental health professionals, patients often complain of other symptoms such as depression, social anxiety or obsessive compulsive disorder, but do not reveal their real concern over body image. Most patients cannot be convinced that they have a distorted view of their body image, due to the very limited knowledge of the disorder as compared to OCD or others.

An absolute cause of body dysmorphic disorder is unknown. However research shows that a number of factors may be involved and that they can occur in combination, including:

A chemical imbalance in the brain. An insufficient level of serotonin, one of the brain's neurotransmitters involved in mood and pain, may contribute to body dysmorphic disorder. Although such an imbalance in the brain is unexplained, it may be hereditary.

Obsessive-compulsive disorder. BDD often occurs with OCD, where the patient uncontrollably practices ritual behaviors that may literally take over their life. A history of, or genetic predisposition to, OCD may make people more susceptible to BDD.

Generalized anxiety disorder. Body dysmorphic disorder may co-exist with generalized anxiety disorder. This condition involves excessive worrying that disrupts the patient's daily life, often causing exaggerated or unrealistic anxiety about life circumstances, such as a perceived flaw or defect in appearance, as in BDD.

Causes

Differentiating type page name here from other Diseases

Epidemiology and Demographics

According to Dr Katharine Phillips (2004) :

Although large epidemiologic surveys of BDD's prevalence have not been done, studies to date indicate that BDD is relatively common in both nonclinical and clinical settings (Phillips & Castle, 2002). Studies in community samples have reported current rates of 0.7% and 1.1%, and studies in nonclinical student samples have reported rates of 2.2%, 4%, and 13% (Phillips & Castle, 2002). A study in a general inpatient setting found that 13% of patients had BDD (Grant, Won Kim, Crow, 2001). Studies in outpatient settings have reported rates of 8%-37% in patients with OCD, 11%-13% in social phobia, 26% in trichotillomania, 8% in major depression, and 14%-42% in atypical major depression (Phillips & Castle, 2002). In one study of atypical depression, BDD was more than twice as common as OCD (Phillips, Nierenberg, Brendel et al 1996), and in another (Perugi, Akiskal, Lattanzi et al, 1998) it was more common than many other disorders, including OCD, social phobia, simple phobia, generalized anxiety disorder, bulimia nervosa, and substance abuse or dependence. In a dermatology setting, 12% of patients screened positive for BDD, and in cosmetic surgery settings, rates of 6%-15% have been reported (Phillips & Castle, 2002).

BDD is underdiagnosed, however. Two studies of inpatients (Phillips, McElroy, Keck et al, 1993, and Grant, Won Kim, Crow, 2001), as well as studies in general outpatients (Zimmerman & Mattia, 1998) and depressed outpatients (Phillips, Nierenberg, Brendel et al 1996), systematically assessed a series of patients for the presence of BDD and then determined whether clinicians had made the diagnosis in the clinical record. All four studies found that BDD was missed by the clinician in every case in which it was present. Thus, underdiagnosis of BDD appears common.

Risk Factors

Screening

Natural History, Complications, and Prognosis

Diagnosis

Symptoms

  • Compulsive mirror checking, glancing in reflective doors, windows and other reflective surfaces.
  • Alternatively, an inability to look at one's own reflection or photographs of oneself; often the removal of mirrors from the home.
  • Compulsive skin-touching, especially to measure or feel the perceived defect.
  • Reassurance-seeking from loved ones.
  • Social withdrawal and co-morbid depression.
  • Obsessive viewing of favorite celebrities or models the person suffering from BDD may wish to resemble.
  • Excessive grooming behaviors: combing hair, plucking eyebrows, shaving, etc.
  • Obsession with plastic surgery or multiple plastic surgeries with little satisfactory results for the patient.
  • In obscure cases patients have performed plastic surgery on themselves, including liposuction and various implants with disastrous results.

Location of imagined defects

In research carried out by Dr. Katharine Philips, involving over 500 patients, the percentage of patients concerned with the most common locations were as follows:

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