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| __NOTOC__ | | __NOTOC__ |
| {{Infobox Disease|
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| Name = Syndrome of inappropriate antidiuretic hormone |
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| Image = |
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| Caption = |
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| DiseasesDB = 12050 |
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| ICD10 = {{ICD10|E|22|2|e|20}} |
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| ICD9 = {{ICD9|253.6}} |
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| ICDO = |
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| OMIM = |
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| MedlinePlus = 003702 |
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| MeshID = D007177 |
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| }}
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| '''For patient information click [[{{PAGENAME}} (patient information)|here]]'''
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| {{Syndrome of inappropriate antidiuretic hormone}} | | {{Syndrome of inappropriate antidiuretic hormone}} |
| {{CMG}}; {{Vbe}} | | {{CMG}}; {{AE}}{{Vbe}} |
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| '''''Synonyms and Keywords:''''' SIADH; syndrome of inappropriate antidiuretic hormone secretion; inappropriate ADH syndrome; Schwartz-Bartter syndrome. | | '''''Synonyms and Keywords:''''' SIADH, Syndrome of inappropriate antidiuretic hormone secretion, Inappropriate ADH syndrome, Schwartz-Bartter syndrome |
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| ==[[Syndrome of inappropriate antidiuretic hormone overview|Overview]]== | | ==[[Syndrome of inappropriate antidiuretic hormone overview|Overview]]== |
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| ==[[Syndrome of inappropriate antidiuretic hormone causes|Causes]]== | | ==[[Syndrome of inappropriate antidiuretic hormone causes|Causes]]== |
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| ==[[Syndrome of inappropriate antidiuretic hormone differential diagnosis|Differentiating Syndrome of inappropriate antidiuretic hormone from other Diseases]]== | | ==[[Syndrome of inappropriate antidiuretic hormone differential diagnosis|Differentiating SIADH from other Diseases]]== |
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| {| class="wikitable"
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| !
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| Disease
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| !Causes
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| |Symptoms
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| |Diagnosis and treatment
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| |- Diagnostic criteria of SIADH include:
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| |SIADH
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| |SIADH is a syndrome characterized by excessive release of [[Vasopressin|antidiuretic hormone]] (ADH or vasopressin) from the [[posterior pituitary]] gland or another source. The result is [[hyponatremia]], and sometimes fluid overload.
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| |symptoms are variable. Ranging from nausea/vomiting,cramps,depressed mood,irritability,confusion and hallucinations. In severe cases seizures ,stupor or coma may result.
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| |Hyponatremia <135 mmol/l
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| Decreased effective serum osmolality<275mosm
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| Urine sodium concentration>40mmol/litre
| | ==[[Syndrome of inappropriate antidiuretic hormone epidemiology and demographics|Epidemiology and Demographics]]== |
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| Plasma uric acid <200;FeUrate>12%
| | ==[[Syndrome of inappropriate antidiuretic hormone risk factors|Risk Factors]]== |
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| Absence of edematous disease like cardiac failure, liver cirrhosis, nephrotic syndrome.
| | ==[[Syndrome of inappropriate antidiuretic hormone screening|Screening]]== |
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| normal adrenal and thyroid function
| | =[[Syndrome of inappropriate antidiuretic hormone natural history, complications and prognosis|Natural History, Complications and Prognosis]]= |
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| |- | | ==Diagnosis== |
| |Cerebral salt wasting | | [[Syndrome of inappropriate antidiuretic hormone history and symptoms|History and Symptoms]] | [[Syndrome of inappropriate antidiuretic hormone physical examination|Physical Examination]] | [[Syndrome of inappropriate antidiuretic hormone laboratory findings|Laboratory Findings]] | [[Syndrome of inappropriate antidiuretic hormone electrocardiogram|Electrocardiogram]] | [[Syndrome of inappropriate antidiuretic hormone x ray|Chest X Ray]] | [[Syndrome of inappropriate antidiuretic hormone CT|CT]] | [[Syndrome of inappropriate antidiuretic hormone MRI|MRI]] | [[Syndrome of inappropriate antidiuretic hormone echocardiography or ultrasound|Echocardiography or Ultrasound]] | [[Syndrome of inappropriate antidiuretic hormone other imaging findings|Other Imaging Findings]] | [[Syndrome of inappropriate antidiuretic hormone other diagnostic studies|Other Diagnostic Studies]] |
| | Cerebral salt wasting is defined as the renal loss of sodium during intracranial disease leading to hyponatremia and a decrease in extracellular fluid volume. | |
| |polyuria,polydipsia,lightheadedness, muscle cramps,orthostatic hypotension,headaches | |
| |The patient is hypovolemic and hyponatremic. | |
| Treatment is with adequate hydration and sodium replacement.
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| |Adrenal insufficiency | |
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| |Adrenal insufficiency ranges from mild nonspecific symptoms to life-threatening shock condition. An important distinction in these patients is the presence of mineralocorticoid deficiency. Those with secondary or tertiary adrenal insufficiency will typically have preserved mineralocorticoid function due to the separate feedback systems.
| | ==Treatment== |
| Adrenal insufficency can be primary, secondary or tertiary.
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| Common causes of primary adrenal insufficiency:
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| * Autoimmune
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| *Iatrogenic
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| *Drugs
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| *Others- adrenal hemorrhage, cancer, infection.
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| *congenital.
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| Secondary adrenal insufficiency refers to decreased adrenocorticotropic hormone (ACTH) stimulation of the adrenal cortex and therefore does not affect aldosterone levels. Traumatic brain injury (TBI) and panhypopituitarism are common causes.
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| Tertiary adrenal insufficiency refers to decreased hypothalamic stimulation of the pituitary to secrete ACTH. Exogenous steroid administration is the most common cause of tertiary adrenal insufficiency.
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| * fatigue
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| * muscle weakness
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| * loss of appetite
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| * weight loss
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| * abdominal pain
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| *diarrhea
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| *Vomiting
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| Chronic disease is characterized by weight loss,sparse axillary hair,hyperpigmentation of the skin,orthostatic hypotension.
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| Acute addisonian crisis is characterized by fever and hypotension. A low sodium with a high potassium level and mild acidosis are also present.
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| |The diagnosis of Addison disease is made through rapid ACTH administration and measurement of cortisol.Lab findings include white blood cell count with moderate neutropenia,lymphocytosis,and eosinophilia;elevated serum potassium and urea nitrogen;low sodium;low blood glucose;and morning low plasma cortisol.
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| The definitive diagnosis is the cosyntropin or ACTH stimulation test. A cortisol level is obtained before and after administering ACTH. A normal person should show a brisk rise in cortisol level after ACTH administration.
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| | [[Syndrome of inappropriate antidiuretic hormone medical therapy|Medical Therapy]] | [[Syndrome of inappropriate antidiuretic hormone surgery|Surgery]] | [[Syndrome of inappropriate antidiuretic hormone primary prevention|Primary Prevention]] | [[Syndrome of inappropriate antidiuretic hormone secondary prevention|Secondary Prevention]] | [[Syndrome of inappropriate antidiuretic hormone cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Syndrome of inappropriate antidiuretic hormone future or investigational therapies|Future or Investigational Therapies]] |
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| Management: The management of Addison disease involves glucocorticoid,mineralocorticoid,and sodium chloride replacement.
| | ==Case Studies== |
| Adrenal crisis: In adrenal crisis,get a cortsol level,then rapidly administer fluids and hydrocortisone. Adrenal crisis may occur in: previously undiagnosed patient with adrenal insufficiency who has undergone surgery,has a serious infection,or any major stressful conditions. Bilateral adrenal infarction or hemorrhage, Patient who is abruptly withdrawn from chronic glucocorticoid therapy
| | [[Syndrome of inappropriate antidiuretic hormone case study one|Case #1]] |
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| |Hypopituitarism:
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| |Hypopituitarism is defined as the partial or complete loss of anterior pituitary function that can result from acquired or congenital causes.
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| Etiology is as follows:
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| *Pituitary tumors
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| *Sellar tumors
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| *Head trauma
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| *Infection
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| *empty sella
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| *infiltration
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| *Idiopathic
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| *congenital
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| Signs and symptoms of hypopituitarism vary, depending on the deficient
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| hormone and severity of the disorder,some of the symptoms may be as follows:
| | [[Category:Medicine]] |
| * Fatigue
| | [[Category:Endocrinology]] |
| * Weight loss
| | [[Category:Nephrology]] |
| * Decreased libido
| | [[Category:Up-To-Date]] |
| * Decreased appetite
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| * Facial puffiness
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| * Anemia
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| * Infertility
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| * Cold insensitivity.
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| * amenorrha,inability to lactate in breast feeding women
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| * Decreased facial or body hair in men
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| * Short stature in children
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| |The diagnosis is based on detailed investigation of symptoms of target endocrine gland function relative to the corresponding pituitary hormone deficiency. The clinical manifestations of hypopituitarism result from the degree of the specific hormone deficiency. A thorough and longitudinal history and physical examination, including visual field testing, are important.<ref name="pmid27936532">{{cite journal |vauthors=Heidelbaugh JJ |title=Endocrinology Update: Hypopituitarism |journal=FP Essent |volume=451 |issue= |pages=25–30 |year=2016 |pmid=27936532 |doi= |url=}}</ref>.
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| Hypopituitarism may involve from one to all endocrine axes regulated by the pituitary (in order of frequency: growth hormone deficiency>secondary hypogonadism>secondary hypothyroidism>secondary adrenal failure).The treatment of permanent hypopituitarism consists of replacement of the peripheral hormones (hydrocortisone, DHEA, thyroxine, testosterone or oestradiol, growth hormone. surgery, and/or radiotherapy to restore normal endocrine function and quality of life. Patients with hypopituitarism require lifelong monitoring of serum hormone levels and symptoms of hormone deficiency or excess. Long-term care and monitoring of patients with hypopituitarism requires a experienced endocrinologist.<ref name="pmid15241506">{{cite journal |vauthors=Hammer F, Arlt W |title=[Hypopituitarism] |language=German |journal=Internist (Berl) |volume=45 |issue=7 |pages=795–811; quiz 812–3 |year=2004 |pmid=15241506 |doi=10.1007/s00108-004-1216-5 |url=}}</ref>
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| |Hypothyroidism
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| |Hypofunctioning of the thyroid gland due to multifactorial etiology ranging from congenital to autoimmune causes described below:
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| *Congenital
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| *Autoimmune
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| *Drugs
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| *Post surgery
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| *post radiation
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| *Infiltrative e.g., amyloid
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| * Fatigue
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| * Constipation
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| * Dry skin
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| * Weight gain
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| * Cold intolerance
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| * Puffy face
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| * Hoarseness
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| * Muscle weakness
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| * Elevated blood cholesterol level
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| * Bradycardia
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| * Myopathy
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| * Depression
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| * Impaired memory
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| | Diagnosis of hypothyroidism is based on blood tests,T3(triiodothyronine),T4(Thyroxine) and TSH (thyroid stimulating hormone). Signs and symptoms are neither sensitive nor specific for the diagnosis. TSH is the most sensitive tool for screening,diagnosis and treatment follow up, when pituitary is normal. The drug of choice for treatment is Levothyroxine.<ref name="pmid28551907">{{cite journal |vauthors=Bashkin A, Nodelman M |title=[THE CLINICAL APPROACH TO DIAGNOSIS AND TREATMENT OF HYPOTHYROIDISM] |language=Hebrew |journal=Harefuah |volume=156 |issue=5 |pages=322–325 |year=2017 |pmid=28551907 |doi= |url=}}</ref>
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| |Psychogenic polydipsia
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| | Also called as primary polydipsia is characterized by polyuria and polydipsia. Causes could be:
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| * Defect in the hypothalamus
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| *Adverse effect of a medication
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| *Traumatic brain injury
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| *Psychiatric disorders such as schizophrenia
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| |polyuria,polydipsia,confusion,lethargy,psychosis,seizures and sometimes, even death. <ref name="pmid17521521">{{cite journal |vauthors=Dundas B, Harris M, Narasimhan M |title=Psychogenic polydipsia review: etiology, differential, and treatment |journal=Curr Psychiatry Rep |volume=9 |issue=3 |pages=236–41 |year=2007 |pmid=17521521 |doi= |url=}}</ref>.
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| |Evaluation of psychiatric patients with polydipsia warrants a comprehensive evaluation for other medical causes of polydipsia, polyuria, hyponatremia, and the syndrome of inappropriate secretion of antidiuretic hormone. The management strategy in psychiatric patients should include fluid restriction and behavioral and pharmacologic modalities. The water deprivation test is the gold standard test to differentiate central or nephrogenic diabetes insipidus (DI) from primary polydipsia (PP) in patients with polyuria and polydipsia. n healthy subjects, water deprivation causes the plasma osmolality to rise above 280–290 mOsmol/kg, which leads to the release of AVP into the circulation. In the collecting ducts of the kidney, AVP binds to the vasopressin type 2 receptor and this is followed by expression of aquaporin 2 channels. This results in increased water retention with a rise in urine osmolality to a maximum of 1000–1200 mOsmol/kg and restoration of plasma osmolality toward the reference range. <ref name="pmid25712898">{{cite journal |vauthors=de Fost M, Oussaada SM, Endert E, Linthorst GE, Serlie MJ, Soeters MR, DeVries JH, Bisschop PH, Fliers E |title=The water deprivation test and a potential role for the arginine vasopressin precursor copeptin to differentiate diabetes insipidus from primary polydipsia |journal=Endocr Connect |volume=4 |issue=2 |pages=86–91 |year=2015 |pmid=25712898 |pmc=4401105 |doi=10.1530/EC-14-0113 |url=}}</ref>
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