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| {{Syndrome of inappropriate antidiuretic hormone}}
| | [[Image:Home_logo1.png|right|250px|link=https://www.wikidoc.org/index.php/Syndrome_of_inappropriate_antidiuretic_hormone]] |
| {{CMG}}; {{AE}} {{Vbe}} | | {{CMG}}; {{AE}}{{Vbe}} |
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| ==Overview== | | ==Overview== |
| [[SIADH]] consists of[[ hyponatremia]], inappropriately elevated[[ urine]] [[osmolality]], excessive urine [[sodium]] and decreased serum [[osmolality]] in a [[euvolemic]] patient without [[edema]]. These findings should occur in the absence of [[diuretic]] treatment with normal [[cardiac, renal]], [[adrenal]], [[hepatic]] and [[thyroid]] function.[[ Hyponatremia]] occurs in about 30% of hospitalized patients and SIADH is the most frequent cause of hyponatremia. Differentiating hyponatremia due to SIADH from other causes of hyponatremia becomes essential to evaluate the treatment plan. [[Syndrome of inappropriate antidiuretic hormone]] must be differentiated from [[Cerebral salt-wasting syndrome|cerebral salt wasting]] , [[adrenal insufficiency]], [[hypopituitarism]], [[hypothyroidism]],[[psychogenic polydipsia]]
| | Syndrome of inappropriate antidiuretic hormone (SIADH) must be differentiated from other causes of [[hyponatremia]], such as [[cerebral salt wasting syndrome]], [[adrenal insufficiency]], [[hypopituitarism]], and [[psychogenic polydipsia]]. |
| | | ==Differentiating Syndrome of Inappropriate Antidiuretic Hormone from other Diseases== |
| ==Differentiating Syndrome of inappropriate antidiuretic hormone from other Diseases== | | [[SIADH]] must be differentiated from cerebral salt wasting, [[ adrenal insufficiency]], [[hypopituitarism]], [[hypothyroidism]], and [[psychogenic polydipsia]].<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><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><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> |
| [[SIADH]] must be differentiated from [[cerebral salt wasting]], [[ adrenal insufficiency]], [[hypopituitarism]], [[hypothyroidism]], [[psychogenic polydipsia]]<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><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><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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| {| class="wikitable"
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| ! align="center" style="background:#4479BA; color: #FFFFFF;" + |Disease
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| ! align="center" style="background:#4479BA; color: #FFFFFF;" + |Causes
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| ! align="center" style="background:#4479BA; color: #FFFFFF;" + |Symptoms
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| ! align="center" style="background:#4479BA; color: #FFFFFF;" + |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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| *[[Nausea/vomiting]]
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| *[[Cramps]]
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| *[[Depressed mood]]
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| *[[Irritability]]
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| *[[Confusion]]
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| *[[ Hallucinations]].
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| *[[Seizures]] ,[[stupor]] or [[coma ]]
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| *[[Hyponatremia ]] <135 mmol/l
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| *[[Decreased effective serum osmolalit]]y<275mosm
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| *[[Urine sodium concentration]]>40mmol/litre
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| *[[Plasma uric acid]] <200;FeUrate>12%
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| *Absence of edematous disease like[[ cardiac failure]], [[liver cirrhosis]],[[ nephrotic syndrome]].
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| *Normal [[adrenal]] and thyroid function
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| | {| style="border: 0px; font-size: 90%; margin: 3px; width: 1000px" align="center" |
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| | ! style="background: #4479BA; width: 200px;" | {{fontcolor|#FFF|Differential Diagnosis}} |
| | ! style="background: #4479BA; width: 300px;" | {{fontcolor|#FFF|Similar Features}} |
| | ! style="background: #4479BA; width: 300px;" | {{fontcolor|#FFF|Differentiating Features}} |
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| | | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[SIADH]] |
| | | style="padding: 5px 5px; background: #F5F5F5;" | |
| | *Excessive release of [[Vasopressin|antidiuretic hormone (ADH or vasopressin)]] from the [[posterior pituitary]] gland or another source. |
| | *[[Hyponatremia]] |
| | *[[Fluid]] overload |
| | *[[Hyponatremia]] <135 mmol/l |
| | *Effective serum [[osmolality]] < 275 mOsm |
| | *Urine [[sodium]] concentration > 40 mMol/l |
| | *Plasma [[uric acid]] < 200 |
| | *Absence of [[edema]]-inducing diseases, such as [[heart failure]], [[liver cirrhosis]], and [[nephrotic syndrome]] |
| | *Normal [[adrenal]] and [[thyroid]] function |
| | | style="padding: 5px 5px; background: #F5F5F5;" | |
| | * [[Weight loss]] (in case of [[malignancy]]) |
| | * History of head [[trauma]] |
| | * History of medication intake |
| | * Positive [[family history]] |
| |- | | |- |
| |Cerebral salt wasting syndrome | | | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[Cerebral salt wasting syndrome]] |
| | | | style="padding: 5px 5px; background: #F5F5F5;" | |
| |[[ Cerebral salt wasting syndrome]] is defined as the[[ renal]] loss of [[sodium]] during intracranial disease leading to [[hyponatremia]] and a decrease in extracellular fluid volume. | | *[[Hyponatremia]] |
| | | *Urine [[sodium]] concentration > 40 mMol/l |
| *[[Trauma]] | |
| *[[Tumor]] | |
| *[[Hematoma]]
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| |The patient is | | | style="padding: 5px 5px; background: #F5F5F5;" | |
| *[[Hypovolemic]] | | *[[Hypovolemia]] |
| *[[Hyponatremic]]. | | *Intracranial [[diseases]], such as: |
| | | **[[Tumor]] |
| |Treatment is with adequate
| | **[[Trauma]] |
| *[[Hydration]] and | | **[[Hematoma]] |
| *[[Sodium]] replacement. | |
| |- | | |- |
| |[[Adrenal insufficiency]] | | | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[Adrenal insufficiency]] |
| | | | style="padding: 5px 5px; background: #F5F5F5;" | |
| |[[Adrenal insufficiency]] ranges from mild nonspecific symptoms to life-threatening [[shock]] like condition. | | *[[Hyponatremia]] |
| 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.
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| Adrenal insufficiency 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]]. Most common causes are:
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| *[[Traumatic brain injury (TBI) ]]
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| *[[Panhypopituitarism]]
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| Tertiary adrenal insufficiency refers to decreased [[hypothalamic]] stimulation of the pituitary to secrete [[ACTH]].
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| Exogenous[[ steroid]] administration is the most common cause of tertiary [[adrenal]] insufficiency.
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| * [[Fatigue]] | |
| *[[ 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
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| *[[Weight loss]] | | *[[Weight loss]] |
| *[[Sparse axillary hair]] | | *Sparse [[axillary]] hair |
| *[[Hyperpigmentation]] of the skin | | *[[Hyperpigmentation]] |
| *[[Orthostatic hypotension]]. | | *[[Orthostatic hypotension]] |
| | | *[[Fever]] |
| Acute [[addisonian]] crisis is characterized by [[fever]] and[[ hypotension]]. A low [[sodium]] with a high[[ potassium]] level and mild [[acidosis]] are also present.
| | *[[Hypotension]] |
| |The diagnosis of [[Addisons]] disease is made through rapid [[ACTH]] administration and measurement of [[cortisol]].Lab findings include:
| | *[[Eosinophilia]] |
| *[[White blood cell]] count with moderate [[neutropenia]],[[lymphocytosis]],and[[ eosinophilia]] | | *[[Hyperkalemia]] |
| *Elevated serum[[ potassium]] and [[urea nitrogen]] | | *[[Hypoglycemia]] |
| *Low [[sodium]] | | *Morning low plasma [[cortisol]] |
| *Low blood[[ glucose]] | |
| * Morning low plasma [[cortisol]]. | |
| 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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| Management: The management of Addison disease involves:
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| *Gluocorticoid
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| *Mineralocorticoid
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| *Sodium chloride replacement.
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| Adrenal crisis:
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| *In adrenal crisis,measure cortisol level,then rapidly administer fluids and hydrocortisone.
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| *Adrenal crisis may occur in previously undiagnosed patient who have:
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| *Undergone surgery
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| *Serious infection
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| *Any major stressful conditions.
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| *Bilateral adrenal infarction or hemorrhage
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| *Patient who is abruptly withdrawn from chronic glucocorticoid therapy
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| |- | | |- |
| |Hypopituitarism: | | | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[Hypopituitarism]] |
| |Hypopituitarism is defined as the partial or complete loss of anterior pituitary function that can result from acquired or congenital causes.
| | | style="padding: 5px 5px; background: #F5F5F5;" | |
| Etiology is as follows:
| | *[[Hyponatremia]] |
| *Pituitary tumors
| | | style="padding: 5px 5px; background: #F5F5F5;" | |
| *Sellar tumors
| | * [[Fatigue]] |
| *Head trauma
| | * [[Weight loss]] |
| *Infection
| | * Decreased [[libido]] |
| *Empty sella
| | * Decreased [[appetite]] |
| *Infiltration
| | * Facial [[puffiness]] |
| *Idiopathic
| | * [[Anemia]] |
| *Congenital
| | * [[Infertility]] |
| | | | * [[Cold intolerance]] |
| Signs and symptoms of hypopituitarism vary, depending on the deficient
| | * [[Amenorrhea]] |
| | | * Inability to lactate in [[breast feeding]] women |
| [[hormone ]] and severity of the disorder,some of the symptoms may be as follows: | | * Decreased [[facial]] or [[body hair]] in men |
| * Fatigue | | * [[Short stature]] in children |
| * Weight loss
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| * Decreased libido
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| * 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
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| *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.
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| A thorough and longitudinal history and physical examination, including visual field testing, are important.
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| Hypopituitarism may involve from one to all endocrine axes regulated by the pituitary
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| In order of frequency: [[growth hormone]] deficiency>[[secondary hypogonadism]]>[[secondary hypothyroidism]]>[[secondary adrenal failure]]).
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| The treatment of permanent hypopituitarism consists of replacement of the peripheral hormones
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| *[[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]].
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| |- | | |- |
| |Hypothyroidism | | | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[Psychogenic polydipsia]] |
| |Hypofunctioning of the thyroid gland due to multifactorial etiology ranging from congenital to [[autoimmune]] causes described below: | | | style="padding: 5px 5px; background: #F5F5F5;" | |
| *Congenital
| | *[[Fluid]] overload |
| *Autoimmune
| | *[[Hyponatremia]] |
| *Drugs
| | | style="padding: 5px 5px; background: #F5F5F5;" | |
| *Post surgery
| | *Defect in the [[hypothalamus]] |
| *Post radiation
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| *Infiltrative e.g., amyloid
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| * Fatigue | |
| * 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:
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| *T3(triiodothyronine)
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| *T4(Thyroxine) and
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| *TSH (thyroid stimulating hormone).
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| 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.
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| *The drug of choice for treatment is [[Levothyroxine]]. | |
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| |[[Psychogenic polydipsia]] | |
| | Also called as[[ primary polydipsia]] is characterized by[[ polyuria]] and [[polydipsia]]. Causes could be:
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| * Defect in the [[hypothalamus]] | |
| *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]] | | *[[Polyuria]] |
| *[[Polydipsia]] | | *[[Polydipsia]] |
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| *[[Lethargy]] | | *[[Lethargy]] |
| *[[Psychosis]] | | *[[Psychosis]] |
| *[[Seizures]] and | | *[[Seizures]] |
| *Sometimes, even [[Death]].
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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:
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| *[[Fluid]] restriction and[[ behavioral]] and [[pharmacologic]] modalities.
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| *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. In 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.
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| |} | | |} |
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| ==References== | | ==References== |
| {{Reflist|2}} | | {{Reflist|2}} |
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| [[Category:Needs content]] | | [[Category:Medicine]] |
| [[Category:Endocrinology]] | | [[Category:Endocrinology]] |
| | [[Category:Nephrology]] |
| [[Category:Neurology]] | | [[Category:Neurology]] |
| [[Category:Nephrology]] | | [[Category:Up-To-Date]] |
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