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    Diabetes Insipidus Journal Reading

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    nadiyasyadina
    This document provides information about diabetes insipidus, including an overview of 8 patients being treated for the condition from June 20 to July 30, 2016. It defines diabetes insipidus as a disease characterized by the passage of large volumes of dilute urine. It then covers the pathophysiology, causes (including neurogenic, nephrogenic, familial, acquired, gestational, and dipsogenic), symptoms and signs, investigations, diagnosis, and management of diabetes insipidus. The key diagnostic test is a fluid deprivation test, and management depends on the type of diabetes insipidus, involving medications like desmopressin or maintaining adequate fluid intake.

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    Diabetes Insipidus Journal Reading

    Uploaded by

    nadiyasyadina
    123 views13 pages
    This document provides information about diabetes insipidus, including an overview of 8 patients being treated for the condition from June 20 to July 30, 2016. It defines diabetes insipidus as a disease characterized by the passage of large volumes of dilute urine. It then covers the pathophysiology, causes (including neurogenic, nephrogenic, familial, acquired, gestational, and dipsogenic), symptoms and signs, investigations, diagnosis, and management of diabetes insipidus. The key diagnostic test is a fluid deprivation test, and management depends on the type of diabetes insipidus, involving medications like desmopressin or maintaining adequate fluid intake.

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    Diabetes Insipidus journal reading

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    This document provides information about diabetes insipidus, including an overview of 8 patients being treated for the condition from June 20 to July 30, 2016. It defines diabetes insipidus as a disease characterized by the passage of large volumes of dilute urine. It then covers the pathophysiology, causes (including neurogenic, nephrogenic, familial, acquired, gestational, and dipsogenic), symptoms and signs, investigations, diagnosis, and management of diabetes insipidus. The key diagnostic test is a fluid deprivation test, and management depends on the type of diabetes insipidus, involving medications like desmopressin or maintaining adequate fluid intake.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    123 views13 pages

    Diabetes Insipidus Journal Reading

    Uploaded by

    nadiyasyadina
    This document provides information about diabetes insipidus, including an overview of 8 patients being treated for the condition from June 20 to July 30, 2016. It defines diabetes insipidus as a disease characterized by the passage of large volumes of dilute urine. It then covers the pathophysiology, causes (including neurogenic, nephrogenic, familial, acquired, gestational, and dipsogenic), symptoms and signs, investigations, diagnosis, and management of diabetes insipidus. The key diagnostic test is a fluid deprivation test, and management depends on the type of diabetes insipidus, involving medications like desmopressin or maintaining adequate fluid intake.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    of 13
    At a glance
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    The key takeaways are that diabetes insipidus is characterized by excessive urine output and can be caused by problems with vasopressin production or the kidneys' response to vasopressin. It has potentially life-threatening consequences if not managed properly.

    The main types are neurogenic diabetes insipidus caused by problems with vasopressin production in the hypothalamus/pituitary and nephrogenic diabetes insipidus caused by the kidneys' inability to respond to vasopressin. Causes include genetic mutations, tumors, trauma and infections.

    Investigations used to diagnose diabetes insipidus include measuring urine and serum osmolality levels during fluid deprivation and after administration of desmopressin to determine the body's response to vasopressin.

    COASS NEURO RSAL PERIODE 20 JUNE - 30JULY

    2016

    Diabetes insipidus
    1. Arini Nisaul I.A 030.11.043
    2. Afifah widyadhari 030.12.005
    3. Andini Yuliana 030.12.018
    4. Fauzan hilman 030.12.102
    5. Nadiya

    030.12.182

    6. Ovia yanli

    030.12.203

    7. Rizky widya kirana

    030.12.236

    8. Tri wira almungis sp. 030.12.271

    What is Diabetes Insipidus?


    Diabetes Insipidusis a disease characterised by the
    passage
    of
    large
    volumes(>3L/24hrs)of
    dilute
    urine(osmolality
    <300
    mOsmol/Kg).
    It
    affects
    approximately 3 in 100,000 people.In some cases the
    volume of urine produced can be as much as 20 litres in a
    24 hour period and therefore rapid dehydration can easily
    occur, leading to death if not managed appropriately.
    Diabetes Insipidus has a number of causes and therefore
    use of the correct investigations is essential to reach a
    definitive diagnosis.

    Pathophysiology
    1.Vasopressin(Anti-Diuretic Hormone)is produced by
    the hypothalamus in response to increased serum
    osmolality
    2.Vasopressin is then transported to the posterior
    pituitary gland
    3.It is then released into the circulatory system via
    the posterior pituitary gland
    4.It then travels to the kidneys where it binds to
    vasopressin receptors on the distal convoluted
    tubules
    5.Thiscauses Aquaporin-2 channels to move from the
    cytoplasm into the apical membrane of the tubules.

    These aquaporin-2 channels allow water to be reabsorbed out of


    the collecting ducts & back into the blood stream.
    This results in both a decrease in volume & an increase in
    osmolality (concentration) of the urine been excreted

    6.The extra water that has been reabsorbed re-enters


    the circulatory system, reducing the serum osmolality
    7.This reduction in serum osmolality is detected by
    the hypothalamus & results in decreased production
    of vasopressin.

    Causes
    Neurogenic
    Diabetes insipidus can occur as a result of decreased circulating levels of Vasopressin(ADH). Vasopressin is
    responsible for instructing the kidneys to retain fluid. Therefore decreased circulating levels of ADH results in
    the production of copious volumes of urine. Because vasopressin is produced by the hypothalamus &
    released by the posterior pituitary gland, pathology impacting either of these glands has the potential to
    cause diabetesinsipidus.
    Acquired

    Familial
    Mutations in the
    Vasopressin
    gene(e.g. Autosomal
    dominant AVP-NPII)
    Results in inadequate
    production of functional
    Vasopressin

    Tumours Pituitary adenomas(20%), Craniopharyngiomas, Metastases


    Trauma 17% of casese.g. Head injury
    Neurosurgery 9% of cases
    Infections meningitis
    Vascular Sheehans syndrome
    Complication of pregnancy in which the pituitary blood supply is causing
    necrosis of the gland
    Sarcoidosis formation of granulomas in pituitary
    Haemochromotosis deposition of iron in pituitary/hypothalamic tissue
    causing damage
    Langerhans cell histiocytosis
    Proliferation ofLangerhanscells which form lesions in many organs
    including
    pituitary stalk
    Idiopathic 25% of cases.

    Causes

    Nephrogenic
    The kidneys are responsible for reabsorbing fluid
    when ADH binds to their receptors. Anything which
    interferes with this binding or damages the kidneys
    has
    the potential to cause diabetesinsipidus.
    Familial
    Acquired

    X-linked recessive mutations


    in the ADH receptor gene
    Autosomal recessive
    aquaporin-2 gene aquaporin 2
    isresponsible for the
    reabsorption of water from
    urine4

    Metabolic hypercalcaemia, hyperglycaemia,


    hypokalaemia
    Drugs lithium, demeclocycline both
    interfere with the binding of ADH
    Chronic renal disease polycystic kidneys
    Amyloidosis
    Post obstructive uropathy

    Causes
    Dipsogenic

    Dipsogenic diabetes insipidus is caused by a defect or damage to the hypothalamus causing


    malfunction of the thirst mechanism. As a result the individual is excessively thirsty regardless
    of their fluid status. The individual therefore consumes large volumes of fluid which suppresses
    secretion of vasopressin and increases urine output. It is dangerous to give a vasopressin
    analogue such as Desmopressin in these circumstances as the individual will continue to feel
    thirsty and consume large volumes of fluids which could result in fluid overload.
    Gestational

    Gestational diabetes insipidus only occurs during pregnancy. During pregnancy the placenta
    produces vasopressinase which breaks down vasopressin. Gestational diabetes insipidus is
    therefore thought to be caused by overproduction of vasopressinase by the placenta causing a
    lack of functional vasopressin.

    Primary Polydipsia

    Primary polydipsia is characterised by an individual consuming large volumes of fluids and as a


    result producing large volumes of dilute urine. The symptoms of primary polydipsia are therefore
    very similar to those of diabetes insipidus however a fluid deprivation test can help distinguish
    the diseases. Most often primary polydipsia is due to a psychological disorder.

    Symptoms & Signs


    Symptoms
    Excessive
    urination(>3L/24hrs)
    Excessive thirst(especially
    for ice cold water)
    Nocturia
    Dehydration
    headache,dizziness,
    fainting, dry mouth

    Signs
    Hypotension
    Dilute urine
    Reduced capillary refill
    time

    Investigations
    Measure urine output confirm more than 3000ml a day
    Exclude diabetes mellitus dipstick urine for glucose & assess blood glucose level
    Exclude renal failure
    Check electrolyte levels
    Hypokalaemia & Hypercalcaemia nephrogenic DI
    Hypernatraemia can develop due to dehydration
    Fluid deprivation test
    Helps determine cause of DI neurogenic, nephrogenic, primary polydipsia
    Patient is allowed fluids overnight
    Patient is then deprived of fluids for 8 hours(or until loss of 5% of body weight if earlier)
    The patient is weighed hourly
    Plasma osmolality is measured every 4 hours
    Urine volume & Osmolality is measured every 2 hours
    At the end of the deprivation period the patient is given 2mcg of IM Desmopressin
    Urine volume & Serum osmolality are then measured over the next 4 hours
    MRI scan head looking for tumours pituitary adenomas, craniopharyngomas

    Diagnosis
    The fluid deprivation test is the most useful in diagnosing diabetesinsipidus
    It can confirm the presence of DI and suggest which type of DI the individual
    likely has
    If the serum osmolality is >305mOsm/kg at any point the patient has DI(stop
    test)

    Diagnosis
    Neurogenic
    If the diagnosis is Neurogenic DI the urine osmolality will be low after fluid deprivation but
    normalise after desmopressin is given. This is because neurogenic DI is caused by the lack of
    vasopressin production therefore giving a synthetic form of vasopressin such as desmopressin
    normalises levels of the hormone resulting in the normalisation of serum & urine osmolality.
    Nephrogenic
    If the diagnosis is Nephrogenic DI then the urine osmolality will remain low throughout regardless
    of desmopressin. This is because the kidneys have a problem which prevents them from been
    able to respond to vasopressin, therefore giving extra synthetic vasopressin will have no effect.
    Primary Polydipsia
    If the diagnosis is Primary Polydipsia the urine osmolality will remain high after fluid deprivation
    as well as after desmopressin is given. This is because the patients vasopressin axis is intact
    and otherwise completely normal.
    Partial DI or Polydipsia
    If the diagnosis is that of Partial DI or Polydipsia the picture may be mixed. The patient may have
    aslightlylow osmolality after fluid deprivation and may not reach normal urine osmolality after
    desmopressin. This kind of picture would require more thorough investigation to determine a

    Management
    Neurogenic
    Give Desmopressin

    Vasopressin analogue
    Binds to v2 receptors on kidney allowing water to be reabsorbed
    Drug can be given orally, intranasally, parenterally or bucally
    Dose varies significantly between patients
    Osmolality & Serum Sodium need monitoring can cause hyponatraemia or hypo-osmolality

    Chlorpropamide & Carbamazepine can be used to increase activity of vasopressin

    Nephrogenic
    Advise patient to maintain adequate fluid intake
    Correct any metabolicderangementshypercalcaemia, hyperglycaemia,
    hypokalaemia
    Stop any drugs that may be to blamelithium, demeclocycline both interfere with
    the binding of ADH
    High dose Desmopressin up to 5mcg IM
    Thiazide diuretics / Prostaglandin Synthase Inhibitors reduce action of
    prostaglandins which can inhibit vasopressins action on the kidney

    Management
    Partial Diabetes Insipidus
    Advise patient to maintain adequate fluid intakeusually
    nodrugs required
    Thirst mechanism must be normal
    Polyuria must be mild (<4L/24hrs)
    Primary Polydipsia
    Often very difficult to manage
    The underlying psychiatric disorder needs to be treated

    Reference
    From http://geekymedics.com/diabetes-insipidus/
    1.Oxford handbook of Endocrinology & Diabetes
    2.Saborio, P.; Tipton, G. A.; Chan, J. C. M. (2000). Diabetes
    Insipidus.Pediatrics in Review21(4): 122129
    3.Makras P, Papadogias D, Kontogeorgos G, Piaditis G, Kaltsas G
    (2005). Spontaneous gonadotrophin deficiency recovery in an
    adult patient with Langerhans cell histiocytosis
    (LCH).Pituitary8(2): 16974
    4.Wildin, Robert (2006).What is NDI?. The Diabetes Inspidus
    Foundation

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