Anti-Diuretic Hormone (Adh) / Vasopressin

ANTI-DIURETIC HORMONE (ADH) / VASOPRESSIN

Q. 1

True about free water clearance is:

 A

Regulated by ADH

 B

Regulated by aldosterone

 C

Increased by furosemide

 D

None of the above

Q. 1

True about free water clearance is:

 A

Regulated by ADH

 B

Regulated by aldosterone

 C

Increased by furosemide

 D

None of the above

Ans. A

Explanation:

A i.e. Regulated by ADH

–         100 mOsm/ kg H20. It does not mean that urine osmolality is greater than that of plasma. It only means that the urine is less than maximally diluted. And urine osmolality is not necessarily elevated inappropriately at all levels of plasma osmolality. 4. Elevated urinary sodium excretion (Turinary Na*) on a normal salt & water intake. It is present in most patients but is neither 100% diagnostic nor its absence rules out the diagnosis. ” align=”left” height=”278″ width=”339″>Concentration and dilution of urine i.e. free water and osmolar clearances are regulated by antidiuretic hormone (ADH) or vasopressinQ.

SIADH is characterized by relatively excessive ADH levels, euvolemia, hypoosmolality (decreased osmolality) of serum, hyponatremia (.1sertim Na*), inappropriately high urine osmolality and elevated urinary Na* excretionQ

Syndrome of Inappropriate ADH Secretion (SIADH)

–  Syndrome of inappropriate ADH secretion (SIADH) is characterized by relatively excessive ADH levels or plasma ADH levels that are elevated above what would be expected on the basis of body fluid osmolality, blood volume and

blood pressure – hence named inappropriate ADH secretion. Patients with SIADH retain water and their body fluids (eg serum) becomes progressively hypoosmotic. In other words, decreased excretion of excess water results in reduced (low)

plasma osmolality (ie hypoosmotic body fluids), hyponatremia (reduced plasma Na*) but the urine is hyper-osmotic (more concentrated) and contain increased urinary

Na* than would be expected on the basis of low body fluid osmolality.

– SIADH is characterized by low plasma osmolality,

hyponatremia (decreased plasma / serum Na*), inappropriately high urine osmolality and significant amounts of sodium in urine (Turinary Na*)

In SIADH, restricted Ovate intake is necessary to prevent cellular overhydration. Declomycin , an agent causing reversible nephrogenic diabetes insipidus (ie ADH deficiency 1/t dehydration, polyduria & polydipsia), may also be useful.

– Bartter & Schwartz clinical criteria for diagnosis of SIADH include

  1. SIADH is most common cause of euvolemic-hypoosmolality. Euvolemia is defined clinically on the basis of absence of signs of hypovolemia (ie tachycardia, orthostatic or postural hypotension decreased skin turgor & dry mucous membranes ) or hypervolemia (generalized edema, ascites etc). Other causes of euvolemic hypoosmolality such as hypothyroidism, hypocortisolism (pituitary ACTH deficiency or Addison’s disease) and diuretics must be excluded.
  2. Hypoosmolality (decreased effective osmolality) of ECF or serum (<275 mOsm/ kg H20) and hyponatremia (reduced plasma Na*); however, pseudo hyponatremia or hyper glycemia must be excluded.
  3. Inappropriately high urine osmolality (concentration) ie > 100 mOsm/ kg H20. It does not mean that urine osmolality is greater than that of plasma. It only means that the urine is less than maximally diluted. And urine osmolality is not necessarily elevated inappropriately at all levels of plasma osmolality.
  4. Elevated urinary sodium excretion (Turinary Na*) on a normal salt & water intake. It is present in most patients but is neither 100% diagnostic nor its absence rules out the diagnosis.

Nephrogenic Syndrome of Inappropriate Antidiuresis

Nephrogenic syndrome of inappropriate antidiuresis (NSIA) occurs d/t gain of function (activating) mutations is V, receptor gene resulting in its constitutive activation even in the absence of ADH. It present with same laboratory findings as those of SIADH including hypoosmolar serum, hyponatremia (4,serum Na*), hyperosmolar urine and Turine Nat But unlike SIADH (where high ADH levels are responsible for water retention by kidneys) patients with NSIA have undertrevels levels of ADH in their plasma.




Q. 2

Greatest stimulator for ADH secretion:

 A

Hyperosmolarity

 B

Hyponatremia

 C

Hypotension

 D

Hypovolemia

Q. 2

Greatest stimulator for ADH secretion:

 A

Hyperosmolarity

 B

Hyponatremia

 C

Hypotension

 D

Hypovolemia

Ans. A

Explanation:

A i.e. Hyperosmolarity


Q. 3

All of the following are true for ADH except:

 A

Post-operative increase in secretion

 B

Neurosecretion

 C

Increased secretion when plasma osmolality is low

 D

Act on disal tubule and icrease permeability

Q. 3

All of the following are true for ADH except:

 A

Post-operative increase in secretion

 B

Neurosecretion

 C

Increased secretion when plasma osmolality is low

 D

Act on disal tubule and icrease permeability

Ans. C

Explanation:

C i.e. Increased secretion when plasma osmolality is low

 


Q. 4

Which paraneoplastic syndrome is not seen with small cell ca lung –

 A

PTH

 B

ACTH

 C

ADH

 D

Carcinoid syndrome

Q. 4

Which paraneoplastic syndrome is not seen with small cell ca lung –

 A

PTH

 B

ACTH

 C

ADH

 D

Carcinoid syndrome

Ans. A

Explanation:

Ans. is ‘a’ i.e., PTH

o Lung carcinoma can be associated with a number of paraneoplastic syndromes, some of which may antedate the development of a gross pulmonary lesion.

o The hormones or hormone-like factors elaborated include :

        Antidiuretic hormone (ADH), inducing hyponatremia owing to inappropriate ADH secretion

        Adrenocorticotropic hormone (ACTH), producing Cushing syndrome

        Parathormone, parathyroid hormone-related peptide, prostaglandin E, and some cytokines, all implicated in the hypercalcemia often seen with lung cancer

        Calcitonin, causing hypocalcemia

        Gonadotropins, causing gynecomastia

        Serotonin & bradykinin, associated with the carcinoid syndrome

o Any one of the histologic types of tumors may occasionally produce any one of the hormones.

o Tumors that produce ACTH and ADH are predominantly small cell carcinomas, whereas those that produce hypercalcemia (due to PTH) are mostly squamous cell tumors.

o The carcinoid syndrome is only rarely associated with small cell carcinoma.


Q. 5

Posterior pituitary secrets-

 A

CH

 B

TSH

 C

ADH

 D

FSH

Q. 5

Posterior pituitary secrets-

 A

CH

 B

TSH

 C

ADH

 D

FSH

Ans. C

Explanation:

Ans. is ‘c’ i.e., ADH

Anterior pituitary has two types of cells : ‑

1. Acidophilic cells

o Somatotrophs            –>         Secrete growth hormone

o Lactotrophs               –>          Secrete prolactin

2. Basophilic cells

o Corticotrophs            –>           Secrete ACTH, POMC, MSH

o Thyrotrophs             –>            Secrete TSH

o Gonodotrophs          –>            Secrete FSH, LH Posterior pituitary secretes ADH and oxytocin.


Q. 6

ADH acts on –

 A

Proximal convoluted tubule

 B

Distal convoluted tubule

 C

Loop of Henle

 D

Collecting duct

Q. 6

ADH acts on –

 A

Proximal convoluted tubule

 B

Distal convoluted tubule

 C

Loop of Henle

 D

Collecting duct

Ans. D

Explanation:

Ans is ‘d’ i.e., Collecting duct

The characteristic feature of cells lining the collecting duct is their responsiveness to Antidiuretic hormone (AD.11).


Q. 7

True about nephrogenic diabetes insipidus in children –

 A

Decreased ADH secretion

 B

Receptor insensitivity in kidney tubules

 C

Decreased ADH

 D

Commonly associated with WILM’s tumor

Q. 7

True about nephrogenic diabetes insipidus in children –

 A

Decreased ADH secretion

 B

Receptor insensitivity in kidney tubules

 C

Decreased ADH

 D

Commonly associated with WILM’s tumor

Ans. B

Explanation:

Ans. is ‘b’ i.e., Receptor insensitivity in kidney tubules

o In nephrogenic diabetes insipidus, level of the ADH is normal.

o The defects lies in the distal tubule where the cells fail to respond to ADH.

o Diabetes inspidus is associated with wolfram syndrome or DIDMOD syndrome not wilm’s tumour.

Wolfram syndrome –> Diabetes insidus, Diabetes mellitus, Optic atrophy, Deafness


Q. 8

Carcinoma of pancreas associated with –

 A

Hypoglycemia

 B

Syndrome of inappropriate secretion of ADH

 C

Erythropoeisis is due to erythropoietin

 D

Hypercalcemia

Q. 8

Carcinoma of pancreas associated with –

 A

Hypoglycemia

 B

Syndrome of inappropriate secretion of ADH

 C

Erythropoeisis is due to erythropoietin

 D

Hypercalcemia

Ans. B

Explanation:

Ans. is ‘b’ i.e., Syndrome of inappropriate secretion of ADH 


Q. 9

SIADH is associated with the following drug :

 A

Vincristine

 B

Erythromycin

 C

5 – FU

 D

Methotrexate

Q. 9

SIADH is associated with the following drug :

 A

Vincristine

 B

Erythromycin

 C

5 – FU

 D

Methotrexate

Ans. A

Explanation:

Answer is A (Vincristine):

Vincristine is known to cause SIADH.

Drugs associated with SIADH : 

  • Vasopressin or desmopressin
  • Chlorpropamide
  • Oxytocin, high dose
  • Vincristine
  • Carbamezapine
  • Nicotine
  • Phenothiazines
  • Cyclophosphamide
  • Tricyclic antidepressants
  • M40 inhibitors
  • Serotonin reuptake inhibitors

Q. 10

SIADH is associated with :

 A

Small cell carcinoma lung

 B

Adeno carcinoma lung

 C

Squamous cell carcinoma lung

 D

Mixed cell tumor lung

Q. 10

SIADH is associated with :

 A

Small cell carcinoma lung

 B

Adeno carcinoma lung

 C

Squamous cell carcinoma lung

 D

Mixed cell tumor lung

Ans. A

Explanation:

Answer is A (Small cell Ca of lung):

Small cell Ca of lung causes SIADH due to ectopic secretion of ADH.


Q. 11

All of the following statements about SIADH are true except:

 A

Serum sodium is low, typically < 135 meq/1

 B

Urinary sodium excretion is low / normal

 C

Water loading test may be used

 D

Vaptans are new FDA approved agents for treatment of SIADH

Q. 11

All of the following statements about SIADH are true except:

 A

Serum sodium is low, typically < 135 meq/1

 B

Urinary sodium excretion is low / normal

 C

Water loading test may be used

 D

Vaptans are new FDA approved agents for treatment of SIADH

Ans. B

Explanation:

Answer is B (Urinary sodium excretion is low / normal):

SIADH is typically characterized by high urinary sodium (Increased rate of excretion of. odium).

Syndrome of Inappropriate ADH Secretion (SIADH) is associated with increased secretion of vasopressin (ADH), which leads to increased absorption of water producing dilutional hyponatremia (serum sodium typically < 135 meq/l) along with concentrated or hyperosmolar urine. Excessive retention of water stimulates compensatory mechanisms that enhance Watriuresis’.

Natriuresis results in increased urinary sodium excretion rate increased urinary sodium concentration) and is believed to compensate for increased volume from inappropriaye ADH secretion preventing a state of clinical hypervolemia, hypertension or edema.

SIADH is associated low serum sodium levels (<135 meg/I) and High urinary sodium

Cardinal features of SIADH include:

 

  • Hyponatremia (dilutional hyponatremia with Na+ < 135 mmo1/1)
  • Decreased plasma osmolality (<280 m osm/kg) with inappropriately increased urine osmolality > 150 m osm).
  • High Urine sodium (over 20 meq4)
  • Low Blood urea Nitrogen < 10 mg/L
  • Hypouricemia (<4 mg/dL)
  • Clinical Euvolemia

 

– Absence of signs of hypervolemia (edema, ascitis)

 

– Absence of signs of hypovolemia (orthostatic hypotension, tachycardia, features of dehydration)

 

  • Absence of cardiac, liver or renal disease
  • Normal thyroid and adrenal function
  • A high BUN suggests a volume contracted state and excludes a diagnosis of SIADH.

Water loading test may be used to help diagnosis of SIADH

Water loading test is recognized as a ‘supplemental criteria’ in establishing a diagnosis of SIADH.

The ‘Water Loading Test’ is of value when there is uncertainity regarding the etiology of modest degrees hypo-osmolality in euvolemic patients but it does not add useful information if the plasma osmolality is < 275 mOsm/kg H2O

 

Test Objective / Principle

Abnormal Water Loading Test Criteria

Fixed quantity of water is given to a patient and the amount of

Abnormal water load

urine produced and changes in blood/urine osmolality are

Inability to excrete at least 90% of a 20m1/kg

recorded.

water load in 4 hours, and/or

Inability to excrete a normal water load (decreased urinary

Failure to dilute urine (osm) to < 100 mOsm/kg

output) or failure to dilute urine is considered abnormal

H-,O.

 

 

 

 

 

 

Vaptans are new FDA approved agents for treatment of SIADH

`Vaptans’ are a new class of drugs that have emerged for treatment of hyponatremia. These medications act as Vasopressin receptors antagonists blocking the action of AVP in renal tubule, pituitary or smooth muscles depending upon receptor selectivity.

Conivaptan ,    itravenous use)

Conivaptan is a combined V1/V2 receptor antagonist is FDA approved for short-term intravenous use fin- treatment of hospitalized patients with SIADH.

Tolivaptan (Oval use)

Tolivaptan is a V2 receptor antagonist that has received FDA approval far oral use

 

100 mOsmol/kg H20 with normal renal function) at some level of hypoosmolality. (Urinary concentration must be inappropriate for Plasma Hyposmolality) • Clinical euvolemia, as defined by the absence of signs of hypovolemia (orthostasis, tachycardia, decreased skin rurgor, dry mucous membranes) or hypervolemia (subcutaneous edema, ascites). • Elevated urinary sodium excretion while on normal salt and water intake. • Absence of other potential causes of euvolemic hypoosmolality: hypothyroidism, hypocortisolism (Addison’s disease or pituitary adrenocorticotropic hormone [ACTH] insufficiency) and diuretic use. Supplemental • Abnormal water load test (inability to excrete at least 90% of a 20 mL/kg water load in 4 hours and/or failure to dilute Uosm to < 100 mOsmol/kg H-0). • Plasma AVP level inappropriately elevated relative to plasma osmolality. • No significant correction of serum [Nal with volume expansion but improvement after fluid restriction " align="left" height="259" width="655">Syndrome of Inappropriate ADH Secretion (SIADH): Concept Review

Differential Diagnosis of Hyponatremia Based on Clinical

 

Criteria for the diagnosis of syndrome of innapropriate antidiuretic hormone` secretion

 

Essential

 

  • Decreased effective osmolality of the extracellular fluid (13„,,, < 275 mOsmol/kg H20).

 

(True hypoosmolality must be present and hyponatremia secondary to pseudohyponatremia or hyperglycemia must be excluded)

 

Inappropriate urinary concentration (Uosm > 100 mOsmol/kg H20 with normal renal function) at some level of hypoosmolality. (Urinary concentration must be inappropriate for Plasma Hyposmolality)

 

  • Clinical euvolemia, as defined by the absence of signs of hypovolemia (orthostasis, tachycardia, decreased skin rurgor, dry mucous membranes) or hypervolemia (subcutaneous edema, ascites).
  • Elevated urinary sodium excretion while on normal salt and water intake.
  • Absence of other potential causes of euvolemic hypoosmolality: hypothyroidism, hypocortisolism (Addison’s disease or pituitary adrenocorticotropic hormone [ACTH] insufficiency) and diuretic use.

 

Supplemental

 

  • Abnormal water load test (inability to excrete at least 90% of a 20 mL/kg water load in 4 hours and/or failure to dilute Uosm to < 100 mOsmol/kg H-0).
  • Plasma AVP level inappropriately elevated relative to plasma osmolality.
  • No significant correction of serum [Nal with volume expansion but improvement after fluid restriction

Assessment of Extracellular Fluid Volume (ECFV)

Clinical Findings

Type 1,

Hypervolemic

Type II,

Hypervolemic

Type III,

Hypervolemic

SIADH

Euvolemic

History

CHF, cirrhosis, or nephrosis

Yes

No

No

No

Salt & water loss

No

Yes

No

No

ACTH- cortisol deficiency and/or

nausea and vomatiting

No

No

Yes

No

Physical examination

Generalized edema, ascites

Yes

No

No

No

Postrlial hypotension

May be

May be

May be

No

Laboratory

BUN, creatinine

High-normal

High-normal

Low-normal

Low-normal

Uric acid

High-normal

High-normal

Low-normal

Low-normal

Serum potassium

Low-normal

Low-normal

Normal

Normal

Serum albumin

Low-normal

High-normal

Normal

Normal

Serum cortisol

Normal-high

Normal-high

Low

Normal

Plasma renin activity

High

High

Low

Low

Urinary sodium (Meg unit of time)

Low

Low

High

High

 


Q. 12

Inappropriate ADH secretion is characterised by the following except:

 A

Hypo-osmolar urine

 B

Water intoxication

 C

Expanded fluid volume

 D

Hypomagnesemia

Q. 12

Inappropriate ADH secretion is characterised by the following except:

 A

Hypo-osmolar urine

 B

Water intoxication

 C

Expanded fluid volume

 D

Hypomagnesemia

Ans. A

Explanation:

Answer is A (Hypo-osmolar urine):

SIADH is characterized by increased vasopressin release leading to increased absorption of water producing a concentrated or hyperosmolar urine.

SIADH

  • The term SIADH is applied to conditions with vasopressin excess. Vasopressin excess is termed inappropriate as this increase occurs despite decreased plasma osmolality.
  • Increased vasopressin acts on renal tubules, resulting in increased absorption of water (increased total body water), a concentrated urineQ and decreasing serum osmolality and hyponatremia Q.
  • Edema does not occur despite increased total body water Q (due to unknown reasons) – Clinical EuvolemiaQ.

SIADH should be suspected in patients who have hyponatremia and concentrated urine (osmolality > 300 mmol/kg) in the absence of edema, orthostatic hypotension and features of dehydration.

Diagnosis is supported by finding of blood urea nitrogen, serum uric acid, creatinine, etc. in low normal or subnormal range Q (as can be expected from hypervolumia).

Increased action of ADH causes increased reabsorption of water, and resulting expanded fluid volume & water intoxication, and this also explains fall in conc. of serum electrolytes such as Mg2+.


Q. 13

Which of the following statements is true about SIADH:

 A

Hypovolemic Hyponatremia

 B

Euvolemic Hyponatremia

 C

Hypervolemic Hyponatremia

 D

Hypervolemic Hypernatremia

Q. 13

Which of the following statements is true about SIADH:

 A

Hypovolemic Hyponatremia

 B

Euvolemic Hyponatremia

 C

Hypervolemic Hyponatremia

 D

Hypervolemic Hypernatremia

Ans. B

Explanation:

Answer is B (Euvolemic Hyponatremia):

SIADH is characterized by Euvolemic Hyponatremia.


Q. 14

In a patient if administration of exogeneus vasopressin does not increase the osmolality of urine the likely cause is

 A

SIADH

 B

Psychogenic polydipsia

 C

Renal Hyposensitivity to ADH

 D

ADH Deficiency

Q. 14

In a patient if administration of exogeneus vasopressin does not increase the osmolality of urine the likely cause is

 A

SIADH

 B

Psychogenic polydipsia

 C

Renal Hyposensitivity to ADH

 D

ADH Deficiency

Ans. C

Explanation:

Answer is C (Renal Hyposensitivity to ADH):

Failure of urine osmolality to rise even after administration of exogenous ADH/vasopressin suggests a diagnosis of Nephrogenic Diabetes Insipidus due resistance to action of vasopressin on the Renal tubule (Renal Hyposensitivity to ADH).


Q. 15

Which of the following is true about nephrogenic diabetes insipidus

 A

Renal tubule is unresponsive to ADH

 B

There is central decrease in secretion of ADH

 C

Serum sodium is low

 D

Urine osmolality is increased after administration of ADH

Q. 15

Which of the following is true about nephrogenic diabetes insipidus

 A

Renal tubule is unresponsive to ADH

 B

There is central decrease in secretion of ADH

 C

Serum sodium is low

 D

Urine osmolality is increased after administration of ADH

Ans. A

Explanation:

Answer is A (Renal tubule is unresponsive to ADH):

Nephrogenic Diabetes Insipidus is charachterized by resistance of action of ADH on Renal tubules or unresponsiveness of renal tubules to the action of ADH or Renal Hyposensitivity to action of ADH.

Serum sodium is typically high (increased), urine osmolality is low and fails to increase after exogenous administration of ADH /vasopression.


Q. 16

Site of action of ADH is:

March 2008

 A

PCT

 B

Vasa recta

 C

Loop of henle

 D

Collecting ducts

Q. 16

Site of action of ADH is:

March 2008

 A

PCT

 B

Vasa recta

 C

Loop of henle

 D

Collecting ducts

Ans. D

Explanation:

Ans. D: Collecting ducts

Because one of its principal physiologic effects is the retention of water by the kidney, vasopressin is often called the antidiuretic hormone (ADH).

It increases the permeability of the collecting ducts of the kidney, so that water enters the hypertonic interstitium of the renal pyramids.

The urine becomes concentrated, and its volume decreases. The overall effect is therefore retention of water in excess of solute; consequently, the effective osmotic pressure of the body fluids is decreased. In the absence of vasopressin, the urine is hypotonic to plasma, urine volume is increased, and there is a net water loss. Consequently, the osmolality of the body fluid rises.


Q. 17

Syndrome of inappropriate ADH secretion is commonly associated with:   

March 2012

 A

Breast carcinoma

 B

Ovarian carcinoma

 C

Lung carcinoma

 D

Hepatocellular carcinoma

Q. 17

Syndrome of inappropriate ADH secretion is commonly associated with:   

March 2012

 A

Breast carcinoma

 B

Ovarian carcinoma

 C

Lung carcinoma

 D

Hepatocellular carcinoma

Ans. C

Explanation:

Ans: C i.e. Lung carcinoma

Paraneoplastic syndrome

  • Paraneoplastic syndromes associated with breast carcinoma are hypercalcemia, dermatomyositis etc.
  • Paraneoplastic syndrome associated with ovarian carcinoma is hypoglycaemia
  • The most frequent causes of SIADH include the secretion of ectopic ADH by malignant neoplasms (particularly small cell carcinomas of the lung), drugs that increase ADH secretion etc.
  • Other paraneoplastic syndromes associated with lungs carcinoma are hypercalcemia (squamous cell carcinoma), cushings syndrome (small cell carcinoma), acanthosis nigricans
  • Paraneoplastic syndromes associated with hepatocellular carcinoma are carcinoid syndrome and polycythemia

Q. 18

ADH acts on ‑

 A

PCT

 B

Loop of Henle

 C

Collecting duct

 D

All sites

Q. 18

ADH acts on ‑

 A

PCT

 B

Loop of Henle

 C

Collecting duct

 D

All sites

Ans. C

Explanation:

Ans. is `c’ i.e., Collecting duct

Antidiuretic hormone (ADH)

ADH (vasopressin) is a nonapeptide secreted by posterior pitutary (neurohypophysis) along with oxytocin.

It is synthesized in hypothalamus (Supraoptic and paraventricular area) nerve cell bodies as large precursor peptide along with its binding protein neurophysin and is transported down the axons to nerve endings in the median eminence and pars nervosa.

The two main physiological stimuli for ADH release are rise in plasma osmolarity and contraction of ECF volume.

Other factors which can influence ADH secretion are:

Inhibit ADH secretion: Cold environemnt, ethyl alcohol

Stimulate ADH secretion: Pain, exercise, stress, sleep and drugs like morphine


Q. 19

Which of the following is the drug of choice for Syndrome of Inappropriate Secretion ofAntidiuretic Hormone (SIADH)?

 A

Demeclocycline

 B

Vasopressin

 C

Thiazide diuretic

 D

Chlorpropamide

Q. 19

Which of the following is the drug of choice for Syndrome of Inappropriate Secretion ofAntidiuretic Hormone (SIADH)?

 A

Demeclocycline

 B

Vasopressin

 C

Thiazide diuretic

 D

Chlorpropamide

Ans. A

Explanation:

Ans. is ‘a’ i.e., Demeclocycline

Syndrome of inappropriateADH (SIADH)

  • Excessive secretion of ADH causes the syndrome of inappropriate ADH (SIADH)
  • In SIADH, ADH secretion occurs irrespective of plasma volume or osmolality.
  • This results in excessive fluid retention which may cause hypertension, edema and hyponatremia.
  • Treatment
  • If the source of excess ADH can not be removed, the only effective therapy for SIADH is
  • restriction of fluid intake

or

  • administration of hypertonic saline.
  • No pharmacologic agent exists that is able to antagonize ADH specifically. Specific ADH antagonists are avail able only for investigational purpose
  • Currently, Demeclocycline and lithium are the only pharmacological t/t effective for SIADH.
  • These are nonspecific ADH antagonists which are of limited use in some situations
  • These two agents antagonize the action of ADH in collecting tubules by inhibiting the formation of CAMP.

Q. 20

All of the following are true about action of ADH, except:

 A

Post-operative increase in secreation

 B

Secreted via neurosecreation

 C

Increased secretion when plasma osmolality is low

 D

Act on distal convoluted tuble and increase permeability

Q. 20

All of the following are true about action of ADH, except:

 A

Post-operative increase in secreation

 B

Secreted via neurosecreation

 C

Increased secretion when plasma osmolality is low

 D

Act on distal convoluted tuble and increase permeability

Ans. C

Explanation:

Ans. c. Increased secretion when plasma osmolality is low



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