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ADH Updated

This document discusses the pathophysiology of abnormal antidiuretic hormone (ADH) secretion. It covers the regulation and receptors of ADH, its action in the kidney, and the pathophysiology of two conditions - syndrome of inappropriate antidiuretic hormone secretion (SIADH) and diabetes insipidus (DI). SIADH is caused by excessive ADH secretion, leading to hyponatremia. DI results from a lack of ADH's antidiuretic effect, causing excessive urine output and water loss. The key differences between the two conditions are also reviewed.

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17 views24 pages

ADH Updated

This document discusses the pathophysiology of abnormal antidiuretic hormone (ADH) secretion. It covers the regulation and receptors of ADH, its action in the kidney, and the pathophysiology of two conditions - syndrome of inappropriate antidiuretic hormone secretion (SIADH) and diabetes insipidus (DI). SIADH is caused by excessive ADH secretion, leading to hyponatremia. DI results from a lack of ADH's antidiuretic effect, causing excessive urine output and water loss. The key differences between the two conditions are also reviewed.

Uploaded by

drgeetanshmittal
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPTX, PDF, TXT or read online on Scribd
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Pathophysiology of

Abnormal ADH
Secretion

• Group 2 – Roll no. 113-119


• Presenter – Raghav Gupta
• Moderator - Dr. Ghanshyam
Index
ADH
Regulation of ADH release
Receptors of ADH
Action of ADH on Kidney
Pathophysiology of SIADH
Pathophysiology of Diabetes Insipidus
SIADH Vs DI
Bibliography
ADH (Anti Diuretic Hormone)

Also known as Arginine Vasopressin

Nonapeptide – 6 member disulfide ring


and a tripeptide tail.

Produced from a single gene on Chr 20


as Prepropressophysin in magnocellular
neurons of SON of hypothalamus.
Regulation of ADH Release
1) Plasma osmolality
• Most sensitive factor
• Normal set point is 285 mOsm/kg
• Increased osmolality stimulates osmoreceptors to cause
ADH release.
2) Diurnal Variation
• Level of ADH varies throughout the day
• ADH levels are higher during the night and lower during
the day
3) Blood volume and pressure :
•Follows inverse relation with ADH release
•Mediated via stretch receptors in low and high pressure vascular
regions
Stretch receptor
NTS CVLM Hypothalamus ADH

4) Drugs and other compounds :


•Clofibrate, Carbamazepine, nicotine and Angiotensin II etc.
stimulates release
•ANP, BNP and Alcohol are the major inhibitors of ADH secretion
Receptors for ADH

V1 V2 V3
Vascular Kidney (DCT and Act on pituitary
endothelium collecting duct) to release ACTH
Liver
Heart
Action of ADH on Kidney
Action of ADH on Kidney

Urea contributes to hyperosmotic


renal medullary intersitium and helps
in the formation of concentrated urine
Syndrome of Inappropriate
hypersecretion of
ADH hormone
Causes of SIADH

1. Most common cause of SIADH is head injury.


2. Tumor - Small cell carcinoma of lung and pancreatic malignancy
3. Lung infection - Necrotizing pneumonia (lung abscess)
4. CNS infection - Meningoencephalitis
5. Drugs – Vincristine, Clofibrate, Carbamazepine, Cyclofosfamide
Pathophysiology of SIADH
Schwartz criteria for diagnosis of SIADH

• Decreased serum osmolality (<275 mOsm/kg)


• Dilutional (true) hyponatremia
• Increased Urine osmolality
• Decreased Serum uric acid (< 4mg/dl)
• BUN < 10mg/dl
• No acid base disorder with normal renal, thyroid and adrenal function.
Will the patient appear
euvolemic, hypervolemic
or hypovolemic in SIADH?
Euvolemic

Increased ADH will increase the ECF volume

• Release of ANP from atrial wall stretching


• Inhibition of Aldosterone

Removal of excess free water from the body


Vasopressin Escape

• Dilutional Hyponatremia is dangerous and


may cause symptoms ranging from minor GI
symptoms to cerebral edema, seizures and
death.
• Thus we have a counter mechanism
Features Of Diabetes Insipidus
• Decrease in 75% or more in the secretion or action of ADH results in Diabetes Insipidus.
• Central Diabetes Insipidus (Decreased secretion of ADH)
Nephrogenic Diabetes Insipidus (Decreased action of ADH, due to defect in gene
encoding V2 receptor or AQP 2)
• Due to absence of ADH water is not reabsorbed from the distal tubules leading to free
water diuresis(polyuria)
1. >7 liters of urine is passed out
2. Decreased Urine osmolality (50 – 300 mOsm/kg)
3. Urine specific gravity : <1.010
• Urine dipstick test for glucose - Negative
Q) Will the patient of DI present in hypovolemic and
hyperosmotic state?

Answer) No, as the Thirst mechanism is still there to


compensate for hypovolemia and hyperosmotic state of
the plasma. It returns the volume and osmolality of the
plasma back to normal.
• Polydipsia
• Nocturnal water craving
• Cold water craving
• Disturb sleep
• Daytime lethargy and
somnolence
Causes of Central/Cranial/Pituitary DI
1. Genetic :
• Autosomal Dominant (AVP – Neurophysin gene)
• X linked recessive
• Autosomal Recessive
a) Type A (AVP – Neurophysin gene)
b) Type B (AVP – Neurophysin gene)
c) Type C (Wolfram’s syndrome)
2. Head trauma
3. Tumor : Craniopharyngioma, metastasis of breast cancer
4. Infiltration: Sarcoidosis, Langerhans cell histiocytosis
5. Infection: TB, HIV and Toxoplasmosis
6. Pregnancy: Placenta produces N terminal aminopeptidase (Vasopressinase)
which cleaves ADH and causes Gestational DI.
SIADH Vs DI
Bibliography
Ganong’s Review of Medical Physiology 26 th Edition
Guyton and Hall Textbook of Medical Physiology 13 th Edition
Berne & Levy Physiology 7th Edition
Harrison’s Principles of Internal Medicine 20 th Edition
Robbins & Cotran Pathologic Basis of Disease 10 th Edition
Thank You

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