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9 - Diabetes Insipidus & SIADH (Notes)

The document discusses the pathophysiology, causes, and diagnostic approach of diabetes insipidus and syndrome of inappropriate antidiuretic hormone. It details the mechanisms of central and nephrogenic diabetes insipidus and inappropriate ADH production. Common causes such as pituitary diseases, drugs, and cancers are explained.

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Meng Bek
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100% found this document useful (1 vote)
74 views9 pages

9 - Diabetes Insipidus & SIADH (Notes)

The document discusses the pathophysiology, causes, and diagnostic approach of diabetes insipidus and syndrome of inappropriate antidiuretic hormone. It details the mechanisms of central and nephrogenic diabetes insipidus and inappropriate ADH production. Common causes such as pituitary diseases, drugs, and cancers are explained.

Uploaded by

Meng Bek
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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ENDOCRINOLOGY Last edited: 3/6/2024

9. DIABETES INSIPIDUS & SIADH


I. PATHOPHYSIOLOGY II. COMPLICATIONS OF DI AND SIADH III. DIAGNOSTIC APPROACH TO DI & SIADH IV. TREATMENT OF DI AND SIADH
A. DIABETES INSIPIDUS (DI) A. DIABETES INSIPIDUS (DI) A. DIABETES INSIPIDUS (DI) A. DIABETES INSIPIDUS (DI)
B. SYNDROME OF INAPPROPRIATE ADH (SIADH) B. SYNDROME OF INAPPROPRIATE ADH (SIADH) B. SYNDROME OF INAPPROPRIATE ADH (SIADH) B. SYNDROME OF INAPPROPRIATE ADH (SIADH)

00:44
I. Pathophysiology
A. Diabetes Insipidus (DI) 00:44

Diabetes Insipidus (DI)


1. Pathophysiology:
o Central DI
 Hypothalamic-posterior pituitary dysfunction →
↓ADH production →
↓H2O reabsorption at the collecting duct
o Nephrogenic DI
 Normal ADH production but ADH receptor dysfunction →
Inadequate ADH response → Central DI
↓H2O reabsorption at the collecting duct

ADH

Nephrogenic
DI

V2-R

H2O

Diabetes Insipidus & SIADH ENDOCRINOLOGY : Note #9 1 of 9


2. Causes of Diabetes Insipidus:
a) Central DI 04:29 b) Nephrogenic DI 08:58
Hypothalamic-Pituitary Dysfunction ADH Receptor Dysfunction
o Pituitary Apoplexy o Lithium use
 Pituitary adenoma hemorrhages →  Assess for a history of bipolar disorder
Vascular compression of the pituitary vessels → o Hypercalcemia
↓Pituitary perfusion → Pituitary infarction →  Assess for the history of hyperparathyroidism or
↓Release of pituitary hormones such as ADH malignancy along with findings of nephrolithiasis,
• Assess for a history of mass effect features: Osteoporosis with pathological fractures,
o Bitemporal hemianopia pancreatitis, and ↓QT-I
 Due to compression of the optic chiasma → Loss of o Hypokalemia
lateral temporal visual fields  Assess for the history of vomiting or diarrhea or
o Secondary Headache diuretic use alongside ECG changes like T-wave
o Sheehan Syndrome inversion, U-waves, and ↑QT-I
 Postpartum hemorrhage → Massive blood loss →
hypotension and DIC → ↓Pituitary perfusion → Nephrogenic DI
Pituitary infarction → ↓Release of hormones such as ADH
• Assess for a patient with recent postpartum hemorrhage
with > 1 L blood loss or hypotension within 24 hours
o Craniopharyngioma
 A tumor that arises from the nasopharynx in children
ADH
(e.g. Rathke’s Pouch) → Migrates to the vicinity of the
pituitary gland → Compression of the pituitary and
pituitary stalk → ↓Release of hormones such as ADH V2-R

• Assess for a history of mass effect features: H2O


o Bitemporal Hemianopia
 Due to compression of the optic chiasma → Loss of
lateral temporal visual fields Lithium Hypercalcemia
Bipolar D/D PTH
o Secondary Headache
Malignancy
o Pituitary removal Hypokalemia
 Transsphenoidal pituitary resection → Loss of pituitary GI losses or Renal losses
tissue → ↓Release of pituitary hormones such as ADH ECG Changes +
• Assess for a prior history of surgery on or near the
pituitary gland
Central DI
Pituitary Macroadenoma
Sheehan Syndrome Apoplexy
(> 10 mm)

Vascular
Compression Compression

Infarction

BV
Transsphenoidal
BP
Resection
and
ADH
DIC
V2-R
H2O

2 of 9 ENDOCRINOLOGY : Note #9 Diabetes Insipidus & SIADH


B. Syndrome of Inappropriate ADH (SIADH) production 12:55

1. Pathophysiology:
SIADH
o ↑Pituitary ADH Release
 Hypothalamic-posterior pituitary dysfunction → Ectopic ADH
↑ADH production → Production
↑H2O reabsorption at the collecting duct
o Ectopic ADH Production Pituitary
 Neoplasm with ADH-producing capabilities → ADH release
↑ADH production →
↑H2O reabsorption at the collecting duct ADH

V2-R

H2O

H2O

2. Causes of SIADH: 15:32

a) ↑Pituitary ADH release b) Ectopic ADH production


i) Intracranial disease o Small cell lung cancer (SCLC) →
o Stroke, Traumatic brain injury (TBI), or Brain tumors → Develop paraneoplastic syndrome →
Stimulate the pituitary → ↑ADH production Tumors produce ADH → ↑ADH production
 Assess for any neurological deficits or recent head injury  Assess for cough, weight loss, or hemoptysis

ii) Pulmonary disease


o COPD, PNA, Intubated patients
→ Stimulate the pituitary → ↑ADH production Ectopic ADH Production
 Assess for any underlying lung disease or hypoxia

iii) Drugs
o SSRIs or carbamazepine →
Stimulate the pituitary → ↑ADH production
SCLC
 Assess medication history

Pituitary ADH Release Paraneoplastic


Syndrome
Intracranial Drugs
Diseases (M/C)
O2 SSRI’s
Stroke Carbamazepine
Pulmonary ICH/SAH TCA’s
Diseases TBI
COPD
PNA
ARDS
Intubated
H2O
ADH
ADH

Diabetes Insipidus & SIADH ENDOCRINOLOGY : Note #9 3 of 9


20:41
II. Complications of DI and SIADH
A. Diabetes Insipidus (DI) 20:41

Hypernatremia
Pathophysiology:
o ↓ADH production (e.g. central DI) or
↓ADH response (e.g. nephrogenic DI) → Hypernatremia (> 145)
↓H2O reabsorption at the collecting duct → Polydipsia
↓Water in the bloodstream → ↑Na+ in the
ADH Hypothalamus
bloodstream +
Presentation: Osmolality
o Polyuria
Na+
 ↓ADH production (e.g. central DI) or
↓ADH response (e.g. nephrogenic DI) → Hypovolemia Dehydration
*(Inadequate Hydration)*
↓H2O reabsorption at the collecting duct →
↑H2O loss in the urine
o Polydipsia H2O Polyuria
 ↓ADH production (e.g. central DI) or Loss
in Urine
↓ADH response (e.g. nephrogenic DI) →
↓H2O reabsorption at the collecting duct →
↓Water in the bloodstream → ↑Serum osmolality →
Stimulation of the hypothalamic thirst center → ↑Thirst
o Dehydration
 Polyuria without adequate hydration →
↓Intravascular volume → Hypovolemia

B. Syndrome of Inappropriate ADH (SIADH) 26:16

Hyponatremia
Pathophysiology: Presentation:
o ↑ADH production → o Cerebral Edema
↑H2O reabsorption at the collecting duct →  Hyponatremia → Water pulled from blood into neurons →
↑Water in the bloodstream → Brain swelling → Cerebral Edema →
↓Na in the bloodstream ↑ICP when Na+ < 120 acutely
• Encephalopathy
Cerebral Edema o Lethargy → Obtunded → Comatose
Hyponatremia (< 135)
• Headache
ADH
• Nausea and vomiting
+ • Pupillary changes (e.g. 3rd nerve palsy)
Acute or ICP +
Na+
< 120
Osmotic Shift
o Seizures
+ H/A N/V Herniation
 Hyponatremia → Water pulled from blood into neurons →
+ Brain swelling → Cerebral Edema → Lowers seizure threshold
Cortical
Seizures
H2O Loss Irritability • Usually, will present with generalized seizures
in Urine
when Na+ < 120 acutely

4 of 9 ENDOCRINOLOGY : Note #9 Diabetes Insipidus & SIADH


32:51
III. Diagnostic Approach to DI & SIADH
A. Diabetes Insipidus (DI) 32:51

Assess for the Presence of Central vs Nephrogenic DI


a) Obtain BMP c) Obtain a Water Deprivation Test
Indications: Indications:
o Suspicion of Hypernatremia in the setting of polyuria and o Differentiate DI from Primary Polydipsia in patients with
polydipsia polyuria
Abnormal Findings: Abnormal Findings:
o Na+ > 145meq/L → Identifies Hypernatremia o DI after water deprivation
 No change in Urine osmolality
b) Obtain Urine and Serum Osmolality • This indicates no presence or function of ADH at the
Indications: collecting duct
o Identifying the cause of Hypernatremia o Primary polydipsia after water deprivation
Abnormal Findings:  ↑Urine osmolality
o DI • This indicates the presence or function of ADH at the
 ↓Urine Osmolality collecting duct
• ↓ADH production (e.g. central DI) or
↓ADH response (e.g. nephrogenic DI) →
↓H2O reabsorption at the collecting duct →
↑H2O loss in the urine
 ↑Serum Osmolality
• ↓ADH production (e.g. central DI) or
• ↓ADH response (e.g. nephrogenic DI) →
↓H2O reabsorption at the collecting duct →
↓Water in the bloodstream

Diabetes Insipidus & SIADH ENDOCRINOLOGY : Note #9 5 of 9


d) Obtain DDAVP Test
Indications:
o Hypernatremia, ↓Urine osmolality, and ↑Serum osmolality →
o determine if it's nephrogenic vs central DI
Abnormal Findings:
o Central DI o Nephrogenic DI
 ↑Urine osmolality  No change in Urine osmolality
• DDAVP administration of ADH (Missing in Central DI)→ • DDAVP administration of ADH (Nephrogenic DI → ADH is
↑ADH levels → not functional) →
↑H2O reabsorption at the collecting duct → ↑ADH levels, but no ADH response →
↓H2O loss in the urine ↓H2O reabsorption at the collecting duct →
↑H2O loss in the urine

6 of 9 ENDOCRINOLOGY : Note #9 Diabetes Insipidus & SIADH


B. Syndrome of Inappropriate ADH (SIADH) 36:00

Assess for the Presence of SIADH

a) Obtain BMP
Indications:
o Suspicion of hyponatremia in the setting of Cerebral Edema
and Seizures
Abnormal findings:
o Na+ < 135meq/L → Identifies Hyponatremia

b) Obtain Urine and Serum Osmolality


Indications:
o Identifying the cause of Hyponatremia
Abnormal Findings:
o SIADH
 ↑Urine Osmolality
• ↑ADH production →
↑H2O reabsorption at the collecting duct →
↓H2O loss in the urine
 ↓Serum Osmolality
• ↑ADH production →
↑H2O reabsorption at the collecting duct →
↑Water in the bloodstream

c) Obtain the Patient's Volume Status


Indications:
o Hyponatremia
Abnormal Findings:
o SIADH
 Euvolemic
• Normal BP and HR
• Normal Mucus membranes and skin turgor
• Normal JVP
• Normal Urine output

d) Obtain TSH with Reflex and Cortisol Levels


Indications:
o Euvolemic Hyponatremia and need to exclude other etiologies
to rule in SIADH
Abnormal Findings:
o SIADH
 Normal TSH with reflex
• Hyponatremia can occur in Hypothyroidism and would
Exclude SIADH
 Normal cortisol levels
• Hyponatremia can occur in Adrenal Insufficiency and
would Exclude SIADH

Diabetes Insipidus & SIADH ENDOCRINOLOGY : Note #9 7 of 9


38:14
IV. Treatment of DI and SIADH
A. Diabetes Insipidus (DI) 38:14

1. Medical Management of DI
Therapies:
o Desmopressin (DDAVP)
o Thiazide Diuretics
Indications:
o Desmopressin (DDAVP)
 Central DI with polyuria and Hypernatremia
o Thiazide Diuretics
 Nephrogenic DI with polyuria and Hypernatremia
Purpose:
o Desmopressin (DDAVP)
 Replace loss of ADH from hypothalamic-pituitary injury
o Thiazide Diuretics
 Promotes mild volume depletion and leads to Na+ loss from
nephron →
Volume depletion triggers ↑RAAS and ↑SNS activity →
↓Na+ and water loss from nephron occurs in response →
Normalize intravascular water balance
Monitoring:
o Monitor urine output for improvement with DDAVP
o Monitor Na+ levels with DDAVP and Thiazide use

8 of 9 ENDOCRINOLOGY : Note #9 Diabetes Insipidus & SIADH


B. Syndrome of Inappropriate ADH (SIADH) 39:24

1. Medical Management of SIADH


Therapies: Monitoring:
o Water Restriction o Monitor K+, Mg2+, and Na+ levels while on loop diuretics
 Limit water intake to < 1500ml/day o Monitor BP while on loop diuretics
o Salt tablets  Can become Hypotensive with Over-Diuresis
o Loop diuretics (e.g. furosemide) o Monitor Na+ levels very closely while on Vaptans, as one can
o Vaptans (Tolvaptan) develop Hypernatremia easily
o 3% Hypertonic saline o Monitor Na+ levels extremely closely (q4hrs) while
Indications: administering 3% Hypertonic Saline, given the risk of
o Water Restriction and salt tablets Osmotic Demyelination Syndrome
 Chronic and/or Asymptomatic Hyponatremia  Prevention of ODS is maintained
o Loop diuretics by preventing Na+ rise of > 6-8meq/L in 24 hours
 Chronic and/or Asymptomatic Hyponatremia with volume • Options to prevent overshooting:
overload o If Na+ shoots above the threshold, give DDAVP to cause
 Chronic and/or Asymptomatic Hyponatremia refractory to water reabsorption to drop in Na+ levels to prevent
water restriction and salt tablets overshooting
o Vaptans o If Na+ shoots above the threshold, give free water to
 Chronic and/or Asymptomatic Hyponatremia not able to cause a drop in Na+ levels to prevent overshooting
abide by water restriction
 Chronic and/or Asymptomatic Hyponatremia refractory to
water restriction, salt tablets and loop diuretics
o 3% Hypertonic Saline
 Acute, Na < 120 and/or symptomatic hyponatremia (e.g.
cerebral edema or seizures)
Purpose:
o Water Restriction and Salt Tablets
 Water restriction
• ↓Water ingested → ↓Water in bloodstream → ↓Water
reabsorbed across collecting duct → ↑Na+ level
 Salt tablets
• NaCl ingested → ↑Na in the bloodstream → ↑Na+ level
o Loop Diuretics
 Block Na/K/2Cl cotransporters in the loop of Henle →
↑Water loss in the urine → ↓H2O in the bloodstream →
↑ Na+ level
o Vaptans
 ADH blocked at the receptor site → ADH response →
↑Water loss in the urine → ↓H2O in the bloodstream →
↑Na+ level
o 3% Hypertonic Saline
 Concentrated NaCl in the bloodstream → ↑↑Na+ in the
bloodstream → ↑↑Na+ level

FIGURE 1. OSMOTIC DEMYELINATION SYNDROME

Diabetes Insipidus & SIADH ENDOCRINOLOGY : Note #9 9 of 9

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