SIADH + DI Flashcards

(32 cards)

1
Q

What causes SIADH?

A

Excess production/release of ADH, most commonly from a tumor secreting ectopic ADH.

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2
Q

What does ADH do in SIADH?

A

Promotes water retention, increasing fluid volume and diluting sodium.

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3
Q

What electrolyte imbalance occurs in SIADH?

A

Hyponatremia (↓ Na) – hypotonic, water accumulates in cells, altering function.

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4
Q

What is the pathophysiology of SIADH?

A

Excess ADH → water retention → ↑ intracellular fluid → diluted Na → hypotonic hyponatremia

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5
Q

Clinical manifestations of mild SIADH?

A

• Decreased urine output (concentrated)
• Anorexia, nausea, vomiting
• Headache, irritability, disorientation, cramps, weakness

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6
Q

Severe symptoms of SIADH (Na <110 mEq/L)?

A

Psychosis, gait disturbances, seizures, coma

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7
Q

Diagnostic criteria for SIADH?

A

• Serum Na <135 mEq/L
• Plasma osmolality <280 mOsm/kg
• Decreased urine volume
• Concentrated urine with high sodium
• Absence of renal, adrenal, or thyroid abnormalities

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8
Q

Mild SIADH treatment?

A

Water restriction: 800–1000 mL/day

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9
Q

Severe SIADH treatment?

A

IV isotonic or hypertonic (3% NaCl) fluids

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10
Q

Pharmacologic treatments for SIADH?

A

• Diuretics to remove excess fluid
• Demeclocycline – reduces kidney response to ADH (long-term therapy)

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11
Q

Goal of treatment for SIADH?

A

Remove underlying cause and correct water/electrolyte imbalance.

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12
Q

What is Diabetes Insipidus?

A

Disorder caused by insufficient ADH or kidney resistance to ADH, leading to inability to concentrate or retain water.

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13
Q

What happens in DI?

A

Water cannot be retained → polyuria, dehydration, hypernatremia.

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14
Q

What are the 4 major types of DI?

A
  1. Central DI – low ADH production; 2. Nephrogenic DI – kidneys resistant to ADH; 3. Dipsogenic DI – excessive water intake; 4. Gestational DI – placental enzyme breaks down ADH during pregnancy
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15
Q

Central DI causes?

A

Brain surgery, head trauma, tumor affecting pituitary gland.

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16
Q

Nephrogenic DI causes?

A

Kidney disease, medications (e.g., lithium), genetic disorders.

17
Q

Dipsogenic DI causes?

A

Excessive water drinking, behavioral or psychiatric disorders.

18
Q

Gestational DI causes?

A

Placental enzyme breaks down ADH; usually resolves after delivery.

19
Q

Common signs of DI?

A

Polyuria, polydipsia, nocturia.

20
Q

Other symptoms of DI?

A

Signs of dehydration (dry mucous membranes, low BP) and hypernatremia (confusion, weakness).

21
Q

How is DI diagnosed?

A

History, physical exam, lab tests.

22
Q

Key lab findings for DI

A

• ↑ Serum Na
• ↓ Urine-specific gravity
• ↓ Urine osmolality

23
Q

what additional history for DI do you need to know?

A

Recent cranial surgery, trauma, pituitary tumor.

24
Q

First step in treatment for Central DI?

A

Treat underlying cause if possible.

25
Fluid management for Central DI?
Oral hydration if possible; IV hypotonic fluids if needed.
26
Medication for central DI
Desmopressin (DDAVP) – synthetic ADH analog. May be lifelong.
27
Diet adjustments for nephrogenic DI
Low salt and low protein diet.
28
Medications for Nephrogenic DI
Thiazide diuretics to reduce urine output.
29
Treatment Approach for Dipsogenic DI?
Behavioral therapy to reduce excessive water intake.
30
Additional support for Dipsogenic DI
May involve mental health professionals.
31
Treatment for Gestational DI
Desmopressin (DDAVP).
32
Prognosis for Gestational DI
Usually resolves after delivery.