vasopressin disorders

Question 1

what is meant by hypotonic polyuria?

Answer 1

• excretion of large volumes of dilute urine because kidneys cannot reabsorb water
• linked to deficiency or resistance to vasopressin

Question 2

hypotonic polyuria conditions and how they differ

Answer 2

central diabetes insipidus
- deficiency of vasopressin

nephrogenic diabetes insipidus
- resistance to ADH - V2 receptor - genetic or aquired

Question 3

management of vasopressin deficiency (central diabetes insipidus)

Answer 3

treat any underlying condition

desmopressin – high activity at V2 receptor

tablets 100-600 micrograms/day
nasal spray 10-20 micrograms/day
injection 1-2 micrograms/day

dose adjusted to response on monitoring of serum sodium

Question 4

management of vasopressin resistance (nephrogenic diabetes insipidus)

Answer 4

try and avoid precipitating drugs

congenital DI - very difficult
free access to water
very high dose desmopressin

Question 5

investigation of hypotonic polyuria

Answer 5

• serum Na less than 135mmol/l - excludes primary polydipsia
• urine osmolality test - less than 800
  AT THIS POINT WE KNOW ITS VASOPRESSIN RELATED POLYURIA
  copeptoin result > 21.4 = ADH resistance
  copeptoin result < 21.4 = ADH deficiency

Question 6

Hyponatraemia

Answer 6

Too much vasopressin release when it should not be released:

main cause = Syndrome of Anti-Diuresis – SIAD

Question 7

Causes of SIAD

Answer 7

• Central Nervous System Disorders
• Tumours
• respiratory causes
• drugs

Question 8

Biochemical Severe serum sodium

Answer 8

< 125mmol/l

Question 9

Signs and symptoms of hyponatraemia

Answer 9

Headache
Irritability
Nausea / vomiting
Mental slowing
Unstable gait / falls
Confusion / delirium
Disorientation

severe:
Stupor / coma
Convulsions
Respiratory arrest

Question 10

what does hyponatreamia morbidity and treatment depend on

Answer 10

whether onset and duration of hyponatraemia is acute or chronic

Question 11

Hyponatremia definition

Answer 11

low levels of sodium (Na⁺) in the blood, typically defined as a serum sodium concentration below 135 mEq/L.

Question 12

SIAD definition

Answer 12

• excessive release of ADH
• main cause of hyponatraemia

Question 13

Treatment for hyponatraemia secondary to SIADH (2)

Answer 13

• Asymptomatic/mild symptoms: Fluid restrict; vaptans (vasopressin antagonist)
• Severe symptoms: 3% hypertonic saline to concentrate blood

Question 14

what are some concequences of water excess and a dec is ECF osmolality?

Answer 14

• Hyponatraemia
• Cerebral overhydration
• Headache
• Confusion
• Convulsions

Question 15

SIAD - management

Answer 15

Diagnose and treat underlying condition

fluid restriction <1L/24 hour

sometimes demeclocycline/ tolvaptan (V2 receptor antagonist)

if Na+ <115 mmol/l AND fitting hypertonic N/Saline on ITU

<8mmol/l increase in Na+ per 24 hour if chronic

Potential risk of osmotic demyelination

Question 16

Hypernatremia definition

Answer 16

• elevated sodium levels
• serum concentration >145 mEq/L
• occurs when body loses too much water or retains too much sodium

Question 17

primary causes of hypernatremea

Answer 17

• dehydration
• inc urine loss - diabetes insipidus
• vomitting diarrhoea
• excess sodium intake

Question 18

mild and moderate symptoms of hypernetropea.

Answer 18

mild
- thirst
- dry mouth
- weakness and fatigue
- inc urine output - diabetes insipidus

moderate to severe
- confusion
- seizures
- coma
- brain hemmorrhage

Question 19

normal plasma and urine osmolality readings

Answer 19

plasma - 275–295 mOsm/kg
urine - 300-700mOsm/kg

Question 20

contrast central and nephrogenic diabetes insipidus and their different treatments

Answer 20

Central Diabetes Insipidus (CDI):

Cause: Vasopressin (ADH) deficiency due to damage to the hypothalamus or posterior pituitary (e.g., brain injury, tumors).

Treatment:
Desmopressin (DDAVP) (vasopressin replacement).
Adequate water intake.

Nephrogenic Diabetes Insipidus (NDI):

Cause: Kidney resistance to vasopressin due to genetic mutations (e.g., V2 receptor), lithium toxicity, or hypercalcemia.
Treatment:
Thiazide diuretics (reduce urine output).
Low-sodium diet and NSAIDs (improve ADH action).