vasopressin disorders Flashcards

1
Q

contrast central and nephrogenic diabetes insipidus and their different treatments

A

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) (synthetic vasopressin).
- 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)
- Desmopressin - non-hereditary forms - can overcome relative resistance

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2
Q

aetiology central and nephrogenic diabetes insipidus

A

central:
reduced secretion ADH
hypo or pitu issue
most commonly idiopathic (not known) 30-50%
can occur secondary to many conditions
- tumours
- hypopituitaryism
- following neurosurgery
- trauma
infection - TB + meningitis
- sarcoidosis (enlargement of lymph nodes)

nephrogenic:
caused by resistance to the effects of ADH:
- inherited - x chromosome
- aquired - chronic lithium use and hypercalcaemia

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3
Q

what is meant by hypotonic polyuria?

A
  • excretion of large volumes of dilute urine because kidneys cannot reabsorb water
  • linked to deficiency or resistance to vasopressin
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4
Q

risk factors diabetes insipidus

A

modifiable:
chronic lithium use

non-modifiable:
hypercalcaemia

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5
Q

investigation diabetes insipidus 1st line

A

urine and serum osmolality
urine osmolality - low
serum osmolality - high

opposite in SIAD

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6
Q

gold standard investigation diabetes insipidus

A

water deprivation/desmopressin stimulation test

  • deprive all fluids 8hrs before
  • measure urine osmolality and administer desmopressin
  • wait 8hrs + measure osmolality again

central (C for changes)
- initial urine osmolality - low
- 8hrs post desmopressin - high

nephrogen - (N for no changes)
- initial urine osmolality - low
- 8hrs post desmopressin - low

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7
Q

explain why theres changes in desomopressin test in central insipidus and not nephrogenic

A

the desmopressin is a synthetic version of vasopressin

in central when there is not enough vasopresin, the desmopressin replaces it and makes it normal and fucntion properly

in nephrogenic its because os a resistance to by adding more synthetic vasopressin (desmopressin) will not make a difference

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8
Q

desmorpressin levels in both types of diabetes insipidus and primary polydypsia

A

primary dolpdypsia:
- before - high
- after - high

central insipidus:
- before - low
- after - high

nephrogenic:
- before - low
- after - high

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9
Q

diabetes insipidus key presentation

A

polyuria and polydypsia

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10
Q

another word for central diabetes insipidus

A

cranial diabetets insepidus

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11
Q

primary polydypsia

A

ADH secretion and function normal but patient drinks an excessive amount of water leading to excessive urine production

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12
Q

hypotonic polyuria conditions and how they differ

A

central diabetes insipidus
- deficiency of vasopressin

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

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13
Q

management of vasopressin deficiency (central diabetes insipidus)

A

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

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14
Q

management of vasopressin resistance (nephrogenic diabetes insipidus)

A

try and avoid precipitating drugs
congenital onset - very difficult
free access to water

  • very high dose desmopressin
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15
Q

investigation of hypotonic polyuria

A
  • serum Na > 135mmol/l - primary polydipsia (drinking more so urinating more)
  • urine osmolality test - < 800
    AT THIS POINT WE KNOW ITS VASOPRESSIN RELATED POLYURIA
    copeptoin result > 21.4 = ADH resistance
    copeptoin result < 21.4 = ADH deficiency

copeptoin - protein released along with ADH release - indicated amount of ADH release

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16
Q

Hyponatraemia

A

Too much vasopressin release when it should not be released:

main cause = Syndrome of Anti-Diuresis – SIAD

17
Q

Causes of SIAD

A
  • Central Nervous System Disorders
  • Tumours
  • respiratory causes
  • drugs
18
Q

Biochemical Severe serum sodium

A

< 125mmol/l

19
Q

Signs and symptoms of hyponatraemia

A

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

severe:
Stupor / coma
Convulsions
Respiratory arrest

20
Q

what does hyponatreamia morbidity and treatment depend on

A

whether onset and duration of hyponatraemia is acute or chronic

21
Q

Hyponatremia definition

A

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

22
Q

SIAD definition

A
  • excessive release of ADH
  • main cause of hyponatraemia

excess water reabsorption ;leading to:
- inc total body water
- euvolemic hyponatraemia (low sodium - same body water)

23
Q

Treatment for hyponatraemia secondary to SIADH (2)

A
  • Asymptomatic/mild symptoms: Fluid restrict; vaptans (vasopressin antagonist)
  • Severe symptoms: 3% hypertonic saline to concentrate blood
24
Q

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

A
  • Hyponatraemia
  • Cerebral overhydration
  • Headache
  • Confusion
  • Convulsions
25
Q

SIAD - management

A

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

26
Q

Hypernatremia definition

A
  • elevated sodium levels
  • serum concentration >145 mEq/L
  • occurs when body loses too much water or retains too much sodium
27
Q

primary causes of hypernatremea

A
  • dehydration
  • inc urine loss - diabetes insipidus
  • vomitting diarrhoea
  • excess sodium intake
28
Q

mild and moderate symptoms of hypernetropea.

A

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

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

29
Q

normal plasma and urine osmolality readings

A

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

30
Q

SIAD investigations

A

Blood test:
Gives a serum sodium reading ->able to confirm hyponatraemia
Serum osmolality will be low (less than 280mOsm/Kg)

Urinary test:
Urine osmolality - high urine osmolality (>100mOsm/Kg)
Urine sodium - high urine sodium (water has been taken out -> high sodium comparatively)

NO 1 TEST DIAGNOSES

31
Q

treatment flowchart SIAD

32
Q

essential diagnostic criteria SIAD

33
Q

complications of desmopressin

A

hyponatraemia due to water retention

34
Q

SIAD aetiology

A
  • post major procedure
  • infection - esp atypical pneumonia and lung absesses
  • head injury
  • medications - thiazine diuretics, carbamazapine, SSRI + NSAIDS)
  • malignancy - small cell lung carcinoma
  • meningitis
35
Q

SIAD main complication

A

osmotic demyelination syndrome
- prevention is imperitive as treatment is only supportive

36
Q

why does diabetes insipidus present with hypernatraemia

A

because so much water is lost when urinating - due to polydypsia

37
Q

excess lithium

A

nephronnic diabetes insipidus

38
Q

thiazide diuretics suffix

A

-semide, -thiazide