Endo - Diabetes Insipidus, SIADH Flashcards
Diabetes Insipidus - what is it?
Lack of ADH
or
Lack of response to ADH
This prevents kidneys from being able to concentrate the urine, leading to classic symptoms of polyuria and polydipsia
Diabetes Insipidus - how can it be classified?
Cranial
Nephrogenic
Diabetes Insipidus - what is nephrogenic diabetes insipidus?
Nephrogenic Diabetes Insipidus (NDI), is when the collecting ducts of kidneys do not respond to ADH
Diabetes Insipidus - what are the causes of NDI?
- Drugs e.g. Lithium
- Electrolyte abnormalities - HYPOkalaemia and HYPERcalcaemia
- Mutations in genetics
Diabetes Insipidus - what is cranial diabetes insipidus, and what are the causes?
Cranial diabetes insipidus (CDI) is reduced secretion of ADH
Causes:
- Idiopathic (most common)
- Brain tumours
- Head injury
- Brain infections - meningitis, encephalitis
Diabetes Insipidus - presentation
Polyuria
Polydipsia
Nocturia
Hypernatraemia
Dehydration
Postural hypotension
Diabetes Insipidus - investigations and their results
Low urine osmolality (diluted urine)
High serum osmolality (concentrated)
Water deprivation test - used to diagnose DI
Diabetes Insipidus - what does the water deprivation test entail?
- Patient has no fluids for 8 hours
- Urine osmolality then measured
- Synthetic ADH administered
- 8 hours later urine osmolality measured again
Diabetes Insipidus - water deprivation results and what they mean?
Cranial DI - patient lacks ADH, kidneys still capable of responding to ADH, so once synthetic ADH given, there will be a response with high urine osmolality
NDI - unable to respond to ADH, so even after giving synthetic ADH there is no response, urine osmolality is still low
Diabetes Insipidus - management
Treat underlying cause
Desmopressin (synthetic ADH) can be used in:
- CDI to replace lack of ADH being secreted
- NDI, give thiazides, low salt/protein diet
SIADH - what is it?
Syndrome of Inappropriate Anti-diuretic Hormone (SIADH), is a condition where there is inappropriately large amounts of ADH
SIADH - where is ADH produced and secreted from, and what is its function?
Produced - hypothalamus
Secreted - posterior pituitary gland
ADH stimulates and increases water reabsorption from collecting ducts in kidneys, INDEPENDENT of sodium
SIADH - causes?
PP secreting too much ADH, or ADH produced from somewhere else like in SCLC
Various causes which can be split into categories,
Drugs:
- SSRIs, Tricyclics
- Carbamazepine
Malignancy:
- SCLC
- Neuroblastoma
Infective:
- Pneumonia
- TB
- HIV
Neurological:
- Stroke
- Subarachnoid haemorrhage
- Subdural haemorrhage
SIADH - what are the symptoms?
Non-specific
- Headache
- Fatigue
- Muscle cramps
- Lethargy
- Anorexia
Large proportion of cases asymptomatic, features only develop with severe HYPONATRAEMIA
SIADH - why does hyponatraemia occur?
- SIADH results in kidneys retaining more water
- Increase in total body water (TBW)
- Leads to dilutional hyponatraemia
- Increase in TBW, causes increase in extracellular fluid volume, which results in increased urinary sodium excretion
SIADH - what are the signs?
Seizures
Reduced GCS
Hyporeflexia
Ataxia
SIADH - how do you diagnose, and what are the results?
SIADH more a diagnosis of exclusion, no single test that definitively diagnoses SIADH
Diagnosis based on clinical chemistry and patients history
Blood tests will show:
Serum Sodium will show hyponatraemia
Serum osmolality - LOW
Urinary tests will show:
Urinary osmolality - HIGH
Urine Sodium - HIGH
SIADH - management
Establish and treat underlying cause, and correct any hyponatraemia SLOWLY, otherwise will lead to osmotic demyelination syndrome
- Fluid restriction, restrict fluid intake to 500ml-1L, may be enough to correct hyponatraemia
- TOLVAPTAN, ADH receptor blockers, powerful, cause rapid Na+ increase, so require 6hr monitoring
SIADH - what is osmotic demyelination syndrome and what are the symptoms?
Complication of long term hyponatraemia (<120mmols/L) being treated too quickly (no more than >10mmol/L over 24 hours)
Symptoms usually occur after 2 days, usually irreversible: dysarthria, dysphagia, paraparesis or quadriparesis, seizures, confusion, and coma,
patients are awake but are unable to move or verbally communicate, also called ‘Locked-in syndrome’
Prevention essential, as treatment only supportive once CPM occurs