endo middle tier Flashcards
types of diabetes insipidus
cranial diabetes insipidus
nephrogenic diabetes insipidus
cranial - lack of vasopressin produced
nephrogenic - enough vasopressin is produced but resistance to vasopressin action
symptoms for diabetes insipidus
both cranial and nephrogenic!
Similar appearance to diabetes mellitus (or primary polydipsia - has polydipsia and polyuria)
- Polyuria 3L+/day
- Polydipsia
- Dehydration
- Low BP
- Lethargy, weakness
Distinct from diabetes mellitus
- No glycosuria (sweet wee with sugar)
- No elevated blood glucose levels
diabetes insipidus osmolality
=high serum osmolality and low urine osmolality
lots of water lost and not reabsorbed in kidneys (no vasopressin action)
diabetes insipidus diagnosis
1) to tell it is diabetes insipiud
2) to distinguish between cranial and nephrogenic diabetes insipidus
1) - Measure urine output - to confirm polyuria
- To distinguish it from DM, do plasma and urine glucose levels (no glycosuria/ elevated blood levels)
- Hyponatremia - due to water loss
- MRI hypothalamus - looking for masses
- Water deprivation test
- – 8h fasting with no fluids
- – Measure urine and serum osmolality hourly
- – Normal response: serum osmolality remains same and urine osmolality increases. Kidneys can concentrate urine.
- – DI: serum osmolality rises, urine unable to be concentrated- remains low osmolality. Kidneys still produce dilute urine, despite dehydration.
2) Desmopressin given
No response over few hours = nephrogenic
Good response over few hours = cranial
causes of cranial diabetes insipidus
Acquired
- idiopathic
- Tumours (rare)- metastases, posterior pituitary
- Trauma
- Infections (TB, encephalitis, meningitis)
- Vascular (sickle cell, infection)
- Inflammation
- Sarcoidosis
Genetic (rare)
- Defect in ADH gene
cranial diabetes management
Treat underlying condition (eg surgery for tumour, treat infection)
Give desmopressin (tablets, nasal spray, injection) -- V2 receptor analogue (fits it, stimulates the action of vasopressin- that is not produced enough here)
Thiazide diureticsmild hypovolemia → kidneys will take up more Na+ and water in proximal tubule
causes of nephrogenic diabetes insipidus
Acquired
- Reduction in medullary concentrating gradient
- – Hypokalaemia
- – Hypercalcaemia
- – Meant to be low NaCl and Ca in blood so more moves back to blood from urine. Meant to be high K in blood so more can be used in the Na/K pumps.
- Antagonism to vasopressin effects
- – Drugs (precipitating drugs? -Lithium chloride, gilbenclamide
- – Renal impairment eg renal tubular acidosis
- – Post obstructive uropathy
- – Prolonged polyuria
Genetic (rare)
- Sickle cell
- Mutation of ADH receptor
nephrogenic diabetes insipidus management
Difficult to treat
Access to water, to rehydrate
Give high dose desmopressin (tablets, nasal spray, injection) (V2 receptor analogue (fits it, stimulates the action of vasopressin))
Thiazide diuretics → mild hypovolemia → kidneys will take up more Na+ and water in proximal tubule
NSAIDs → lower urine volume and plasma Na as it inhibits prostaglandin synthase - and prostaglandins inhibit ADH action so it prevents that
SIADH pathophysiology
too much vasopressin, inappropriate release (despite very dilute plasma)
Increased insertion of aquaporin 2 channels in the apical membrane of the collecting duct
(opposite to cranial diabetes insipidus)
SIADH osmolality
low (lots of water)
is SIADH hypo/eu/hypervolemic
retention of water –> intracellular volume increases (cells swell) but EUvolemic
- as volume rises, aldosterone is suppressed and ANP is released which increases renal excretion, so ps volume normal
SIADH causes
- Head injury/ haemorrhage , subdural hematoma
- Tumour (eg lung, prostate, pancreas, thymus, lymphoma, CNS)
- Meningitis
- Thrombosis
- Lupus
- Pulmonary lesions (TB, pneumonia, asthma, CF, lung abscess)
- Alcohol withdrawal
- Drugs: (SSRIs, sulfonylurea (DMT2) , cyclophosphamide (immunosuppressant), carbamazepine (anti-convulsant), some chemo )
SIADH signs and symptoms
why do u/ why do u not get oedema
- concentrated urine
- due to brain cell swelling:
- – reduction in GCS
- – fits, coma, confusion, drowsy, irritable
- Weakness
- Aches
- Anorexia, Nausea
- Malaise
NO !! Oedema !! – oedema is ECF increase whereas SIADH is euvolemic, only the intracellular fluid increases
SIADH investigations
- Low serum Na+, high urine Na+
- Low plasma osmolality, high urine osmolality
- Euvolaemia
- Need to distinguish between frail elderly patients’ hyponatraemia from salt and water depletion
- – Give 1-2L of 0.9%saline
- – If sodium depleted, will respond well as will fill in their defecit
- – SIADH will have no response, as the Na will be excreted in order to balance the low osmolality
No hypokalemia (low aldosterone! aldosterone ), No hypotension, no hypovolemia Normal adrenal, renal, thyroid function
SIADH treatment
Treat underlying condition (eg stop causative drug)
Increase Na in serum (hospital visits)
Restrict fluids (used for general low Na)
- 500-1000mL /day
- This will increase Na+ concentration (less fluid excess so less excretion including Na excretion)
Vasopressin antagonist = tolvaptan (oral)
Blocks V2 receptor
Promotes water excretion (less absorbed), without affecting electrolytes
Demeclocycline
Inhibits the action of ADH on the kidneys - resistant to its action – induces nephrogenic DI
If severe and you are worried about circulatory overload – loop diuetic = furosemide
