Endocrinology Flashcards
WHO diagnostic criteria for DM
If symptomatic: fasting glucose >=7.0mmol/L or random glucose >=11.1mmol/L
If asymptomatic the above criteria must be demonstrated on two separate occasions
OR:
HbA1c >= 6.5% (48) is diagnostic
HbA1c 6-6.5% ?prediabetes
HbA1c <6.0% DM excluded
Side effects of insulin and MoA
Hypoglyaemia, weight gain, lipodystrophy (alternate injection sites)
Beta blockes reduce hypoglycaemic awareness
MoA: Glucose utilisation and glycogen synthesis, Inhibits lipolysis, Reduces muscle protein loss, Increases cellular uptake of K+ (NaKATPase)
Side effects of metformin and mechanism of action
GI upset, lactic acidosis, cant use in eGFR <30
MoA: Increases insulin sensitivity, and decreases hepatic gluconeogenesis
Side effects of sulfonylureas (gliclazide) and MoA
Hypoglycaemia, weight gain, hyponatraemia
MoA: Stimulates pancreatic beta cells to secrete insulin
Side effects of thiazolidinediones (pioglitazone)
Weight gain, fluid retention (Contraindicated in HF)
Side effects of SGLT-2 inhibitors (-gliflozins) and MoA
UTI, weight loss
MoA: Inhibits reabsorption of glucose in the kidney (hence UTI as a side effect)
Side effects of GLP-1 agonists
N+V, pancreatitis, weight loss
Management of T2DM
Lifestyle modification first.
Metformin first line drug.
If HbA1c still >7.5% (58), add a gliptin or sulfonylurea or pioglitazone or SGLT-2 inhibitor (dual therapy)
If still >7.5% (58) add another of the above drugs (triple therapy)
If still not effective use insulin.
Or:
If triple therapy not effective, not tolerated or if contraindicated AND BMI >35 do metformin + sulfonylurea + GLP-1 mimetic (eg. exenatide)
Guidelines for monitoring T1DM
Check HbA1c every 3-6m, target <6.5%
Self monitor at least 4 times/day (before each meal and before bed) - monitor more if ill, having hypoglycaemic episodes, sport, pregnancy
Target 5-7mmol/L on waking and 4-7mmol/L before meals/other times of the day
Management of T1DM
Multiple daily injection basal-bolus insulin regimen:
twice-daily insulin detemir is regime of choice, with rapid-acting insulin before meals (novorapid)
Consider adding metformin if BMI >= 25
T2DM risk factor modification
BP: target <140/80 (or <130/80 if end-organ damage), ACE-i first line regardless of age
QRISK2 >10% (10year cardiovascular risk of >10%) should be offered 20mg atorvastatin OD (primary prevention)
If secondary prevention (known IHD/PAD) give atorvastatin 80mg OD
Sick day rules in DM
Check BMs at least every 4 hours, drink at least 3L in 24h, if unable to eat then drink sugary drinks, pt's should be able to check Ketone levels Continue oral hypoglycaemics even if not eating (stress response increases BMs) - possible exception is metformin (risk of dehydration -> lactic acidosis -> AKI) Continue insulin (risk of DKA if stopped)
Presentation of diabetic foot disease
neuropathy: loss of sensation
Ischaemia: absent foot pulses, reduced ABPI, intermittent claudication
Calluses, ulceration, Charcot’s arthropathy, cellulitis, osteomyelitis, gangrene
Diabetic foot disease sceening
At least annually. Palpate for both dorsalis pedis pulse and posterior tibial artery pulse
Use a 10g monofilament on various parts of the sole to check sensation
DKA diagnostic criteria
Glucose >11 or known DM
pH <7.3
Bicarb <15
Ketones >3 or urine ketones ++
Management of DKA
Fluid replacement (approx 6-8L dehydrated)
Correct hypokalaemia - 1L 0.9% NaCl over first hour and then add KCl into subsequent bags
If K >5.5 in first 24hr dont add KCl into bags
If K 3.5-5.5 add 40mmol/L into bags
If K <3.5 seek senior help
IV fixed rate insulin: 0.1unit/kg/hr
When glucose <15 add 5% dextrose infusion
Long acting insulin should be continued, short acting insulin should be stopped
Complications of DKA
Gastric stasis
VTE
Arrhythmias (hyperkalaemia, hypokalaemia)
Iatrogenic complications due to fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia)
ARDS
AKI
Cerebral oedema and DKA
Due to IV fluid therapy too much too quickly
Children/young adults most vulnerable - 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology
Usually 4-12hrs following commencement of treatment
CT head and senior review
Mannitol or hypertonic saline
DM and DVLA
If on insulin/sulfonylureas, pt can drive as long as: not had severe hypoglycaemia in prev 12m, driver has full hypoglycaemic awareness, regular BM monitoring at least BD and at times relevent to driving, no other debarring complications of DM
No need to inform DVLA if on tablets that don’t induce hypoglycaemia, or if diet-controlled DM
Hyperosmolar hyperglycaemic state
- at risk population group
- where are they managed
- clinical features
Typically presents in the elderly with T2DM
Medical emergency - managed in HDU or ITU
Osmotic diuresis, severe dehydration, electrolyte deficiencies
Clinical features: fatigue, lethargy, N+V, altered consciousness, headaches, papilloedema, weakness, hyperviscosity (MI, stroke, peripheral artery thrombosis), dehydration, hypotnesion, tachycardia
Complications of hyperosmolar hyperglycaemic state
MI, stroke, peripheral artery thrombosis
Less common: seizures, cerebral oedema, central pontine myelinolysis
Pathophysiology of hyperosmolar hyperglycaemic state
Hyperglycaemia results in osmotic diuresis with associated loss of Na and K
Severe vol depletion -> raised serum osmolarity (>320mosmol/kg) -> serum hyperviscosity
Diagnosis of hyperosmolar hyperglycaemic state
Hypovolaemia Marked hyperglycaemia (>30) without significant ketones or acidosis Significantly raised serum osmolarity (>320mosm/kg)
Management of hyperosmolar hyperglycaemic state
Normalise osmolality gradually, replace fluids and electrolytes, normalise blood glucose gradually
Fluid losses estimated to be 100-220ml/kg (7-16L in 70Kg)
IV 0.9% saline is first line (rate depends on patient and comorbidities) - aim to replace 50% of losses in first 12hrs and the remaining in the next 12h
Vigorous fluid replacement alone will result in gradual decline in plasma glucose and serum osmolarity
Insulin should NOT be used because rapid decline in glucose may be harmful
Causes of hypoglycaemia
Insulinoma
Self administration of insulin/sulphonylureas
Liver failure
Addisons disease
Alcohol
Nesidioblastosis in children (beta cell hypertrophy)
Insulinoma features
- what is it
- clinical features
Most common pancreatic endocrine tumour (islets of langerhans)
Hypoglycaemia early in the morning or just before meal
Rapid weight gain
high insulin, raised proinsulin:insulin ratio
High C peptide
Diagnosis and treatment of insulinoma
Supervised, prolonged fasting (up to 72 hours) - hypoglycaemia and increased plasma insulin
CT pancreas
Treatment: surgical excision (diazoxide and somatostatin if not eligible for surgery)
Clinical features of thyrotoxicosis
Symptoms: diarrhoea, weight loss, increased appetite, swear, heat intolerance, palpitations, tremor, irritability, anxiety, oligomenorrhoea/infertility
Signs: tachycardia/AF, warm moist skin, fine tremor, palmar erythema, thin hair, lid lag, lid retraction
Causes of thyrotoxicosis
Graves, toxic nodular goitre, toxic adenoma, ectopic thyroid tissue, exogenous (levothyroxine overdose), acute phase of subacute (De Quervain’s) thyroiditis, amiodarone
Investigations of thyrotoxicosis
TSH down, T4 and T3 up Thyroid autoantibodies (anti-thyroid peroxidase antibodies, TSH receptor autoantibodies, thyroglobulin autoantibodies)
Treatment of thyrotoxicosis
Beta blockers for rapid control of symptoms
Carbimazole (SE: agranulocytosis, get urgent FBC if sore throat/infection)
Radioiodone
Thyroidectomy - risk of damage to recurrent laryngeal nerve (hoarseness) and hypoparathyroidism. Pt will become hypothyroid so levothyroxine required
Features of thyroid eye disease
Exophthalmos, conjunctival oedema, optic disc swelling, ophthalmoplegia
Inability to close the eyelids -> sore dry eyes -> exposure keratopathy
NO SPECS
- No signs or symptoms
- Ocular irritation (dryness, FB sensation)
- Soft tissue involvement (conjunctival chemosis/oedema)
- Proptosis (exophthalmos)
- Extraocular muscle fibrosis
- Corneal exposure and ulceration if severe
- Sight loss (due to corneal ulceration, compressive optic neuropathy or ↑ IOP)
Management of thyroid eye disease
topical lubricants, steroids, radiotherapy, surgery
Smoking is the most important risk factor (stop smoking to prevent TED)
TFT results for
- thyrotoxicosis
- primary hypothyroidism
- secondary hypothyroidism
- sick euthyroid syndrome
- subclinical hypothyroidism
- poor compliance with thyroxine
- steroid therapy
- thyrotoxicosis: TSH low free T4 high
- primary hypothyroidism: TSH high free T4 low
- secondary hypothyroidism: TSH low free T4 low
- sick euthyroid syndrome: TSH low free T4 low
- subclinical hypothyroidism: TSH high free T4 normal
- poor compliance with thyroxine: TSH high free T4 low
- steroid therapy: TSH low free T4 normal
Graves disease features
Commonest cause of thyrotoxicosis
Typically seen in women aged 30-50y
TSH receptor stimulating autoantibodies, and anti-thyroid peroxidase autoantibodies
Typical features of thyrotoxicosis, plus: exophthalmos, ophthalmoplegia, pretibial myxoedema, thyroid acropachy
Clinical features of thyroid storm
Fever >38.5, tachycardia, confusion, agitation, N+V, HTN, HF, abnormal LFTs (jaundice)
Primary vs secondary vs congenital hypothyroidism
Primary - problem with the thyroid gland (eg. autoimmune disease affecting thyroid tissue)
Secondary - disorder of the pituitary gland or lesion compressing pituitary
Congenital - thyroid dysgenesis or thyroid dyshormonogenesis
Clinical features of hypothyroidism
Weight gain, lethargy, cold intolerance, dry/cold/yellowish skin, non-pitting oedema, dry/coarse hair, constipation, menorrhagia, decreased deep tendon reflexes, carpal tunnel syndrome
Subacute (DeQuervains) thyroiditis
- precipitating event
- investigations
- management
- Following a viral infection
- Ix: thyroid scintigraphy (globally reduced uptake of iodine-131)
- Mx: usually self-limiting, thyroid pain may respond to aspirin/NSAIDs, steroids if severe or is hypothyroidism develops
Causes of primary and secondary hypothyroidism
Primary: Hashimotos (Most common. Autoimmune. Women more common), DeQuervains thyroiditis, Riedel thyroiditis, after thyroidectomy/radioiodine, drug therapy (lithium, amiodarone, carbimazole), dietary iodine deficiency
Secondary: Down’s, Turner’s, coeliac, pituitary failure (compression from external features or from pituitary itself)
Management of hypothyroidism
Levothyroxine
Check TFTs 8-12wks after thyroxine dose change
Therapeutic goal is normalisation of TSH (0.5-2.5)
Increase levothyroxine by 25-50mcg in pt who becomes pregnant (monitor carefully)
Side effects and interactions of levothyroxine
SE: hyperthyroidism, reduced bone mineral density, worsening angina, AF
Interactions: iron and calcium carbonate -> reduce absorption of levothyroxine (give at least 4 hours apart)
Congenital hypothyroidism
- risks if not diagnosed
- features
- screening
If not diagnosed and treated within first four weeks it causes irreversible cognitive impairment
Features: prolonged neonatal jaundice, delayed mental and physical milestones, short stature, puffy face, macroglossia, hypotonia
Children are screened at 5-7 days using heel prick test
Actions of PTH
Released in response to hypocalcaemia
Acts on the bone to increase osteoclast activity -> bone releases calcium and phosphate into the blood
Acts at the kidney to increase calcium reabsorption and increase phosphate excretion
Also acts at the kidney to increase hydroxylation and activation of Vit D -> vit D then acts to increase calcium absorption from the intestine
What is the difference between PTH and PTHrp
PTHrp has all the same effects as PTH however it cannot activate vitamin D
Primary vs secondary vs tertiary vs malignant hyperparathyroidism (calcium and PTH levels)
Primary: increased calcium levels and increased PTH levels.
Secondary: reduced calcium levels and increased PTH levels.
Tertiary: increased calcium, significantly increased PTH.
Malignant: increased calcium, and reduced PTH (PTHrp is not detected in PTH assay)
Primary hyperparathyroidism
- causes
- presentation
- tests
- treatment
Causes: adenoma, hyperplasia, parathyroid cancer
Presentation: often asymptomatic, detected with hypercalcaemia on routine tests
Other signs/sx: tiredness, weakness, depression, pancreatitis, ulcers, bone pain, fractures, osteopenia/osteoporosis, dehydration, renal stones, abdo pain, thirsty, HTN
Tests: increased calcium and PTH, reduced phosphate, increased ALP (bone activity), 24hr urinary calcium increased. Technetium-MIBI subtraction scan
X-ray may show pepperpot skull.
Check BP.
Treatment: total parathyroidectomy is definitive Mx. Cinacalcet (calcimimetic) offered if surgery inappropriate (increased sensitivity of parathyroid cells to Ca)
Secondary hyperparathyroidism
- causes
- treatment
Causes: reduced vit D intake, CKD.
hypocalcaemia leads to excessive secretion of PTH
Treatment: correct cause. Phosphate binders, vit D, cinacalcet, parathyroidectomy
Tertiary hyperparathyroidism
-causes
Causes: occurs after prolonged secondary hyperparathyroidism, causing glands to become hyperplastic and release PTH regardless of calcium levels -> increased calcium, significantly increased PTH.
Often seen in CKD.
Cancers releasing PTH-rp
Squamous cell lung cancers
Breast cancers
Renal cell carcinomas
Primary hypoparathyroidism
- causes
- presentation
- tests
- treatment
-causes: autoimmune gland failure, congenital (Di George)
-presentation: hypocalcaemia, cramps, perioral numbness, Trousseau’s sign (carpopedal spasm), Chvostek sign
-tests: low calcium, high phosphate (or normal), normal ALP, low PTH
Treatment: calcium supplements + calcitriol
-tests
Secondary hypoparathyroidism causes
Radiation, surgery (thyroidectomy, parathyroidectomy), hypomagnesaemia (Mg required for PTH secretion)
Pseudohypoparathyroidism vs pseudopseudohypoparathyroidism
pseudo: Failure of target cells to respond to PTH. Short metacarpals, round face, short stature, calcified basal ganglia.
pseudopseudo: morphological features of pseudo but with normal biochemistry
Multiple endocrine neoplasia type 1 vs type 2a vs type 2b associated features (3Ps, 2Ps, 1P)
MEN1: hyperparathyroidism, pituitary tumours, pancreatic tumours (insulinoma, gastrinoma). Most common presentation is hypercalcaemia
MEN2a: hyperparathyroidism, phaeochromocytoma (also medullary thyroid cancer)
MEN2b: phaeochromocytoma (also medullary thyroid cancer and neuromas)
MEN1 gene is a tumour suppressor gene, MEN2 gene is a proto-oncogene
Cortisol negative feedback
Corticotropin releasing factor released from hypothalamus -> stimulates ACTH secretion from pituitary -> stimulates glucocorticoid (cortisol) production and androgen production by adrenal cortex
Causes of Cushing’s syndrome
Oral steroids Cushings disease (pituitary adenoma -> increased ACTH) Ectopic ACTH (SCLC, carcinoid tumours) Adrenal adenoma/hyperplasia McCune-Albright syndrome
Signs and symptoms of Cushings syndrome
Symptoms: weight gain, mood change (depression, irritability, psychosis), hirsutism, irregular menses, erectile dysfunction, acne, proximal weakness, recurrent achilles rupture
Signs: central obesity, plethoric, moon face, buffalo hump, supraclavicular fat distribution, skin and muscle atrophy, bruises, purple striae, osteoporosis, hypertension, hyperglycaemia, infections, poor healing
Signs of a cause (eg. abdo mass)
Cushings syndrome investigations
Overnight dexamethasone suppression test (dex 1mg PO at midnight, serum cortisol measured at 8am)
Normal: suppressed cortisol
Cushings syndrome due to oral steroids: cortisol not suppressed by low dose dex
Cushings disease: cortisol not suppressed by low dose dex, but suppressed by high dose dex
Ectopic ACTH: not suppressed by low or high dose dex
24hr urinary free cortisol
Other results:
Hypokalaemic metabolic alkalosis
Impaired glucose tolerance
HTN
Treatment of Cushings syndrome
- treat underlying cause
- cushings disease: remove pituitary adenoma (trans-sphenoidally)
- adrenalectomy
What is addison’s disease
Primary adrenocortical insufficiency, caused by destruction of adrenal cortex leading to glucocorticoid (cortisol) and mineralocorticoid (aldosterone) deficiency
Clinical features of addisons disease
lethargy, weakness, anorexia, N+V, weight loss, salt craving, hyperpigmentation of palmar creases, vitilligo, loss of pubic hair in women, low BP, hypoglycaemia, hyponatraemia, hyperkalaemia
Causes of hypoadrenalism
Addisons disease TB Mets Meningococcal septicaemia HIV Antiphospholipid syndrome Pituitary disorders (tumour, irradiation, infiltration) -> secondary hypoadrenalism Long term exogenous gluocorticoid therapy
Investigations for addisons disease
Synacthen test: plasma cortisol measures before and 30 mins after giving synthetic ACTH.
No reponse in addisons because the ACTH has no where to act (due to adrenal destruction).
Alternative: 9am serum cortisol (low in addisons but not diagnostic)
Other results: hyperkalaemia, hyponatraemia, hypoglycaemia, met acidosis, hypercalcaemia, uraemia, anaemia, eosinophilia
Treatment and follow up for addisons disease
A combination of hydrocortisone and fludrocortisone (PO)
Wear a steroid bracelet
Add 5-10mg hydrocortisone before exercise
Double steroids in illness
Follow up: yearly BP, yearly U+E, watch for other autoimmune diseases
Addisonian crisis
- causes
- presentation
- management
Causes: sepsis, surgery, adrenal haemorrhage, steroid withdrawal
Presentation: shock (tachycardia, hypotension, vasoconstriction, oliguria, weak, confused, comatose), hypoglycaemia
Management: hydrocortisone 100mg IM/IV, normal saline fluid boluses or with dextrose if hypoglycaemia, continue hydrocortisone 6 hourly until patient is stable
Convert to oral after 24 hours and reduce back to maintenance over 3-4 days
Causes of primary hyperaldosteronism
Conn’s syndrome (adrenal adenoma)
Bilateral idiopathic adrenal hyperplasia
Clinical features of primary hyperaldosteronism
Hypertension
Hypokalaemia (muscle weakness, cramps, paraesthesia, polyuria, polydipsia)
Alkalosis
Investigations for primary hyperaldosteronism
First-line: plasma aldosterone/renin ratio (high aldosterone alongside low renin = diagnosis)
High resolution CT abdomen and adrenal vein sampling used to differentiate between unilateral and bilateral sources of aldosterone excess
Management of primary hyperaldosteronism
Adrenal adenoma: surgery
Bilateral adrenocortical hyperplasia: aldosterone antagonist (spironolactone)
Phaeochromocytoma
- what is it
- associations
- features
- tests
- management
- Rare catecholamine secreting tumour
- 10% are familial, associated with MEN type 2, neurofibromatosis, and von Hippel-Lindau syndrome
- Features: HTN, headaches, palpitations, sweating, anxiety
- tests: 24hr urinary colection of metanephrines, and CT abdo
- Mx: surgery is definitive, but pt should be medically stabilised first with alpha blocker (phenoxybenzamine) followed by a beta blocker (propranolol)
Features of Klinefelters
Primary hypogonadism (47XXY) Tall Small, firm testes Lack of secondary sexual characteristics Infertile Gynaecomastia Elevated gonadotrophin levels but low testosterone
Diagnosed by karyotype
Kallmann’s syndrome
Secondary hypogonadism (hypogonadotrophic hypogonadism) X-linked recessive (males) Lack of smell Delayed puberty Hypogonadism Sex hormones low LH and FSH levels inappropriately low/normal normal/above average height
Cleft lip/palate and visual/hearing defects may be seen
Congenital adrenal hyperplasia
- inheritance pattern
- what is it
A group of autosomal recessive disorders affecting adrenal steroid biosynthesis
Different types: 21-hydroxylase deficiency (90%), 11-beta hydroxylate deficiency, 17-hydroxylase deficiency
CAH affects adrenal steroid biosynthesis -> in response to resultant low cortisol levels the anterior pituitary secretes high levels of ACTH -> adrenal androgen production -> virilisation in females and precocious puberty in males
Indications, administration and side effects of GH therapy
Indications: proven GH deficiency, Turners, Prader-Willi, chronic renal insufficiency before puberty
Administration: SC
SE: headache, benign intracranial HTN, fluid retention
Acromegaly causes
Excess GH secondary to a pituitary adenoma (95% of cases), or due to ectopic GHRH or GH production by tumours (eg. pancreatic tumour)
Acromegaly features
Coarse facial appearance, spade like hands, increased shoe size, large tongue, prognathism (jaw protrusion), interdental spaces, excessive sweating, oily skin, raised prolactin (galactorrhoea)
Pituitary tumour features (hypopituitarism, headache, bitemporal hemianopia)
Some patients also have MEN-1
Complications of acromegaly
HTN, diabetes, cardiomyopathy, colorectal cancer
Acromegaly investigations
Serum IGF-1 levels are first-line (raised in acromegaly)
If IGF-1 levels are raised, diagnosis can then be confirmed by doing OGTT test (GH should be suppressed in hyperglycaemia, in acromegaly there is no suppression of GH following OGTT)
(IGF-1 = insulin-like growth factor 1)
Pituitary MRI may show a pituitary tumour
Acromegaly management
Trans-sphenoidal surgery is first-line in majority of patients
Somatostatin analogue (octreotide) inhibits release of GH (may be used as surgery adjunct)
Dopamine agonists (bromocriptine) effective in some patients
Pituitary adenoma investigations
Pituitary blood profile (GH, prolactin, ACTH, FH, LSH, TFTs)
Formal visual field testing
MRI brain with contrast
there are different types of pituitary adenomas - prolactinoma is the most common, followed by non-secreting adenomas
Pituitary adenoma DDx
Pituitary hyperplasia, craniopharyngioma, meningioma, brain mets, lymphoma, hypophysitis, vascular malformation (eg. aneurysm)
Management of pituitary adenoma
Hormonal: bromocriptine/dopamine agonist (first line for prolactinoma), octreotide/somatostatin analogue
Surgery (trans-sphenoidal transnasal hypophysectomy)
Radiotherapy
Features of excess prolactin in men vs. women
Men: impotence, loss of libido, galactorrhoea
Women: amenorrhoea, galactorrhoea
Causes of raised prolactin
Prolactinoma, pregnancy, oestrogens, physiological (stress, exercise, sleep), acromegaly, PCOS, primary hypothyroidism
Drugs: metoclopramide, domperidone, phenothiazines, haloperidol, SSRI, opioids
Dopamine inhibits prolactin release, therefore dopamine antagonists promote prolactin secretion
Side effects of glucocorticoids
- Head: insomnia, mania, depression, psychosis, intracranial HTN
- Eyes: glaucoma, cataracts
- Blood/immuno: neutrophilia, immunosuppression (infections, reactivation of TB)
- MSK: growth suppression in children, osteoporosis, proximal myopathy, avascular necrosis of femoral head
- GI: peptic ulcer, acute pancreatitis
- Endocrine: DM, weight gain, hirsutism, hyperlipidaemia, Cushing’s syndrome
nephrogenic vs cranial diabetes insipidus
- causes of nephrogenic
- causes of cranial
Passage of large volumes of dilute urine due to impaired water absorption by the kidney, because of:
Nephrogenic: impaired response of the kidney to ADH
-causes: inherited, hypokalaemia, hypercalcaemia, lithium, demeclocycline, CKD, post-obstructive uropathy
Cranial: reduced ADH secretion from the posterior pituitary
-causes: idiopathic, congenital, tumour, mets, trauma, hypophysectomy, sarcoidosis, haemorrhage, meningoencephalitis
Symptoms of diabetes insipidus
polyuria, polydipsia, dehydration, hypernatraemia
Tests for diabetes insipidus
U+E (hypernatraemia, hypokalaemia), hypercalcaemia, glucose (exclude DM), serum and urine osmolalities
Diagnosis: 8-hour water deprivation test (no drink for 8 hours -> measure urine osmolality -> should increase in the presence of dehydration, but doesnt if DI)
Can then differentiate between cranial and nephrogenic by giving desmopressin at the end of the 8 hours -> if osmolality then increases (=cranial), if it doesnt (=nephrogenic)
Management of diabetes insipidus
Cranial: desmopressin (synthetic ADH)
Nephrogenic: treat cause. If it persists trial bendroflumethiazide
