Aetiology of Hypoaldosteronism
primary - primary adrenal insufficiency, congenital adrenal hyperplasia, aldosterone synthase deficiency
secondary -
- disease in pituitary or hypothalamus
hyporeninaemic hypoaldosteronism - renal dysfunction - most commonly diabetic nephropathy
- NSAIDs
- ciclosporin
symptoms of hypoaldosteronism
muscle weakness
Nausease
heart palpitation
arrhythmia
low BP
investigation and management of hypoaldosteronism
bloods - aldosterone, U&E ( hypyerkalaemia, hyponatraemia), renin
renin:aldosteronism ratio (1 - low aldo, high renin, 2 - low aldo and low renin)
treatment - fludrocortisone + hydrocortison + diuretics (if renal cause)
what is hirsutism
development of androgen dependent terminal hair (coarse, pigmented) following a male-pattern distribution (face, chest, abdomen, back)
causes of hirsutism
excessive androgen excess
- PCOS
- idiopathic hirsutism
- hyperprolactinemia
- Cushing syndrome - androgenic meds
- androgen-secreting ovarian tumor/adrenal tumor
clinical features of hirsutism
virilization over a short period of time - RED FLAG for androgen-secreting ovarian or adrenal tumour
excessive hair growth
Male-pattern alopecia
deepening of voice
clitoromegaly
inc muscle bulk
oligomenorrhea / infertility
differentials for hirsutism
hypertrichosis - a condition of excessive hair growth in non-male pattern distribution, which is of hereditary origin or occurs following use of certain medications (glucocorticoids, phenytoin, minoxidil, ciclosporin
investigation and management for hirsutism
refer to endocrinology
bloods - FBC, total testosterone, sex hormone binding globulin, cancer markers eg CA125
• use Ferriman-Gallway visual scale – rank the amount of hair in 9 different areas of the body to assess level of hirsutism
treatment - depends on causes
what is another name for hyperosmolar hyperglycaemic coma (HHC)
non-ketonic hyperglycaemic hyperosmolar syndrome
which population of patients does HHC occur in
T2DM
pathophysiology of HHC
- in T2DM, some amount of insulin present in the blood stream cell is insulin resistance so cannot use insulin to remove glucose from blood hypglycaemia
- the presence of glucose in the blood inc blood osmolarity leading to water being draw out of cells and follow glucose to kidney where it is excreted dehydration and hyperosmolarity
- present of insulin inhibits ketogenesis and so non-ketonic state
what initial investigation would you see in HHC
profound hyperglycaemia (glucose > 33.3)
hyperosmolarity > 320
volume depletion
abscence of significant ketoacidosis - pH >7.3, HCO3 > 15
causes of HHC
infection inadequate insulin or oral antidiabetic therapy acut illness nursing home resident post-operatve TPN cushing syndrome
clinical features of HHC
• hyperglycaemia
o fatigue and weight loss and weakness + abdo pain due to hyperglycaemia
• dehydration and hyperosmolarity o frequent urination and thirst o hypotension o altered mental state (no glucose for brain cells), eventually coma (serum osmolality levels >330 to 340 mmol/kg (>330-340 mOsm/kg) and is most often more hyponatraemic than hyperglycaemic in nature. o seizures o hypothermia o focal neurological signs
investigation for HHC
serum osmolarity
serum blood glucose
serum or urine keton
VBG
U&E – hypo/hyperkalaemia, hypo/hypernatraemia, hypophosphataemi, hypomagnesaemia
ECG - can show abnor T or Q or ST segments, U waves (hypokalaemia), tall T wave (hyperkalaemia)
treatment for HHC
o IV fluids + potassium replacement (if < 3.5)
o IV insulin
o early ICU involvement
o vasopressor
what are the 2 types of diabetes inspididus
1) craniogenic - lack of ADH hormone
2) nephrogenic - lack of response to ADH hormone
causes of craniogenic diabetic inspidius
idiopathic brain tumor head injury brain malformation brain infection - meningitis, encephalitis, tuberculosis brain surgery or radiotherapy
causes of nephrogenic diabetic inspidius
due to collecting ducts of the kidnets do not respond to ADH
- drugs - particularly lithium
- mutation in the AVPR2 gene on the X chromosome that codes for ADH receptor
- intrinsic kidney disease
- electrolyte disturbance (hypokalemia and hypercalcemia)
clinical features of diabetes inspidius
polyruia polydipsia dehydration postural hypotension hypernatraemia
differentials for diabetes inspidius
diabetes mellitus
primary polydipsia
investigation for diabetes inspidius
Initially
U&Es –> hypernatraemia
urine osmolality - low
serum osmolality - high
water deprivation test - initially patient should avoid taking any fluids for 8 hours (fluid deprivation), then urine osmolality is measured and synthetic ADH (desmopressin) is administered. 8 hours later urine osmolality is measured again
how do you interpret the water deprivation test results
in craniogenic DI, urine osmolality
- after deprivation - low, after ADH - becomes high (as kidney stills working)
In nephrogenic DI, urine osmolality
- after deprivation - low, after ADH - remains low (as kidney no longer able to respond to DH)
in primary polydipsia - urine osmolality after water deprivation remains high
treatment for diabetes inspidius
desmopressin - synthetic ADH
- in mild case, conservative treatment
- in cranogenic DI - low dose desmopressin
- in nephrogenic DI - high dose desmopressin
