Endocrine2.txt

hyperglycaemic hyperosmolar non ketotic coma

DM2, it’s a hyperglycaemic emergency

• Infection
• Acute MI
• Stroke

• Decreased insulin activity
• High serum glucose levels
• Osmotic diuresis
• Volume loss
• Ketogenesis does not occur as endogenous insulin levels are enough to inhibit hepatic ketogenesis. However glucose production by the liver is unrestrained
• If eat lots of sugary fluids, can lead to really high glucose levels and raised plasma osmolality

• Raised G
• Elevated plasma osmolality [2(Na+K) + urea + glucose]
• hyperNa+
• identify precipitant

• Dehydrated (secondary to osmotic diuresis and no compensatory polydipsia)
• Reduced consciousness
• Plasma osmolality > 340mOsm/kg
• Focal CNS signs: sensory/motor/seizures, LMN signs
• Vomit

• Hypovolaemic shock
• Confusion
• Coma
• Thromboelmbolism due to hyperviscosity state
• Untreated → death

• ITU, iv access
• Fluids: 0.9% saline – careful for 2 reasons
• 1) not too fast as may have cardiac disease – danger of pulmonary oedema – so monitor CVP
• 2) if too fast give fluids, change from high Na to low Na quickly – affects brain
• iv soluble insulin infusion pump titrated to plasma glucose
• K+ replacement titrated
• Full dose of anticoagulant –because blood is very viscous

• BM
• ABG, bicarb
• K+
• Plasma osmolality
• Lab glucose

• Cerebral oedema
• Pulmonary oedema – too much fluid replacement
• Central pontine myelinolysis

• Paracetamol OD
• Salicylate OD
• Alcohol excess

• macrocyctic - assoc. with pernicious anaemia
• microcytic - blood loss from menorrhagia

• muscle weakness
• paraesthesia
• cramps
• nocturia
• polyuria
• thirst
• hypertension
• all features of hypoK+

no

• K+ low
• renin low

• Conn's: solitary aldo producing adenoma (2/3)
• bilateral adrenocortical hyperplasia (1/3)

• surgery: laparoscopic adrenalectomy
• use spironolactone pre-op to control HTN and to treat low K+

medical: spironolactone/amiloride/eplerenone (doesn't cause gynaecomastia)

• 1. HTN with low K+
• 2. refractory HTN not responding to 3 antiHTN drugs
• 3. HTN before 40yrs

• aldosterone/renin ratio increased is HIGH
• must stop all antiHTN for 2 weeks and spiro for 6 weeks. use alpha blockers to control HTN as they don't affect the test
• patient has to be sitting up for 2 hrs!

• assess the effect of POSTURE
• maestre renin, aldo and cortisol when lying down then after being upright for 4 hrs
• renin production increases on standing causing more aldo prod
• this is exaggerated in BAH but no effect in Conns as aldo production is autonomous

• high renin release from reduced renin perfusion
• eg RAS, accelerated HTN, diuretics, CCF or hepatic failure

• bronchospasm
• diarrhoea
• tricuspid stenosis
• flushing

sympathetic paraganglia cells which are collections of adrenaline secreting chromaffin cells usually found in adrenal medulla

• 10% malignant
• 10% bilateral
• 10% extra adrenal - paraganliomas
• 10% familial (MEN2/von Hippel-Lindau)

sustained or episodic, not controlled by treatment

• general: sweat, heat intol, pallor, flushing
• neuro: headache, visual disturbances, seizures
• CV: palps, tight chest, SOB, faints (postural drop), pulm oedema
• GI: abdo pain, nausea, constipation

• persistent HTN
• heart failure
• dilated CM
• arrythmia
• stroke - cerebral haemorrhage
• death due to hypertensive crisis

3 x 24h urinary free catecholamines test

• abdo CT/MRI
• MIBG chromaffin seeking isotope scan - good for extraadrenal tumours

• surgery
• pre-op: alpha (phenoxybenzamine) and beta block (alpha before beta to avoid crisis from unopposed alpha stimulation
• post-op: do 24h urine catecholamines 2 wks post op, monitor BP as risk of very LOW

• help!
• phentolamine: non selective alpha blocker to (vasodilates via alpha1)
• or labetalol: mixed alpha and beta blocker
• when BP controlled give phenoxybenzamine (alpha block)
• also give B1 blocker e.g. atenolol/bisoprolol/metoprolol to control any tachycardia with phenoxybenzamine
• then surgery after 6wks

• postural hypo,
• dizzy,
• tachycardia,
• nasal congestion,
• miosis

• slow degeneration due to demyelination of nerves in dorsal column
• caused by untreated syphilis
• one of the symptoms is impotence

• low T3/T4
• but feel normal - asymp (due to adaptation?)

when have symptoms but normal values

• parafollicular C cells
• calcitonin

• 50% excellent
• 50% if invasive get local recurrence or spread to bone/lung

• hyoptension
• hyponatraemia
• collapse

• rapid withdrawal of long term steroid therapy
• sepsis/stress in chronic adrenal dysfunction
• perinatal haemorrhageic necrosis - after prolonged difficult labour because don't have many clotting factors likely to bleed
• adrenal haemorrhage - heparin/warfarin/DIC
• post partum infarction
• warehouse friderichson syndrome: infection N.Meningitidis bacteraemia, low BP shock, DIC, bleed into adrenal gland
• trauma

• lethargy, depression, anorexia, wt loss
• hypotension (low aldo)
• hyperpigmentation: melanocytes stimulated by excess ACTH

• low Na
• high K
• high urea
• low glucose (as low cortisol)

• autoimmune: destruction of cells = 80%
• TB, mets, amyloid, haemochromatosis, lymphoma, AIDS = 20%

• acth dependent:
• cushing's disease due to ACTH pituitary tumour,
• ectopic ACTH (small cell lung cancer, carcinoid tumour) specific features due to LOTS of acth: hyperpigmentation, hypokalaemic met al (inc cortisol acts on MR), wt LOSS, hyperglycaemia. classical cushing's features may be absent.
• non-acth dependent:
• iatrogenic - pharmacological doses of steroids (commonest)
• adrenal adenoma or carcinoma
• adrenal nodular hyperplasia

• overnight dexamethasone suppression test. give dex at midnight and should cause -ve feedback, less ACTH and less cortisol at 8am
• 24h urinary free cortisol

• highest: 8am
• lowest: midnight
• check cortisol at midnight, if raised its cushing's syndrome

• 1. measure plasma ACTH - if undetectable then ADRENAL tumour likely then CT the glands.
• if ACTH is detectable then distinguish pituitary from ectopic ACTH production:
• 2. HIGH dose dex sup test: if cortisol levels are suppressed after 2days then its cushing's disease (i.e. pituitary cause) as pit retains SOME feedback
• 3. if not suppressed then it is ectopic ACTH - CT neck, thorax, abdomen for small cell lung cancer and carcinoid tumours

• maturity onset diabetes of the young
• rare autosomal dominant form of DM2 affecting young people with a positive family history

• steroids
• thiazides

• pancreatic: pancreatitis, surgery (removal of pancreas), haemochromatosis, cystic fibrosis, pancreastic cancer
• endocrine: cushing's, acromegaly, phaeochromacytoma, thyrotoxicosis, glucagonoma

• fasting plasma glucose can be high but < 7.0mmol/l
• OGTT 2h glucose 7.8 - 11.1
• manage with exercise and diet
• RF for DM

• fasting plasma glucose: 6.1-6.9
• manage with exercise and diet
• RF for DM

• short synACTHen stimulation test
• give ACTH but cortisol stays low due to adrenal insufficiency

• lack of an enzyme involved in cortisol steroid synthesis
• therefore -ve feedback to pituitary as low cortisol
• more ACTH is released and get adrenal hyperplasia
• but the steroid production pathway is diverted to ANDROGENS --> virilisation

• 21 hydroxyls deficiency: salt wasting due to low ado, virilisation of females (cliteromegaly, labial fusion), at birth vomit, dehydrate, collapse, low Na, high K
• 11B hydroxyls deficiency: salt sparing as still produce corticosterone which has mineralocorticoid activity. may get HTN in adulthood, also features of high androgens

3, 4, 6, V1, V2

prolactinoma > GH > PRL & GH, ACTH

• headache
• visual field defect: bitemporal hemianopia due to optic chiasm compression
• palsy of CN 3, 4, 6 if pressure to cav sin
• DI if stalk affected (ADH is made in hypothal and stored in post pit)

rapid pituitary enlargement due to haemorrhage into a tumour causing SUDDEN mass effects

• from rathke's pouch (origin of ant pit)
• rare, most common in children

• hypopituitarism
• growth failure, amenorrhoea, loss of libido
• hyopthal features: DI, hyperphagia so get obese, sleep disturbance
• tumour mass effect: headache, visual field defect

GnRH deficiency

• hypogonadotrophic hypogonadism
• fails to get proper erection
• anosmia
• cleft palate
• renal abnormalities
• cerebral abnormalities e.g. colour blindness

x-linked

metyrapone: blocks cortisol synthesis

hyperthyroid due to muscle wasting

• primary: problem with the testes
• secondary: due to low gonadotrophins

• local trauma, radio, chemo, torsion
• orchitis - mumps, HIV
• renal failure
• cirrhosis
• alcohol excess (toxic to leydig cells)
• chromosomal: Klinefelters 47 XXY: delayed sexual development, small tests, gynaecomastia

• hypopituitary
• kallmanns: isolated GnRH deficiency, anosmia, colour blindness
• prader-willi syndrome

• GnRH deficiency - hypogonadism
• anosmia
• colour blindness