Diabetic ketoacidosis (DKA):
- Absolute insulin deficiency – occurs in DM T1 but NOT T2!
- Lack of insulin = hyperglycaemia (=osmotic diuresis and dehydration) = raised ketone levels = metabolic acidosis
- Precipitants: infection, missed insulin dose (hospital stay/psychological reasons), MI, trauma, undiagnosied DM T1
- p/c: thirst, polyuria, dehydration ( – even hypovolaemic shock), vomiting, abdo pain, tachycardic, tachypnoea and Kussmaul’s respirations (due to acidosis), decreased consciousness (normaltiredcoma), ketotic (peardrop) fetor on breath.
- Ix: BMs typically >20mmol/L, ketonuria, high urine potassium due to acidosis – but low body potassium, acidotic (= pH 7.0-7.2), decrease in bicarbonate (=due to acidosis usage) and dcrease in PCO2 as a result of hyperventilation
- Ix precipitant:microbiology, CXR, ECG, FBC, cardiac enzymes…
- Mx: fluid (3-5L in <6h), IV insulin (6 units), potassium replacement (10-20mmol/h) after initial insulin and fluid replacement (must be AFTER as risk of hypokalaemia – as insulin drives potassium into cells). May need bicarbonate, nasogastric tube inserted for gastoparesis. Tx underlying cause.
- Prognosis: need insulin longterm. Risk of mortality <5%
Hyperosmolar non-ketotic coma (HONK):
- Found in DM T2 but NOT T1!
- Insulin elevels are sufficient to prevent ketosis but insufficient to prevent hyperglycaemia
- Precipitants: infection, MI, sugary drinks
- p/c: thirst and polyuria – leading to progressive dehydration, impaired concentration levelscoma, hyperviscosity (=thrombotic complications=DVT/stroke)
- Ix: glucose often very high >50mmol/L, sodium often >160mmol/L, plasma osmolality is increased, acidosis is absent/mild. Urine = no ketones, but high glucose
- Ix of precipitant: ECG, cardiac enzymes, microbiology
- Mx: central venous monitoring in elderly/cardiac disease patients, IV fluids +/- potassium replacement. IV insulin 3units/h, anticoagulation.
- Prognosis:mortality is very high 20-40%. If they survive, can be managed in the future with their normal hypoglycaemic agents
- Rare complication of metformin treatment
- p/c: similar to acidaemia = malaise, anorexia, vomiting, hyperventilation (Kussmaul’s resps), normal glucose levels, no ketones in urine, an ABG shows profound acidosis with high base excess. Increased anion gap.
- Tx: supportive and withdraw metformin!
- More obvious in women than men
- Women p/c: menstrual disturbance or infertility, galactorrhoea (in 30-80%)
- Men p/c: galactorrhoea (<30%), erectile dysfunction, infertility, features of macroadenoma and mass effect
- o Prolactin levels can be very high.
- o If pathology is microadenoma – full assessment of anterior pituitary function is needed
- Women tend to present earlier due to clearer symptoms – due to earlier presentation – women are more likely to have microprolactinoma (caused by stress, renal failure, hypothyroidism, PCOS, pregnancy, lactation, seizures – rule these causes out early).
- Mx of prolactinomas:
- Drugs: dopamine agonists (=bromocriptine, cabergoline) inhibit prolactin secretion and cause tumour shrinkage. s/e: N&V, postural hypotension
- Surgery: trans-sphenoidal removal if drug intolerance – or if failure to shrink with dopamine agonists
- RT: prevent re-growth after drug or surgical tx.
- Prolonged excessive GH secretion in adults (excessive GH in children = gigantism)!
- Extremely rare: 5/mil. M=F. 40-60yo.
- Underlying pathologies include:
- o Benign pituitary tumour (macroadenomas more common than microadenomas)
- o Pituitary carcinoma (v rare)!
- o GH-releasing hormone (GHRH) secreting carcinoid tumour (v rare)!
- Pathophysiology: results from insulin-like growth factor (IGF-1) which mediates the effects of GH = increased sweating, headache, tiredness, lethargy, joint pains, pituitary fossa mass effects (=visual field defects, hypopituitarism).
- O/E: characteristic facial appearance (=course, frontal bossing, large sinuses, large tongue, prognathism, separation of teeth), deep voice, carpal tunnel syndrome, hand and foot enlargement and organomegally (=goitre, HSM).
- Complications: CVD and mortality from HTN, impaired glucose tolerance and DM (in 10%). Cardiac failure, IHD, CVA, obstructive sleep apnoea, colonic polyps, carcinoma, osteoporosis, joint disease (in 50%)
- o Lab: IGF-1 is high, GH is not supressed by oral glucose
- o MRI scan of pituitary and visual field assessment
- Tx: aim is to normlaise GH and reduce associated high mortality
- o Surgery:
- Trans-sphenoidal adenomectomy or craniotomy for very large tumours
- Pituitary RT: if tumour not fully removed – useful to reduce growth
- o Drugs:
- Somatostatin analogues (=octreotide, lanreotide) suppress GH in 60%
- Dopamine agonists (=bromocriptine, cabergoline) lower but rarely normalise GH