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