Endocrinology Flashcards
What are the parameters for a diagnosis of diabetes mellitus?
Fasting glucose >7 mmol/l
Random glucose >11.1 mmol/l
2h 75g OGTT >11.1 mmol/l
HbA1C > 48 mmol/mol
What markers are there for T1DM that can be measured in serum?
GAD or IA2 antibodies - usually high
C- peptide (blood/ urine) - less sensitive
What are markers associated with monogenetic diabetes?
HNF 1 & 4 alpha, risk factors for premature CVD
How do you treat suspected diabetes with weight loss?
Weight loss indicates insulin insufficiency. Start a basal bolus insulin regime
How do you prescribe long-term insulin therapy?
Based on weight i.e. 0.3-0.5 x weight (in kg), 50% short acting and 50% long acting
If using BD mix give 2/3 with breakfast (to al7so cover lunch) and 1/3 before dinner
What are some side effects of SGLT2 inhibitors? e.g. gliflozin
These prevent kidneys from reabsorbing glucose, leading to glucose excretion in the urine
Weight loss, risk of UTI, thrush, euglycaemic DKA
What are some common precipitants of DKA?
Infection (e.g. gastroenteritis), 1st presentation, MI, non-compliance/ wrong dosing
How do you treat DKA?
Normal saline over 1, 2, 2, 4, 4, 6 hours (with K replacement)
FRII 0.1 x weight
10% glucose IV when BG falls below 14
What do you monitor in DKA?
Hourly monitoring of blood glucose and ketones, and 2 hourly monitoring of VBG - K+ and bicarb initially.
Closely monitor fluid balance (hyperglycaemia causes osmotic diuresis a/w polydipsia, polyuria)
A patient with abdo pain and vomiting presents with hyponatremia. How do you treat?
Give 100mg IM hydrocortisone and saline
How do you make a diagnosis of DKA?
Ketones >3 (CBK) or significant ketonuria (>2+ on dip)
Blood glucose >11* or known BM (in women who are pregnant and patients on SGLT2 inhibitors may be normal)
Bicarb <15 and/ or venous pH <7.3
*Dapagliflozin may lead to euglycaemic DKA
What are some indications of DKA severity i.e. potential referral to ITU?
Ketones > 6 [<0.6] Bicarb <5 pH <7 K+ <3.5 GCS <12 SpO2 <92% RA sBP <90mmHg HR <60 or >100 Anion gap >16 [3-11]
What must you check before initiating K+ replacement?
Check Mg levels - if deficiency present, replace this first.
When do you replace K+ in DKA?
What is the fastest rate that K+ should be replaced?
If K+ >5.5, no replacement required. If 3.5-5.5, generally 40mmol replacement. If <3.5, senior review for more invasive replacement.
Maximum 10mmol/ h. Up to 20mmol/h if patient is critically unwell and on continuous monitoring.
When do you stop FRII in DKA?
Normal blood pH (acidosis resolved)
Ketones <0.3 for 2 subsequent hourly readings
BMs normalised
Patient eating and drinking so can return to normal insulin regime
What are some complications of DKA?
Cerebral oedema (esp in children) - drowsiness, headache ~ due to fluid shifts Hypokalaemia (or hyper) Hypoglycaemia Pulmonary oedema/ ARDS Co-morbid issues e.g. sepsis
When are HbA1c measurements unreliable?
In haemolysis (rapid RBC turnover), altered Hb, interference with erythropoiesis/ erythropocyte destruction. pregnancy. Use fructosamine instead to monitor chronic hyperglycaemia or OGTT to diagnoses diabetes.
Why is bilirubin and ALT raised in haemolysis?
Unconjugated bilirubin is released due to breakdown of RBC
ALT is present in RBC
Patients with panhypopituitarism usually have:
- Early clinical evidence of gonadotrophin deficiency
- Impaired glucose tolerance
- A rise in serum growth hormone in response to hypoglycaemia
- Raised BP
- A high serum TSH
- True. Due to low LH and FSH.
- False. Should be normal
- False.
- False. Would be low.
- False.
What hormones are produced by the pituitary?
AP - FSH, LH, ACTH, TSH
PP - GH, Prolactin
An increased plasma total ALP activity is seen in patients with…
Paget’s, obstructive jaundice, fractures, hepatic mets
NOT in immobilisation, myeloma
What are some examples, mechanism and side effects of DPP-4 inhibitors?
DPP-4 inhibitors such as sitagliptin inhibit the peripheral breakdown of GLP-1, leading to greater release of insulin into the bloodstream in response to intestinal carbohydrate. They rarely cause hypoglycaemia and do not cause weight gain.
What are some examples and side-effects of GLP-1 mimetics?
Examples are exenatide and liraglutide, which are both given subcutaneously. Side effects include weight loss (may be given in conjunction with insulin to minimise weight gain), nausea and vomiting.
What are some examples and side effects of thiazolidinediones/ PPARy agonists?
An example is pioglitazone. May lead to increased risk of bladder cancer, fractures, weight gain/ fluid retention.
How do you treat patients with HHS?
Start fluids i.e. 1L over 1 hour and continue as osmolality falls (ensure at rate of ~ 5mmol/h). When this is normalised, reassess electrolytes and start fixed rate insulin at 0.05units/ kg/ h. Also start on LMWH.
What antibiotics cover pseudomonas?
Ciprofloxacin, gentamicin, piptaz
What investigation can you carry out for subacute thyroiditis, and what would the results be?
Thyroid scintigraphy. You would see globally reduced uptake of iodine-131. You would also see a raised ESR and hyperthyroidism in the 1st 3-6 weeks, and hypothyroidism in weeks-months before normalising.
What are the most common causes of hypercalcaemia? What may lead to a falsely raised calcium reading?
Malignancy and primary hyperparathyroidism. An abnormal albumin (<34 or >54). As serum calcium may be bound to albumin, albumin concentration may affect total calcium results.
What is the most common cause of primary hyperaldosteronism?
Bilateral idiopathic adrenal hyperplasia (70%)
May also be caused by an adrenal adenoma i.e. Conn’s syndrome - usually unilateral
Differentiate using high-res CT abdo and adrenal vein sampling
How do you treat primary aldosteronism?
Bilateral adrenal hyperplasia - spironolactone
Adrenal adenoma - adrenalectomy
What does raised TSH with normal free T4 in a patient on thyroxine indicate?
Suggests poor compliance, TSH level reflects that over recent days/ weeks body has been thyroxine deficient and that patient just started taking thyroxine before blood test.
What medical condition may result in an over-estimation of HbA1C?
Spleen conditions resulting in splenectomy, which leads to increased lifespan of RBCs. Also vitamin B12/ folic acid deficiency (macrocytic anaemia), iron deficiency anaemia.
What conditions result in lower-than-expected HbA1C?
Sickle-cell anaemia
GP6D deficiency
Hereditary spherocytosis
Patient with Addison’s disease has gastroenteritis and presents to ED. How do you adjust her steroid replacement?
Double hydrocortisone dose, same fludrocortisone dose
What is the 1st line Tx for diabetic neuropathic pain?
Amitryptiline, duloxetine, gabapentin, pregablin. Tramadol may be used as ‘rescue therapy’ for exacerbations or topic capsaicin for localised pain.
What causes Graves’ disease?
It is an autoimmune condition, caused by IgG antibodies to TSH receptors in thyroid (TSHR-Ab), in the context of hyperthyroidism.
What are causes of primary hyperthyroidism?
Graves’ disease or thyroid nodules e.g. toxic multi-nodular goitre and solitary toxic adenoma.
What are causes of secondary hyperthyroidism?
Beta-HCG can mimic the action of TSH on the thyroid gland - this occurs in pregnancy and in b-HCG secreting tumours e.g. choriocarcinoma, teratomas.
What are the most common forms of transient thyroiditis?
De Quervain’s, postpartum thyroiditis (<2 mths following birth) and amiodarone-induced thyroiditis type 2 (inflammation and released of stored hormones). These may exhibit thyrotoxic and hypothyroid phases.
How does amiodarone cause thyroid problems?
Excess iodine load may lead to increased synthesis of thyroid hormone or impaired synthesis, leading to hypothyroidism (AIH type 1) , or direct inflammation resulting in release in thyroid hormone (type 2)
What are the long term side effects of amiodarone?
Amiodarone is an antiarrythmic that contains large amounts of iodine. It may cause bradycardia, hypothyroidism / hyperthyroidism, pulmonary toxicity, ocular deposits, and liver function derangements.
What syndrome is a/w medullary thyroid cancer?
MEN Type 2.
What is the main risk factor for Graves’ ophthalmopathy?
Smoking - this increases the risk by 7-8 x
What are some Tx options for Graves’ opthalmopathy?
Steroids, irradiation, eye drops, surgery
Note: RAI is contraindicated in active/ severe eye disease
How do you investigate Graves’ disease?
TSHR-Ab indicates Graves’. If this is negative, do a thyroid uptake scan - diffuse uptake observed in antibody negative Graves’ disease OR scattered uptake by multiple lesions
How do you investigate a potential thyroid malignancy?
Ultrasound +/- FNA
How do you treat hyperthyroidism?
Thioamides i.e. carbimazole and propylthiouracil.
What are Tx options for Graves’ disease?
Radioactive iodine (RAI) - typically 1st line; CI in pregnancy, breastfeeding, active eye disease (may worsen this) Anti-thyroid meds - 1st line in mild disease/ increased chance of remission Surgery e.g. hemi or total thyroidectomy - 1st line in tracheal compression, suspected malignancy, other options unsuitable
What are the key features of thyroid storm?
A medical emergency a/w high mortality - Tx in ITU/ HDU w consultant led care and specialist endo input. (1) Beta blockers (2) Anti-thyroid medication (3) Steroids (4) Lugol's iodine (1h later) Closely monitor BMs.
What are causes of primary, secondary and tertiary hypothyroidism?
Primary - thyroid gland failure e.g. thyroiditis
Secondary - pituitary disease and reduced TSH
Tertiary - hypothalamic disease causing reduced TRH
What is the most common cause of hypothyroidism in developed countries?
Chronic autoimmune thyroiditis, characterised by high levels of thyroid autoantibodies. It may present with a non-tender goitre (firm, rubbery, smooth) OR an atrophic thyroid gland.
What may cause a painful goitre?
Subacute thyroiditis i.e. de Quervain’s/ postpartum.
What causes Sheehan’s syndrome?
In post partum haemorrhage causing hypovolemic shock, the increased vascular supply to pituitary gland (in pregnancy) may lead to ischaemia of the gland (esp if existing tumour) and global reduction in pituitary hormone secretion.
What is the Wolff-Chaikoff effect?
Decreased thyroid synthesis after a large iodine intake. Amiodarone-induced hypothyroidism (AIH) results from an inability to escape this effect.
What causes congenital hypothyroidism?
Underdeveloped thyroid gland/ ectopic gland or dys-hormonogenesis. This is screened for in the heel prick test to see if newborn will require long-term levothyroxine therapy.
What does the presence thyroid acropachy indicate?
Hyperthyroidism. This manifests as digital clubbing, soft tissue swelling of hands/ feet, periosteal new bone formation.
What are the symptoms of myxoedema coma?
Altered mental status, bradycardia, hypothermia, hypoglycaemia. This occurs in patients with undiagnosed hypothyroidism or those w/o meds.
When to test for hypothyroidism?
Classical symptoms, indicative conditions, psychiatric illness, menstrual irregularities
What antibodies are associated with chronic autoimmune thyroiditis?
Thyroid peroxidase antibodies (TPO Abs) are positive in >90% of patients with chronic autoimmune thyroiditis - this is the most common one but other antibodies may be present as well. Non specific and may be raised in T1DM and pregnancy.
How do you treat primary hypothyroidism in different patient groups?
18-65y, no CVS disease - levothyroxine, starting with 1.6mcg/kg (titrate up by 25mcg, aim for TSH 0.4-4.5 mU/L)
>65yo, CVS disease - levothyroxine, starting with 25-50mcg (lower dose) and titrate up by 25mcg
Pregnancy - levothyroxine, specialist care, aim to be euthyroid prior to conception
What are treatment targets in DKA?
Ketones - fall by 0.5 mmol/l/h
Bicarb - rise by 3 mmol/l/h
Glucose - fall by 3 mmol/l/h
What is needed for diagnosis of HHS?
Serum glucose >30 (grey bottle)
Raised osmolality >320 (2 Na + urea + glucose)
Mild or absent ketones - serum <3; urine -/trace/+
What can trigger HHS?
Infection e.g cystitis, pyelonephritis, pancreatitis
Hypovolemic
High dose steroids
Fall/ long-lie/ LOC (check for rhabdo)
What are some complications of HHS and HHS treatment?
HHS - venous/ arterial thrombosis, seizures, coma, electrolyte derangements
HHS Tx - cerebral oedema, osmotic demyelination syndrome, electrolyte derangements
How do you treat HHS?
0.9% NaCl, aim for 2-3L at 6h, 3-6L at 12h (continuously re-assess and treat)
If glucose falls <14, give 5% or 10% dextrose
Treat with FRII only if there is ketosis (or if fluid resus does not cause adequate fall in glucose) – long term insulin Tx may be started if poor glycaemic control
What are the aims of Tx HHS?
Fall in glucose of 5mmol/h
Fall in osmolality of 3-8mmol/h
