Endocrine and metabolic Flashcards
T1DM
- diagnosis
- management
Random blood glucose >11.1mmol/L
Management:
1st line - basal bolus regime:
1 long-acting insulin (e.g. Levemir) taken regular (bolus)
1 rapid-actinging insulin (e.g. novorapid, Humalog) taken before meals
T2DM
- diagnosis
- management
- what point is considered ‘pre-diabetes’
T2DM is diagnosed with an Hba1c >48 mmol/L and/or a fasting blood glucose >7 mmol/L. If the patient is asymptomatic, two separate abnormal test results are required.
Management:
* Hba1c >48 mmol/L despite lifestyle changes → metformin first-line
* HbA1c >58 mmol/L despite maximal dose metformin → dual therapy
* HbA1c >58 mmol/L despite dual therapy → triple therapy or insulin therapy + metformin
* First-line insulins in T2DM are intermediate acting (e.g., Humulin I).7.
Pre-diabetes is between 42-47mmol/mol
Diabetic peripheral neuropathy: management
1st line: amitrityline, duloxetine, gabapentin or pregablin
Rescue therapy: tramadol
Localised pain: topical capsaicin
Pain management clinics
Diabetes drug class and side-effects
Biguanides (metformin)
Sulfonylureas (gliclazide)
SGLT-2 inhibitors (dapagliflozin)
DPP-4 inhibitors (linagliptin, sitagliptin)
Thiazolidinediones (pioglitazone)
GLP-1 agonists (liraglutide, exenatide)
**Biguanides (metformin): ** Nausea and vomiting, abdominal pain, diarrhoea
Lactic acidosis
Sulfonylureas (gliclazide): Weight gain, hypoglycaemia
SGLT-2 inhibitors (dapagliflozin) UTIs, Fournier’s gangrene, DKA
DPP-4 inhibitors (linagliptin, sitagliptin):
Pancreatitis
**Thiazolidinediones (pioglitazone): **
Fluid retention, weight gain
Contraindicated in heart failure
Bladder cancer
GLP-1 agonists (liraglutide, exenatide):
Nausea and vomiting, reduced appetite
Pancreatitis
Addisons disease
- pathophysiology
- causes
- investigations
- management
Pathophysiology: caused by decreased production of the steroid hormones cortisol (glucocorticoid) and aldosterone (mineralocorticoid) by the adrenal gland.
Causes:
* Autoimmune (developed world)
* Tuberculosis (developing world)
* Haemorrhage (Waterhouse–Friderichsen syndrome)
Investigations:
* U&Es—Hyperkalaemia, hyponatraemia
* Blood glucose—Hypoglycaemia is common.
* Early morning cortisol is initial test.
* The short Synacthen test is the gold standard.
Management:
* Glucocorticoid—Hydrocortisone 2 × –3 × daily, with double dose during acute illness
* Mineralocorticoid—Fludrocortisone once daily
Hyperthyroidism:
TFTs for subclinical, primary and secondary
Mx
Subclinical: T4 ↔ TSH ↓
Primary: T4 ↑ TSH ↓
Secondary T4↑ TSH ↑ or ↔
TSH receptor antibodies (Graves’ disease)
Mx:
symptomatic - BBs e.g. propanolol
antithyroid:
1st line - carbimazole
2nd line - propylthiouracil
Radioiodine treatment for Graves and toxic multi nodular goitre
Surgical thyroidectomy
Hypothyroidism
- subtypes
- investigations
- Mx
Subtypes:
1. Hashimoto’s thyroiditis (autoimmune inflammation of the thyroid gland)
2. De Quervain’s thyroiditis (self-limiting post-viral infection, painful goitre, raised inflammatory markers)
3. Riedel’s thyroiditis (fibrosis causing hard non-tender goitre),
4. postpartum thyroiditis (autoimmune, initially thyrotoxicosis then hypothyroidism that normalises by 12 months)
5. iatrogenic post-thyroidectomy or radioiodine
6. drugs (e.g., lithium, amiodarone)
7. congenital hypothyroidism.
Investigations: \
* Antithyroid peroxidase (anti-TPO) antibodies—Hashimoto’s thyroiditis
* Inflammatory markers (raised in De Quervain’s thyroiditis)
Subclinical: T4 ↔ TSH ↑
Primary: T4 ↓ TSH↑
Secondary T4↓ TSH ↓ or ↔
Mx:
* Lifelong thyroxine (T4) replacement with levothyroxine, initially 1.6 mcg/kg once daily
* Check TSH levels every 3 months, then yearly once stable.
* Lower dose if over 65 years old or cardiovascular risk factors
Hyperparathyroidism
- pathophysiology
- classification
- presentation
- investigation
- management
Parathyroid hormone (PTH) is produced by the four parathyroid glands located on the posterior surface of the thyroid gland in response to low calcium levels.
* Primary hyperparathyroidism—Most common type and due to a parathyroid adenoma, hyperplasia
* Secondary hyperparathyroidism—Caused by renal impairment/vitamin D deficiency leading to low calcium levels & elevated PTH
*** Tertiary hyperparathyroidism **-longstanding secondary hyperparathyroidism leading to parathyroid hyperplasia
Sx - Usually asymptomatic. Possible symptoms include bone pain, abdominal pain, dehydration, polydipsia, polyuria, depression, anxiety, impaired concentration, poor sleep, fatigue, nausea, anorexia, and constipation.
Investigations
* PTH level
* Bone profile (calcium, phosphate)
* U&Es—Poor renal function may suggest secondary or tertiary hyperparathyroidism.
Management
* Primary
* Parathyroidectomy. If surgery is contraindicated, medical therapy with cinacalcet may be trialled to reduce calcium and PTH levels.
* Bisphosphonates or HRT to reduce fracture risk
* Secondary—Treat underlying cause with calcium supplements and phosphate-binding agents.
Hypoparathyroidism:
- causes
- presentation
- investigation
- management
Causes:
* Post-surgical (most common)
* Autoimmune
* DiGeorge syndrome
Presentation (asymptomatic or signs similar to hypocalcaemia)
* * * Myalgia, spasms, cramps
* * * Paraesthesia or numbness
* * * Memory impairment or slowed thinking
* * * Dry hair, brittle nails
* * * Chvostek’s sign—Tapping over facial nerve (CN VII) causes twitching of facial muscles.
* * * Trousseau’s sign—Carpopedal spasm when BP cuff is inflated above systolic BP
Investigations:
* Parathyroid hormone (PTH) is reduced.
* Bone profile (↓ calcium, ↑ phosphate)
* Magnesium and vitamin D may be low.
* ECG—Low calcium can cause prolonged QT interval.
* Pseudohypoparathyroidism refers to end-organ PTH resistance causing hypocalcaemia and hyperphosphataemia with elevated PTH level.
Management
* Correct hypocalcaemia
* Calcium and vitamin D sups
* Human recombinant PTH i
* Thiazide diuretics if hypercalciuria is present
MEN1 and MEN2
- associated tumours
MEN-1:
Pituitary adenoma
Primary hyperparathyroidism
Pancreatic neuroendocrine tumour (e.g., gastrinoma, insulinoma)
MEN-2A:
Medullary thyroid cancer
Phaeochromocytoma
Primary hyperparathyroidism
MEN-2B:
Medullary thyroid cancer
Phaeochromocytoma
Marfanoid body habitus
Mucosal neuromas
Cushing’s syndrome
- causes
- investigations
- management
Causes:
* Exogenous steroid use (most common)
* Pituitary adenoma (Cushing’s disease)
* Adrenal adenoma
* Small cell lung cancer (paraneoplastic)
Investigations:
Cushings syndrome e.g. adrenal adenoma : cortisol not surpressed, ACTH surpressed
Cushings disease (i.e. pituitary adenoma → ACTH secretion): cortisol & ACTH surpressed
**Ectopic **= both surpressed
Management (depend on underlying cause)
Cushing’s disease (pituitary adenoma)—Trans-sphenoidal resection
* Adrenal adenoma—Resection/adrenalectomy
* Ectopic ACTH—Treat underlying cancer.
Hyperaldosteronism (Conns syndrome)
- causes
- where is aldosterone produced?
- Sx
- investigations
- Mx
Aldosterone is a mineralocorticoid hormone produced in the zona glomerulosa of the adrenal cortex. It is released in response to angiotensin II as part of the renin–angiotensin–aldosterone system (RAAS).
Causes:
* Bilateral adrenal hyperplasia is most common.
* Adrenal adenoma (= Conn’s syndrome)
* Adrenal carcinoma (rare)
Features:
* HTN
* Hypokalaemia e.g muscle weakness
Investigations:
* Aldosterone/renin ratio would be increased.
* U&Es—Low K+, mildly elevated or normal Na2+
* Spironolactone and diuretics should be stopped 6 weeks before testing, as they will affect the measurements.
* CT adrenals
* Adrenal venous sampling (determines laterality and if any masses are functional)
Mx:
* Unilateral hyperplasia or adenoma—Laparoscopic adrenalectomy
* Bilateral hyperplasia—Aldosterone antagonist (e.g., spironolactone)
Diabetes Insipidus
- Cranial DI vs nephrogenic DI causes
- DI presentation
- investigations
- management
Cranial DI (most common) - neurosurgery, cranipharyngioma, head trauma, infection (meningitis)
Nephrogenic DI - drugs, lithium, electrolyte abnormalities, CKD, genetic
Presentation:
* Polydipsia (excess thirst)
* Polyuria (excess urine volume)
* Nocturia (waking at night to pass urine)
* Signs of fluid depletion (e.g., dry mucous membranes, reduced skin turgor, tachycardia)
Investigations:
* Serum osmolality will be raised.
* Urine osmolality is reduced.
* Water deprivation test:
Primary polydipsia
- after fluid dep: ↑
- after desmopressin: ↑
Cranial DI:
- after fluid dep: ↓
- after desmopressin: ↑
Nephrogenic DI:
- after fluid dep: ↓
- after desmopressin: ↓
Management:
* Encourage hydration and correct electrolytes.
* Cranial DI—Desmopressin (synthetic ADH)
* Nephrogenic DI—Thiazide diuretics
Phaeochromocytoma
- what is it?
- presentation
- investigation
- initial Mx
- definitive Mx
A rare catecholamine (adrenaline)-producing tumour of the chromaffin cells of the adrenal medulla.
Presentation:
* HTN
* Headaches
* Palpitations
* Sweating
* Anxiety
Investigation:
* 24-Hour urinary metanephrines and plasma free metanephrines.
* CT abdomen and pelvis to image the adrenals
Initial Mx: alpha blockers (e.g., phenoxybenzamine), then add beta blockers (e.g., propranolol). Starting a beta blocker before an alpha blocker may precipitate a hypertensive crisis
Definitive Mx: adrenalectomy
Hypopituitarism
- causes
- presentation
Causes:
* Pituitary adenoma (functional or non-functional)—Most common cause in adults
* Craniopharyngioma
* Pituitary surgery or radiotherapy, trauma
* Pituitary apoplexy (haemorrhage into or ischaemic infarction of an adenoma)—Consider if sudden severe headache
* Sheehan syndrome—Pituitary ischaemic necrosis secondary to a postpartum haemorrhage
Presentation: depends on the hormone which is deficient
- GH: short stature if during childhood; in adulthood, causes obesity
Prolactin: problems with lactation
FSH and LH: amenorrhoea, infertility, ↓ libido
ACTH: adrenal insufficiency (fatigue, postural hypotension)
TSH Secondary hypothyroidism (tiredness, cold, constipation)
Oxytocin: deficits in cognitive empathy
ADH/vasopressin: diabetes insipidus
