Endocrine Flashcards
Recognise the presenting symptoms of Paget’s disease of bone
- Bony deformity / pain / arthritis / fracture
- Nerve impingement
- Sensorineural hearing loss (from VIII nerve compression)
- High-output CF (vascularity of Paget bone –> increased blood volume –> increased strain on heart)
(UpToDate, Mirza)
Identify appropriate investigations for Paget’s disease of bone
Bloods: LFTs (for ALP), serum ALP, (bone ALP needed if liver disease), serum calcium, serum 25-hydroxyvitaminD, CRP, ESR
Imaging: plain x-ray, bone scan
Bone biposy: only if ?malignant disease
(UpToDate)
Generate a management plan for Paget’s disease of bone
- Conservative: regular follow-up, education, preventative measures (avoid high-impact activities), physio, hearing aids
- Medical
- 1st line: bisphosphonates (zoledronic acid)
- adjunct calcium (carbonate) + vitD (ergocalciferol)
- analgesia (WHO ladder, usually paracetamol or NSAID)
- 2nd line: calcitonin (if not tolerating bisphosphonates. Use together CI)
(BMJ)
Identify the possible complications of Paget’s disease of bone
Long-term:
- Malignant change (1% osteosarcoma)
- Spinal stenosis
- Sensorineural deafness
- Arthritis
- High-output cardiac failure
(BMJ, Mirza)
T2DM: outline the targets for HbA1c monitoring
Monitoring:
- HbA1c (every 3-6m until stable, then every 6m)
- Lifestyle modifications / 1 non-hypo-causing mx = target 6.5% (48mmol/mol)
- Lifestyle modifications + 1 hypo-causing mx = target 7.0% (53mmol/mol)
- If on single drug and HbA1c 7.5+% (58mmol/mol), intensify mx
- Be flexible with targets if hypoglycaemia risks (falls)
(NICE)
T2DM: what are the indications for home glucose monitoring?
Indications for home glucose monitoring in T2DM:
- Taking insulin
- Hypoglyaemic episodes (or ?hypoglycaemic episode)
- On oral mx that may induce hypoglycaemia + drives/machinery
- Pregnant or planning to get pregnant
- Starting a course of steroids
Pts self-monitoring skills and need for self monitoring should be assessed annually
(NICE)
Explain the aetiology / risk factors of primary hyperaldosteronism
Bilateral idopathic adrenal hyperplasia (70%)
Adrenal adenoma = Conn’s Syndrome
Adrenal carcinoma (rare)
Familial hyperaldosteronism (early onset)
(Passmedicine)
Identify appropriate investigations for primary hyperaldosteronism
Bloods: UEs (K+), plasma aldosterone:renin ratio (morning, ambulatory)
Imaging: high-resolution CT abdo
Special tests: adrenal venous sampling (to see if flow of excess aldosterone is bilateral), fludrocortisone suppression test
(UpToDate)
Identify the possible complications of primary hyperaldosteronism
Short: aldosterone-antagonist-induced hperkalaemia, perioperative complications (bleeding, infection, wound hernia, anaesthetic)
Long: stroke, MI, HF, AF, impaired renal function
(BMJ)
Generate a management plan for primary hyperaldosteronism
- Medical
- Aldosterone-R antagonist: either
- spironolactone. SE: gynaecomastia
- eplerenone: avoid if hyperK, hepatic impairment
- amiloride
- glucocorticoid (IF familial hyperaldosteronism)
- Aldosterone-R antagonist: either
- Surgical
- Lap adrenalectomy (if adenoma + surgical pt)
- (+ pre and post op medical tx)
(BMJ)
Summarise the prognosis for patients with primary hyperaldosteronism
Medical mx usually reduces HTN and always resolves hypokalaemia
Surgical mx has 50-60% cure rate. Low recurrence
(BMJ)
T2DM: outline the choice of glycaemic control
See image
Targets:
- HbA1c (every 3-6m until stable, then every 6m)
- Lifestyle modifications / 1 non-hypo-causing mx = target 6.5% (48mmol/mol)
- Lifestyle modifications + 1 hypo-causing mx = target 7.0% (53mmol/mol)
- If on single drug and HbA1c 7.5+% (58mmol/mol), intensify mx
- If pt not meeting target, but not breaching 58 mmol/mol, consider increasing dose of current therapy
(Hypo-causing mx: sulphonylureas, insulin)
What are the criteria for diagnosing T2DM?
- Pt symptomatic:
- random glucose >11.1 mmol/l (or after OGTT)
- fasting glucose >7.0 mmol/l (HbA1c 48)
- Pt asymptomatic: the above must be demonstrated on 2 separate occasions
(Passmedicine)
What are the criteria for diagnosing prediabetes?
Prediabetes:
Impaired fasting glucose: 6.0-6.9 mmol/L (HbA1c 42-47)
Impaired glucose tolerance: fasting glucose <7 mmol/L + OGTT (2h) of 7.8-11 mmol/l
(passmedicine)
What are the causes of raised prolactin levels?
6 Ps:
- pregnancy
- prolactinoma
- physiological
- polycystic ovarian syndrome
- primary hypothyroidism
- phenothiazines, metoclopramide, domperidone
Explain the causes of SIADH
- Malignancy: small cell lung cancer, pancreas, prostate
- Neurological: stoke, subarachnoid haemorrhage, subdural haemorrhage
- Infections:
- Lung (TB, pneumonia)
- Brain (meningitis, encephalitis, abscess)
- Drugs: 2’ines’, 2 ‘ides’ and 2 antidepressants
- Vincristine + carbemazepine
- Glizlazide (sulphonylureas) + cyclophosphamide
- SSRIs + TCAs
(passmedicine)
Generate a management plan for phaeochromocytoma
• Medical
o Alpha-blockade: eg phenoxybenzamine (irreversible, a1+a2).
Reduces alpha-mediated vasoconstriction. Central action reduces sympathetic outflow
o Labetolol – mixed alpha and beta blocker. Used in chronic hypertension associated with phaeos. NEVER USE BETA-BLOCKERS IN ISOLATION – will stop NA’s vasodilator effect and can lead to a hypertensive crisis
(ARBs, ACE-Is, diuretics can also be harmful as phaeo’s inhibition of renin-angiotensin system + sweating + increased metabolic rate –> dehydration)
• Surgical (>3cm lesion)
o Resection of tumour
- Consider IV saline before operation to maintain higher circulating volume to avoid BP crashing after surgery
- Peri-operative doxazosin – alpha 1 receptor blocker. Vasodilation. Chosen over phenoxybenzamine as is less potent, shorter-acting and more easily reversed. Risk of alpha blockade + minimal catecholamine production + surgical bleeding –> serious hypotension
Identify the possible complications of phaeochromocytoma
Immediate: acute hypertensive crisis (–> cerebral haemorrhage, MI, arrhythmia), neurological complications (hypertensive encephalopathy, seizure, CVA)
Post-operative: hypotension, arrythmias
(BMJ)
Summarise the prognosis for patients with phaeochromocytoma
Mortality: 5y survival 95% in benign disease, 50% in malignant disease
Surgery curative in 85%
(BMJ)
Define phaeochromocytoma
Neuroendocrine tumour of the chromaffin cells of the adrenal medulla. Hypertension and hyperglycaemia are often found.
- 10% of cases are bilateral.
- 10% occur in children.
- 11% are malignant (higher when tumour is located outside the adrenal).
- 10% will not be hypertensive.
- Usuall smaller than 10cm
(passmedicine)
Generate a management plan for carcinoid syndrome
Management
- somatostatin analogues e.g. octreotide (suppresses 5HT release)
- diarrhoea: cyproheptadine may help
- treat underlying malignancy
(passmedicine, path)
Identify appropriate investigations for carcinoid syndrome
- urinary 5-HIAA (main 5HT metabolite)
- plasma chromogranin A y
(passmedicine, path)
Define carcinoid syndrome
Tumours of enterchromaffin cells (bowel, lung, ovaries, testes), produce 5HT, slow growing –> bronchoconstriction, flushing, diarrhoea –> carcinoid crisis (life threatening vasodilatation: hypotension, tachy, bronchoconstriction, hyperglycaemia)
(path)
Identify the possible complications of carcinoid syndrome
- Early: carcinoid crisis (hypotension, tachy, arrhythmias), bowel obstruction
- Late: carcinoid heart disease (valvular damage –> heart failure), pellagra (dementia, diarrhoea, dermatitis due to deficiency of tryptophan –> niacin deficiency)
(BMJ)
