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Medicine Y6 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Recognise the presenting symptoms of Paget’s disease of bone

A
  • 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)

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2
Q

Identify appropriate investigations for Paget’s disease of bone

A

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)

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3
Q

Generate a management plan for Paget’s disease of bone

A
  • 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)

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4
Q

Identify the possible complications of Paget’s disease of bone

A

Long-term:

  • Malignant change (1% osteosarcoma)
  • Spinal stenosis
  • Sensorineural deafness
  • Arthritis
  • High-output cardiac failure

(BMJ, Mirza)

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5
Q

T2DM: outline the targets for HbA1c monitoring

A

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)

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6
Q

T2DM: what are the indications for home glucose monitoring?

A

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)

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7
Q

Explain the aetiology / risk factors of primary hyperaldosteronism

A

Bilateral idopathic adrenal hyperplasia (70%)

Adrenal adenoma = Conn’s Syndrome

Adrenal carcinoma (rare)

Familial hyperaldosteronism (early onset)

(Passmedicine)

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8
Q

Identify appropriate investigations for primary hyperaldosteronism

A

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)

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9
Q

Identify the possible complications of primary hyperaldosteronism

A

Short: aldosterone-antagonist-induced hperkalaemia, perioperative complications (bleeding, infection, wound hernia, anaesthetic)

Long: stroke, MI, HF, AF, impaired renal function

(BMJ)

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10
Q

Generate a management plan for primary hyperaldosteronism

A
  • Medical
    • Aldosterone-R antagonist: either
      • spironolactone. SE: gynaecomastia
      • eplerenone: avoid if hyperK, hepatic impairment
      • amiloride
      • glucocorticoid (IF familial hyperaldosteronism)
  • Surgical
    • Lap adrenalectomy (if adenoma + surgical pt)
    • (+ pre and post op medical tx)

(BMJ)

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11
Q

Summarise the prognosis for patients with primary hyperaldosteronism

A

Medical mx usually reduces HTN and always resolves hypokalaemia

Surgical mx has 50-60% cure rate. Low recurrence

(BMJ)

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12
Q

T2DM: outline the choice of glycaemic control

A

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)

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13
Q

What are the criteria for diagnosing T2DM?

A
  • 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)

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14
Q

What are the criteria for diagnosing prediabetes?

A

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)

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15
Q

What are the causes of raised prolactin levels?

A

6 Ps:

  • pregnancy
  • prolactinoma
  • physiological
  • polycystic ovarian syndrome
  • primary hypothyroidism
  • phenothiazines, metoclopramide, domperidone
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16
Q

Explain the causes of SIADH

A
  • 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)

17
Q

Generate a management plan for phaeochromocytoma

A

• 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
18
Q

Identify the possible complications of phaeochromocytoma

A

Immediate: acute hypertensive crisis (–> cerebral haemorrhage, MI, arrhythmia), neurological complications (hypertensive encephalopathy, seizure, CVA)

Post-operative: hypotension, arrythmias

(BMJ)

19
Q

Summarise the prognosis for patients with phaeochromocytoma

A

Mortality: 5y survival 95% in benign disease, 50% in malignant disease

Surgery curative in 85%

(BMJ)

20
Q

Define phaeochromocytoma

A

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)

21
Q

Generate a management plan for carcinoid syndrome

A

Management

  • somatostatin analogues e.g. octreotide (suppresses 5HT release)
  • diarrhoea: cyproheptadine may help
  • treat underlying malignancy

(passmedicine, path)

22
Q

Identify appropriate investigations for carcinoid syndrome

A
  • urinary 5-HIAA (main 5HT metabolite)
  • plasma chromogranin A y

(passmedicine, path)

23
Q

Define carcinoid syndrome

A

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)

24
Q

Identify the possible complications of carcinoid syndrome

A
  • 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)

25
Q

What are the features of McCune-Albright Syndrome?

A
  • Hyperfunctioning endocrine system
    • Precious puberty
    • Cushingoid
    • Hypophosphataemia
  • Cafe-au-lait spots
  • Polyostotic fibrous dysplasia

Genetic condition, mutation in G-protein

26
Q

What are the main features of Kallman Syndrome?

A
  • Hypogonadotrophic hypogonadism
    • hypogonadism
    • infertility
    • variable puberty
  • Anosmia - differentiates it from other causes of hypogonadotrophic hypogonadism

(500 SBAs)

27
Q

Give common causes of erythema nodosum

A
  • IBD
  • Sarcoidosis
  • TB
  • Streptococcal infection
  • Drugs: salicylates, sulphonamides

(Meeran)

28
Q

Generate a management plan for diabetic ketoacidosis in an adult

A

Medical (ABCDE)

  • IV 0.9% saline: start with fluid challenge of 1L over ~30 mins (running free). Usually depleted by 5-8L.
  • Monitor BM, ECG, electrolytes, ABG
  • Insulin: After ~1h, 0.1 units / kg/h fixed dose IV infusion
  • 5% dextrose: once BM >15mmol/L:
  • K+: 40 mmol/L into fluids, unless levels >5.5 mmol/L
  • Investigate causes: FBC, cultures, CXR

(Meeran, passmedicine)

29
Q

Give features of acromegaly

A
  • coarse facial appearance, spade-like hands, increase in shoe size
  • large tongue, prognathism, interdental spaces
  • excessive sweating and oily skin
  • features of pituitary tumour: hypopituitarism, headaches, bitemporal hemianopia
  • raised prolactin in 1/3 of cases → galactorrhoea
  • 6% of patients have MEN-1

(passmedicine)

30
Q

Give potential complications of acromegaly

A
  • Bitemporal hemianopia
  • hypertension
  • diabetes (>10%)
  • cardiomyopathy
  • colorectal cancer

(passmedicine, Meeran)

31
Q

Generate a management plan for acromegaly

A
  • Medical:
    • Octreotide (lanreodie can be given monthly)
    • Radiotherapy
  • Surgical
    • Transphenoidal hypophysectomy

(Meeran)

32
Q

Generate a mangement plan for Cushing’s Syndrome

A
  • Treat underlying cause
    • Reduce steroids
    • Tumour: radiotherapy, surgery
  • Medical
    • Block cortisol synthesis
      • Ketoconazole
      • Metyrapone

(Path, meeran)

33
Q

Summarise the prognosis for patients with Cushing’s syndrome

A

Untreated tx has 5y survival of 50%

Responds well to tx (features can fade w/i a year)

(BMJ)

34
Q

Generate a management plan for SIADH

A

Treat underlying cause

1st: fluid restriction
2nd: desmeclocycline (inhibits ADH)
* (500SBAs)*

35
Q

What is the triple assessment for patients with a thyroid nodule?

A
  • Clinical examination
  • USS
  • FNAC

(AS)

36
Q

Give causes of cervical lymphadenopathy

A

LIST

  • Lympoma + Leukaemia
  • Infection
    • bacterial: tonsillitis, dental abscess, TB
    • viral: EBV, HIV
  • Sarcoidosis
  • Tumours: ENT, breast, lung, gastric

(AS)

37
Q

Insulinoma: triad

A

Whipple’s triad

Episodic hypoglycaemia + CNS dysfunction (anxiety, confusion) + releived by glucose

(250 SBAs)

Medicine Y6 (14 decks)

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