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GCUH FRACP Writtens 2020 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What features do you expect to see in MEN1, and what is the associated gene? Name 3 features.

A

“3 Ps”

Parathyroid (95%) - hyperparathyroidism

Pituitary (70%)

Pancreas (50%)

MEN1 gene

Also adrenal and thyroid

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2
Q

What features do you expect to see in MEN1, and what is the associated gene? Name 3 features.

A

“3 Ps”

Parathyroid (95%) - hyperparathyroidism

Pituitary (70%)

Pancreas (50%)

MEN1 gene

Also adrenal and thyroid

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3
Q

What features do you expect to see in MEN2A, and what is the associated gene? Name 2 features.

A

“2 Ps”

Parathyroid (60%)

Phaeochromocytoma

RET oncogene

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4
Q

What features do you expect to see in MEN2B, and what is the associated gene? Name 3 features.

A

Phaeochromocytoma

Marfanoid body habitus

Neuromas

RET oncogene

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5
Q

Name 5 autoantibodies you might expect to see in T1DM

A

Anti-GAD (glutamic acid decarboxylase)

Anti-IAA (insulin autoantibodies)

Anti-ICA (islet cell antibodies)

Anti-IA2A

Anti-ZnT8

T1DM generally starts when patients have 2 or more autoantibodies

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6
Q

Name 3 potential “triggering” factors for T1DM

A

Congenital rubella

Hygiene (possibly)

Obesity (probably)

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7
Q

What HbA1c level ought to be targeted in T1DM?

A

<7.0

<8.0 if severe hypoglycaemia

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8
Q

In diabetes, what are the reference ranges for microalbuminuria and macroalbuminuria with urine ACR?

A

Micro - 2.5 to 25 M; 3.5 to 35 F

Macro - > 25 M, >35 F

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9
Q

What 3 parameters are required to diagnose DKA?

A

Glucose >14

Ketosis

pH < 7.30 (bicarbonate <20)

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10
Q

What 3 parameters are required to diagnose HHS?

A

Glucose > 30

Minimal ketosis

Osmolality > 320

Usually glucose is >56 and age is >65

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11
Q

How do DPP4 (gliptin) inhibitors work?

A

Boost endogenous GLP-1/GIP (incretin), inhibiting glucagon release and and in turn increasing insulin secretion

Works only at mealtimes; no CV benefit

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12
Q

How do GLP-1 analogues (e.g. exenatide) work?

A

Direct stimulation of beta islet cells

Often results in weight loss

Risks of pancreatitis and nausea

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13
Q

For T2DM, after inadequate control following conservative measures and metformin, what medications would you consider in patients with CVD? Name 2

A

GLP-1

SGLT2i

Either one will do. Give both if one isn’t working, or consider insulin, TZD, SU or DPP4 if not on GLP-1.

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14
Q

For T2DM, after inadequate control following conservative measures and metformin, what medications would you consider in patients with CKD or HF? Name 2

A

Preferably SGLT2i

If eGFR does not allow that, then GLP-1

Following that, consider insulin, SU or DPP4 (if not on GLP-1)

Do NOT give TZD in setting of HF

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15
Q

For T2DM, after inadequate control following conservative measures and metformin, what medications would you consider in patients who have a compelling need to minimise hypoglycaemia? Name 4

A

DPP4i

GLP-1

SGLT2i

TZD

Add the others as needed; if still inadequate, consider later generation sulphonylureas or insulin

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16
Q

For T2DM, after inadequate control following conservative measures and metformin, what medications would you consider in patients with a compelling need to minimise weight gain or promote weight loss? Name 2

A

SGLT2i

GLP-1

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17
Q

Which GLP-1 agonists are proven to significantly reduce CVD?

A

Albiglutide

Dulaglutide

Exenatide and lixosenatide are not shown to reduce CVD - unclear why

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18
Q

What BP should be aimed for in diabetic patients?

A

140/90

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19
Q

What are the risks and benefits of intensive glycaemic control in diabetic patients?

A

Decreased HbA1c and macrovascular complications

22% increase in mortality, however

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19
Q

What are the risks and benefits of intensive glycaemic control in diabetic patients?

A

Decreased HbA1c and macrovascular complications

22% increase in mortality, however

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20
Q

When should diabetic patients be given statins?

A

<40 years, no risk factors for CVD - no statins

<40 with risk factors, start moderate-high dose

All else, give

Ezetimibe with statin is recommended

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21
Q

In which diabetic patients is fenofibrate beneficial alongside ezetimibe/statin?

A

Patients with increased triglycerides and decreased HDL

No significant CV benefit for other patients otherwise

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22
Q

What are the benefits of using GFR rather than ACR in diabetic patients to monitor renal function? Name 3 benefits.

A

More specific

Indicates renal function

Rarely regresses (ACR microalb -> normoalb-> macroalb is typical)

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23
Q

Name 5 hormones involved in predisposition to obesity.

A

MC4-R (dominant)

Ob/ObR or LEP/LEPR (leptin)

POMC (MSH)

FTO

BDNF

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24
Q

In which parts of the nervous system is weight regulated? Name 2 places.

A

Hypothalamus - Arcuate nucleus -Neuropeptide-Y nerves

POMC nerve fibres

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25
Q

Which 3 hormones stimulate hunger?

A

Neuropeptide-Y

Ghrelin

Leptin

All the other hormones suppress hunger

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26
Q

What drugs can be given to obese patients to encourage weight loss? Name 4.

A

Liraglutide

Orlistat

Duromine

Bupriopion + naltrexone

Topiramate can be used but is off-label

It’s better to use multiple low dose drugs than one high dose drug - drug use should be lifelong

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27
Q

Define osteoporosis with 2 criteria.

A

T-score < -2.5

Fractures with minimal trauma include wrist, vertebra and hip

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28
Q

What is the recommended daily intake of Ca?

A

1000mg/day

1300mg/day in women >50 and men >70

Baseline dietary intake 750mg to 1240mg daily

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29
Q

What is the risk associated with over supplementation of Ca?

A

Increased risk of MIs (30% vs placebo)

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30
Q

What is the risk of excessive vitamin D supplementation?

A

Increased risk of falls and fractures

31
Q

What are the varying levels of deficiency for vitamin D?

A

Vit D > 50 is considered adequate

30 - 49 is mild deficiency

12.5 to 29 is moderate deficiency

<12.5 is severe deficiency

32
Q

Where are atypical fractures generally seen?

A

Proximal third femur shaft

Incomplete fractures involve the lateral cortex

The median duration on bisphosphonates for atypical fractures is 7 years; concomitant steroid use seen in 34% of patients

33
Q

Which population of patients are at increased risk of ONJ while on bisphosphonate therapy?

A

Oncology patients - 1-15%

Also high dose and long duration, but not to nearly the same extent

34
Q

What are the indications for starting teriparatide? Name 3.

A

BMD < -3.0

2 or more minimal trauma fractures

AND

At least one new symptomatic # after at least 12 months of continuous antiresorptive therapy

Course is limited to 18 months

35
Q

What are the contraindications for giving teriparatide? Name 5.

A

Malignancy

Renal stones

Gout

Paget’s

Skeletal irradiation

36
Q

How are small pituitary causing acromegaly tumours managed surgically?

A

Selective trans-sphenoidal microadenectomy

37
Q

How are large pituitary tumours causing acromegaly managed surgically?

A

Total hypophysectomy +/- XRT (stereotactic or megavoltage) +/- somatostatin analogue

38
Q

Name 4 ACTH-independent causes of Cushing’s.

A

Adrenal adenoma

Adrenal carcinoma

Micronodular hyperplasia (primary pigmented nodular adrenal disease - PPNAD)

Macronodular hyperplasia (ACTH-independent macronodular adrenal hyperplasia - AIMAH)

39
Q

Name 3 ACTH-dependent causes of Cushing’s.

A

Cushing’s disease

Ectopic ACTH syndrome

CRH syndrome

40
Q

Name 2 causes of pseudo-Cushing’s

A

Depression

ETOH

41
Q

How do you interpret test results from an evening plasma cortisol test?

A

<50nm/L excludes Cushing’s syndrome

> 207 excludes pseudo-Cushing’s

Next step is plasma ACTH

42
Q

How do you interpret an overnight low dose dexamethasone suppression test?

A

<50nm/L excludes Cushing’s syndrome (can say <140 for sensitivity purposes)

Next step is plasma ACTH

43
Q

How do you interpret plasma ACTH results?

A

<5 = ACTH-independent cause of CS

> 15 = ACTH-dependent cause of CS

5-15 = equivocal, probably ACTH-dependent

44
Q

What is pre-operative prep that is given prior to pituitary surgeries, irradiation and bilateral adrenalectomies for CS? Name 3.

A

Metyrapone

Ketoconazole

Mifepristone

If failed other therapies, consider pasireotide

45
Q

How are patients evaluated for treatment success following pituitary surgery for Cushing’s disease?

A

Measure 0800hrs plasma 24 hours post last hydrocortisone administration 3-7 hours post-OP

Cure if undetectable plasma cort (<28) or ACTH (<5-10)

Persistently detectable plasma cort = incomplete resection and almost certain recurrence, even in normal range

46
Q

Which gene mutation is associated with primary pigmented nodular adrenal disease (PPNAR)?

A

PPKAR1A mutation

Associated with Carney complex

47
Q

Name 6 non-pharmaceutical causes of hyperprolactinaemia.

A

CKD

Seizure

Post-partum

PRLoma

Macroadenoma with stalk disruption

Stalk trauma

48
Q

Name 3 causes for Conn’s syndrome

A

Aldosterone-producing adenoma

Idiopathic/bilateral hyperplasia

Adrenal Ca

49
Q

How do you interpret the results of an aldosterone suppression test?

A

Abnormal is >240

Normal is <140

50
Q

How does copeptin testing work?

A

Measure baseline copeptin

Give hypertonic Na to Na 150

Copeptin normally increases; if not, it is suggestive of diabetes insipidus

51
Q

How do you approach a unilateral adrenal tumour based on age?

A

<40 - adrenalectomy

> 40 - incidentaloma is most likely - consider adrenal vein sampling

52
Q

What features on CT or MRI are suggestive of a benign adrenal tumour? Name 5 features.

A

Smooth border

Round/ovoid shape

Homogenous border

Low intensity signal (<10 HU)

Isodense with liver MRI

Carcinoma = hyperdense vs liver, heterogeneous, microcalcification

53
Q

What conditions are associated with phaeochromocytoma? Name 4

A

MEN2A

MEN2B

VHL

NF-1

Also genes SDBH (most important) and SDHD (assoc with head and neck tumours rather than paragangliomas, unlike the others)

54
Q

Which imaging modalities can be used to assess for phaeochromocytomas? Name 3

A

CT

MRI

GaTATE scanning

MIBG is not used so much anymore

55
Q

Which populations do multinodular goitres typically affect? Name 3.

A

Older adults

Women

People from iodine-deficient areas

56
Q

What are the pathophysiological processes of AIT types I and II?

A

Type I - increased synthesis T4 due to iodine load (T4 ++ T3 -)

Type II - thyrocyte cytotoxicity

Both feature 5’ deiodinase inhibition

USS shows increased vascularity in type I but decreased in type II

57
Q

Name 4 causes of subclinical hyperthyroidism.

A

Multinodular goitre

Grave’s disease

Over-replacement of thyroxine

Iodine exposure

58
Q

How do you manage thyroid storms? 11 points.

A

HDU/ICU admission

Beta-blocker (propranolol or esmolol to maintain HR <100)

Rehydrate

Control fever

Avoid aspirin

PTU

Lugol’s iodine

Hydrocort/pred

Cholestyramine (clears T4)

Plasmapheresis

59
Q

What clinical and diagnostic features would you expect to see with subacute thyroiditis? 5 points.

A

HLA-B35 in 75%

Thyrotoxicosis

High ESR/CRP/leuks

High thyroglobulin

USS - enlarged hypoechoic gland with decreased vascularity

Typically there is thyrotoxicosis, hypothyroidism then recovery.

60
Q

What are the different types of thyroid cancer, in order of incidence?

A

Papillary

Follicular

Poorly differentiated

Anaplastic

Medullary

61
Q

How is papillary thyroid cancer diagnosed?

A

FNA

62
Q

How is follicular thyroid cancer diagnosed?

A

Excision biopsy or hemithyroidectomy

It may be adenoma or carcinoma hence FNA not reliable

63
Q

How is follicular thyroid cancer differentiated from follicular adenomas? And what signalling pathway defects are implicated?

A

Capsular and vascular invasion

MEK or ERK system defects

64
Q

What are negative prognostic features for follicular thyroid cancer? Name 3.

A

Age > 40

Tumour size > 4cm

Local extension or distant mets

Spread to lymph nodes is very common (>80%), but spread beyond the neck is <10% - generally indolent without causing death.

65
Q

What is the treatment for follicular thyroid cancers?

A

Total thyroidectomy with remnant ablation radio-iodine

Surveillance with thyroglobulin measurement, whole body iodine scan and neck USS

TKI therapy for non-iodine avid recurrent and progressive disease

66
Q

What are the indications for surgery with primary hyperparathyroidism? 6 criteria.

A

Serum Ca 2.9 or above

Urine Ca >10mmol/day

eGFR <60

Nephrolithiasis/calcinosis

T-score < -2.5 in spine, neck of femur, total hip or distal third radius

Age < 50

67
Q

What is the pathophysiology of familial hypocalcuric hypercalcaemia?

A

Inactivating mutation of calcium sensing receptor in PTH glands and kidneys

68
Q

What is the pathophysiology of autosomal dominant hypocalcaemia?

A

Activating mutation of calcium-sensing receptor in PTH glands and kidney i.e. increased sensitivity of receptors to ionised calcium

PTH therefore decreased at normal calcium levels

69
Q

Which gene is implicated in vitamin D dependent rickets type 1a?

A

VDDR-1A gene CYP27B1

Vitamin D activation gene

70
Q

Which gene is implicated in vitamin D dependent rickets type 1b?

A

VDDR-1A gene CYP2R1

Vitamin D activation gene

71
Q

Which gene is implicated in vitamin D dependent rickets type 2?

A

HNRNPC - vitamin D receptor co-activator

72
Q

What are the diagnostic criteria for PCOS?

A

2 out of 3 of…

Oligomenorrhoea/anovulation

Clinical or biochemical hypoandrogenism

Polycystic ovaries

73
Q

What biochemical abnormalities would you expect to see with PCOS? 3 abnormalities.

A

Elevated free serum testosterone

Low SHBG

Androstenedione or DHEAS often mildly elevated

Elevated free androgen index subsequently

74
Q

What 2 criteria (either/or) do you require in order to make a diagnosis of primary ovarian insufficiency?

A

2 x FSH >40 at least 1 month apart

Or

Decreased oestradiol and increased FSH

Then go on to clarify aetiology e.g. Fragile X (FMR1), Polyendocrine Syndrome Type 1 (AIRE) etc.

75
Q

How quickly do you aim to correct Na in SIADH normally, and how quickly do you aim to correct it in severe cases?

A

Aim to increase Na by 4-6 mmol/L per 24 hours

If severe - aim to increase by 4-6 mmol/L per 2-3 hours (give hypertonic Na 2ml/kg over 15 mins)

GCUH FRACP Writtens 2020 (14 decks)

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