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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
In which parts of the nervous system is weight regulated? Name 2 places.
Hypothalamus - Arcuate nucleus -Neuropeptide-Y nerves POMC nerve fibres
25
Which 3 hormones stimulate hunger?
Neuropeptide-Y Ghrelin Leptin All the other hormones suppress hunger
26
What drugs can be given to obese patients to encourage weight loss? Name 4.
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
27
Define osteoporosis with 2 criteria.
T-score < -2.5 Fractures with minimal trauma include wrist, vertebra and hip
28
What is the recommended daily intake of Ca?
1000mg/day 1300mg/day in women >50 and men >70 Baseline dietary intake 750mg to 1240mg daily
29
What is the risk associated with over supplementation of Ca?
Increased risk of MIs (30% vs placebo)
30
What is the risk of excessive vitamin D supplementation?
Increased risk of falls and fractures
31
What are the varying levels of deficiency for vitamin D?
Vit D > 50 is considered adequate 30 - 49 is mild deficiency 12.5 to 29 is moderate deficiency <12.5 is severe deficiency
32
Where are atypical fractures generally seen?
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
Which population of patients are at increased risk of ONJ while on bisphosphonate therapy?
Oncology patients - 1-15% Also high dose and long duration, but not to nearly the same extent
34
What are the indications for starting teriparatide? Name 3.
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
What are the contraindications for giving teriparatide? Name 5.
Malignancy Renal stones Gout Paget's Skeletal irradiation
36
How are small pituitary causing acromegaly tumours managed surgically?
Selective trans-sphenoidal microadenectomy
37
How are large pituitary tumours causing acromegaly managed surgically?
Total hypophysectomy +/- XRT (stereotactic or megavoltage) +/- somatostatin analogue
38
Name 4 ACTH-independent causes of Cushing's.
Adrenal adenoma Adrenal carcinoma Micronodular hyperplasia (primary pigmented nodular adrenal disease - PPNAD) Macronodular hyperplasia (ACTH-independent macronodular adrenal hyperplasia - AIMAH)
39
Name 3 ACTH-dependent causes of Cushing's.
Cushing's disease Ectopic ACTH syndrome CRH syndrome
40
Name 2 causes of pseudo-Cushing's
Depression ETOH
41
How do you interpret test results from an evening plasma cortisol test?
<50nm/L excludes Cushing's syndrome >207 excludes pseudo-Cushing's Next step is plasma ACTH
42
How do you interpret an overnight low dose dexamethasone suppression test?
<50nm/L excludes Cushing's syndrome (can say <140 for sensitivity purposes) Next step is plasma ACTH
43
How do you interpret plasma ACTH results?
<5 = ACTH-independent cause of CS >15 = ACTH-dependent cause of CS 5-15 = equivocal, probably ACTH-dependent
44
What is pre-operative prep that is given prior to pituitary surgeries, irradiation and bilateral adrenalectomies for CS? Name 3.
Metyrapone Ketoconazole Mifepristone If failed other therapies, consider pasireotide
45
How are patients evaluated for treatment success following pituitary surgery for Cushing's disease?
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
Which gene mutation is associated with primary pigmented nodular adrenal disease (PPNAR)?
PPKAR1A mutation Associated with Carney complex
47
Name 6 non-pharmaceutical causes of hyperprolactinaemia.
CKD Seizure Post-partum PRLoma Macroadenoma with stalk disruption Stalk trauma
48
Name 3 causes for Conn's syndrome
Aldosterone-producing adenoma Idiopathic/bilateral hyperplasia Adrenal Ca
49
How do you interpret the results of an aldosterone suppression test?
Abnormal is >240 Normal is <140
50
How does copeptin testing work?
Measure baseline copeptin Give hypertonic Na to Na 150 Copeptin normally increases; if not, it is suggestive of diabetes insipidus
51
How do you approach a unilateral adrenal tumour based on age?
<40 - adrenalectomy >40 - incidentaloma is most likely - consider adrenal vein sampling
52
What features on CT or MRI are suggestive of a benign adrenal tumour? Name 5 features.
Smooth border Round/ovoid shape Homogenous border Low intensity signal (<10 HU) Isodense with liver MRI Carcinoma = hyperdense vs liver, heterogeneous, microcalcification
53
What conditions are associated with phaeochromocytoma? Name 4
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
Which imaging modalities can be used to assess for phaeochromocytomas? Name 3
CT MRI GaTATE scanning MIBG is not used so much anymore
55
Which populations do multinodular goitres typically affect? Name 3.
Older adults Women People from iodine-deficient areas
56
What are the pathophysiological processes of AIT types I and II?
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
Name 4 causes of subclinical hyperthyroidism.
Multinodular goitre Grave's disease Over-replacement of thyroxine Iodine exposure
58
How do you manage thyroid storms? 11 points.
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
What clinical and diagnostic features would you expect to see with subacute thyroiditis? 5 points.
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
What are the different types of thyroid cancer, in order of incidence?
Papillary Follicular Poorly differentiated Anaplastic Medullary
61
How is papillary thyroid cancer diagnosed?
FNA
62
How is follicular thyroid cancer diagnosed?
Excision biopsy or hemithyroidectomy It may be adenoma or carcinoma hence FNA not reliable
63
How is follicular thyroid cancer differentiated from follicular adenomas? And what signalling pathway defects are implicated?
Capsular and vascular invasion MEK or ERK system defects
64
What are negative prognostic features for follicular thyroid cancer? Name 3.
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
What is the treatment for follicular thyroid cancers?
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
What are the indications for surgery with primary hyperparathyroidism? 6 criteria.
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
What is the pathophysiology of familial hypocalcuric hypercalcaemia?
Inactivating mutation of calcium sensing receptor in PTH glands and kidneys
68
What is the pathophysiology of autosomal dominant hypocalcaemia?
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
Which gene is implicated in vitamin D dependent rickets type 1a?
VDDR-1A gene CYP27B1 Vitamin D activation gene
70
Which gene is implicated in vitamin D dependent rickets type 1b?
VDDR-1A gene CYP2R1 Vitamin D activation gene
71
Which gene is implicated in vitamin D dependent rickets type 2?
HNRNPC - vitamin D receptor co-activator
72
What are the diagnostic criteria for PCOS?
2 out of 3 of... Oligomenorrhoea/anovulation Clinical or biochemical hypoandrogenism Polycystic ovaries
73
What biochemical abnormalities would you expect to see with PCOS? 3 abnormalities.
Elevated free serum testosterone Low SHBG Androstenedione or DHEAS often mildly elevated Elevated free androgen index subsequently
74
What 2 criteria (either/or) do you require in order to make a diagnosis of primary ovarian insufficiency?
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
How quickly do you aim to correct Na in SIADH normally, and how quickly do you aim to correct it in severe cases?
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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