Endocrinology Flashcards

1
Q

What effect does biotin have on thyroid function?

A

Can cause spurious results on TFTs, as it interferes with assay.
Can cause false positive Graves-like appearance

Patients taking biotin should hold the supplement for two days prior to assessing thyroid function and longer if they are taking more than 10 mg a day.

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2
Q

What are the main associations with MEN2 syndrome?

WHat is the main difference between MEN2A and MEN2B?

A

MEN2A = medullary thyroid cancer, pheochromocytoma, and primary parathyroid hyperplasia

MEN2B = MTC + pheochromocytoma but not hyperparathyroidism

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3
Q

What are the main associations with MEN1 syndrome?

A

3Ps

Tumours of

  • parathyroid glands
  • anterior pituitary
  • enteropancreatic endocrine cells
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4
Q

2011B40

A 52 year old male presents with flushing, watery diarrhoea and wheezing. Urinary 5HIAA is 120mg/dL (2-8). A CT of the abdomen shows multiple liver metastases.

What is the site of primary tumour?
A. colon
B. oesophagus
C. rectum
D. small intestine
E. stomach
A

Small intestine

Distribution frequency =
GIT – 55%
- Small intestine – 45%, most commonly in the ileum
- Rectum 20%, Appendix 16%, Colon 11%, Stomach 7%

Bronchopulmonary system – 30%

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5
Q

What is the most common clinical presentation of carcinoid syndrome?

A

Chronic flushing (85%) & diarrhea (80%)

Result of serotonin (and other vasoactive substances) secretion into the systemic circulation

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6
Q

What test has >90% sensitivity and specificity for carcinoid syndrome diagnosis?

A

24-hour urinary excretion of 5-hydroxyindoleacetic acid (5-HIAA)
- Values >100 md/day indicative of carcinoid syndrome (normal 2-8mg/day)

5-HIAA is an end product of serotonin metabolism

5-HIAA is most useful in patients with primary midgut (jujunoileal, appendiceal, ascending colon) carcinoid tumours, which produce the highest levels of serotonin

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7
Q

What the effect of SGLT2 inhibitors on glucagon and insulin levels?

A

It decrease glucose levels, which leads to reduction in insulin and increase in glucagon

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8
Q

What is the main orexigenic hormone from the stomach that promotes hunger?

A

Ghrelin

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9
Q

What are the main hunger-promoting hormones from the arcuate nucleus of the hypothalamus?

A
Agouti-related peptide (AgRP)
Neuropeptide Y (NPY)
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10
Q

Where is leptin secreted from?

What are its main effects?

A

Secreted by adipocytes

Acts as the body’s marker of fat stores
An increase will stimulate melanocortin, which suppresses appetite

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11
Q

What is the main difference between Roux-en-Y and Sleeve gastrectomy in terms of weight loss mechanism?

A

Both are restrictive, but Roux-en-Y is also malabsorptive

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12
Q

What is the most effective treatment for morbid obesity?

A

Bariatric surgery

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13
Q

What is the proven most effective T2DM prevention strategy?

A

Intensive lifestyle program with diet and exercise

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14
Q

What are the effects of insulin on glucose utilisation, proteins and fats?

A

Glucose utilisation

  • Stimulates uptake of glucose by skeletal muscle and fat
  • Inhibits hepatic gluconeogenesis by decreasing free fatty acids to liver -> decreased gluconeogenesis

Fat

  • Promotes storage of triglycerides in adipose tissue
  • Inhibits lipolysis of stored triglycerides from adipose tissue

Protein
- Increases protein synthesis

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15
Q

What are incretins?

What is their function?

A

They are insulin secretagogues.

  • Amplification effect -> determines up to 70% of post-prandial insulin production
  • After meal, GLP1 / GIP peptide hormones bind to pancreas -> production of insulin
  • DPP4 cleaves GLP1, rendering it inactive
  • Incretin effect is impaired in DM
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16
Q

Which transporter in the kidney is responsible for up to 90% of PCT reabsorption of glucose?

A

SGLT2 - Sodium glucose co-transporter 2

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17
Q

Which hypoglycaemic agents promote weight loss?

A

Metformin

GLP-1 agonists

SGLT2 inhibitors

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18
Q

Which hypoglycaemic agent can improve BP?

A

SGLT2 inhibitors via weak diuretic affect

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19
Q

Which hypoglycaemic agents have shown to reduce CV death?

A

Empagliflozin

Liraglutide

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20
Q

What are the main auto-abs in T1DM? (4)

A

GAD
IA2
Insulin
ZnT8

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21
Q

What is the duration of action of Ryzodeg 70/30?

A

42 hours

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22
Q

What are 4 key advantages of insulin pumps over injections?

A

Reduced HbA1c
Reduced severe hypos
Improved QoL
May decrease mortality (CV and overall)

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23
Q

What is the role of RANK Ligand in bone?

A

Cytokine which is essential for development and survival of osteoclasts -> promotes bone resorption

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24
Q

Is bone mineral density a more sensitive or specific marker of fracture risk?

A

Specific

Low sensitivity

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25
Q

At what BMD range do most fractures occur?

A

Osteopenic range -> -1 -> -2.5

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26
Q

What is the biggest risk factor for fracture in osteoporosis?

A

Previous fracture

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27
Q

Which type of bone is most affected in steroid-induced OP?

A

Trabecular (cancellous)

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28
Q

What is the PBS criteria for bone health treatment in long-term steroid use?

A

> 7.5mg/day of prednisolone for over 3 months + T-score <1.5

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29
Q

What are the three ways in which PTH acts to increase serum calcium?

A
  1. Promotes formation of calcitriol in kidneys, which increases GIT absorption of Ca and Phos
  2. Mobilises calcium from bone by promoting resorption
  3. Increases renal calcium reabsorption
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30
Q

What is the best way to distinguish between factitious hypoglycaemia and insulinoma?

A

C-peptide level

- will be high in insulinoma

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31
Q

What diagnosis is consistent with diffusely increased uptake on Thyroid Uptake Scan?

A

Graves Disease

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32
Q

What are the indications for treating subclinical hypothyroidism? (3 definitive)

A

Treat if ->

- TSH >10
- Symptomatic 
- Pregnant (TSH >4)

Consider if:

- Age <65 
- Heart failure
- TPO / Tg ab positive 
- Dyslipidaemia
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33
Q

What are the indications for treating subclinical hyPERthyroidism? (5)

A

Treat if =

- TSH <0.1
- Symptoms 
- AF
- Heart failure
- Osteoporosis
34
Q

Why is there hyperpigmentation in primary adrenal insufficiency?

A

Due to increased production of proopiomelanocortin (POMC), a prohormone that is cleaved into the biologically active hormones -> ACTH, MSH, and others.

The elevated MSH results in increased melanin synthesis, causing hyperpigmentation.

35
Q

What is the most common cause of primary adrenal insufficiency?

What are the other common causes?

A

Autoimmune adrenalitis is responsible for 70 to 90%

Remainder =

  • infectious diseases
  • replacement by metastatic cancer or lymphoma
  • adrenal hemorrhage / infarction
  • drugs
36
Q

What are the tests to diagnosis primary adrenal insufficiency?

A

Early morning cortisol and ACTH

Short Synacthen to detect response to ACTH stimulation

Check plasma renin levels (will be elevated)

37
Q

When is ongoing mineralocorticoid replacement required in adrenal insufficiency?

A

In primary only
-> adrenal insufficiency secondary to hypopituitarism only requires glucocorticoid replacement; mineralocorticoid replacement is not required because the renin–angiotensin–aldosterone axis remains intact

38
Q

What should be done to the mineralocorticoid dosing for a patient with primary adrenal insufficiency who is acutely unwell?

A

Nothing ->

Acute adjustment of the mineralocorticoid dose is not required for stress or intercurrent illness.

39
Q

How is primary adrenal insufficiency treatment monitored?

What is the role of ACTH?

A

At each review, measure serum sodium and potassium and plasma renin concentrations.
Plasma renin concentration in the upper-normal reference range indicates optimal mineralocorticoid replacement.
Clinically, assess for features of glucocorticoid/mineralocorticoid excess/deficiency

ACTH does not correlate well with appropriateness of replacement, so is not used

40
Q

Acute treatment for adrenal crisis?

A

Hydrocortisone 100 mg intravenously, initially, then 50 mg intravenously, every 6 hours until stable and tolerating oral intake.

Hypovolaemia -> IV NaCl 0.9%
Correction of hypoglycaemia
Severe hyperkalaemia -> usually responds to IV fluids and hydrocortisone therapy —do not use intravenous insulin and glucose.

41
Q

What dose of prednisolone would be expected to lead to adrenocortical suppression?

A

Oral prednis(ol)one at a dose of 10 mg or more daily for more than 3 weeks

42
Q

What is the most common cause of adrenal dysfunction in children?

A

Congenital adrenal hyperplasia

43
Q

What enzyme is most commonly deficient in CAH?

What hormonal imbalances does this lead to?

A

21-hydroxylase

Leads to cortisol and aldosterone deficiency, with androgen excess

44
Q

What is the usual presentation of Nonclassical congenital adrenal hyperplasia?

What is it (usually) caused by?

A

Androgen excess without glucocorticoid deficiency.
Females -> hirsutism and menstrual irregularity; may be clinically indistinguishable from PCOS.
Can be asymptomatic
In men often very subtle, hard to pick up

Caused by a PARTIAL deficiency of the 21-hydroxylase enzyme, leading to androgen excess without symptoms of glucocorticoid deficiency

45
Q

Most common cause of hypopit in adults?

A

PItuitary adenoma

46
Q

Why can thyroxine not be commenced in hypopit until cortisol is corrected?

A

Levothyroxine increases the clearance of cortisol, and can precipitate adrenal crisis in a patient with low glucocorticoid reserve.

47
Q

In adults with growth hormone deficiency who can receive recombinant GH replacement, how is dose titrated / monitored?

A

Titrate the somatropin dose to achieve a plasma IGF-1 concentration in the middle of the age-adjusted reference range.

48
Q

What is the effect of oestrogen therapy on GH levels in GH deficiency?

A

Oral oestrogen decreases sensitivity to growth hormone, increasing the dose requirement if on replacement.

49
Q

How is diabetes insipidus diagnosed?

A

Water deprivation test -> measures response of plasma and urine osmolality to water deprivation. In DI, fluid restriction does not lead to appropriate concentrating of urine (which would appear as increased urine osmolality >600)

Differentiating between central and nephrogenic -> give desmopressin
- urine osmolality will increase in response to desmopressin if the patient has central diabetes insipidus, but not nephrogenic diabetes insipidus

50
Q

Management of central diabetes insipidus?

A

Drink to thirst

Oral Desmopressin, adjusted to electrolytes

51
Q

What is the difference between micro and macro prolactinoma?

A

Micro <10mm diameter

Macro >10mm

52
Q

What are 1st line treatment options for prolactinoma?

A

Dopamine agonists -

  • cabergoline
  • bromocriptine
53
Q

What is the management of prolactinoma during pregnancy?

A

Prolactinomas can enlarge in pregnancy
- risk depends on size of the prolactinoma before pregnancy.

Smaller masses -> stop dopamine agonist therapy when pregnancy is confirmed.
Monitor - assess the woman regularly throughout pregnancy for signs of prolactinoma enlargement (eg headache, visual disturbance).

Macro

  • Formal assessment of visual fields is recommended each trimester
  • MRI if the patient becomes symptomatic
  • If enlargement on MRI -> treatment with Bromocriptine

Large mass -> Consider surgical debulking before pregnancy.
Use bromocriptine pre-emptively

54
Q

What is the 1st line treatment for acromegaly?

A

Surgery -> Trans-sphenoidal microadenomectomy

55
Q

What is the 2nd line Rx for acromegaly, after surgery?

A

Somatostatin analogue

  • lanreotide
  • octreotide
  • Pasireotide if non-responsive to the 1st two options

Adjunct if required -> dopamine agonist

56
Q

What is Pegvisomant?

A

3rd line agent for acromegaly

GH receptor antagonist

PBS approved for refractory IGF-1 to somatostatin analogue

57
Q

Initial screening test for suspected primary aldosteronism?

A

Plasma aldosterone-to-renin ratio (elevated)

58
Q

Which anti-hypertensives do NOT interfere with plasma aldosterone-to-renin ratio, and can be taken by the patient when tested?

A

Diltiazem, verapamil
Prazosin
Hydralazine

59
Q

After initial screening, how is Conn’s dx confirmed?

A
  1. Aldosterone suppression test to confirm
    - Oral sodium load for 3 days OR IV NaCL load for 4 hours
    - Aldosterone should be suppressed <140
  2. Adrenal CT
    - Tumour on CT and aged <40 -> reliably the cause
    - May be incidentaloma in age >40
  3. Adrenal vein sampling -> To check for lateralisation
60
Q

What is the medical management of Conn’s?

A

MRA ->

  • Spironolactone
  • Eplerenone (less effective but better tolerated)
61
Q

Screening tests for Phaeo?

A

Plasma free metanephrines / normetanephrines

Urine total metanephrines

62
Q

In Phaeo, why must alpha-adrenergic blockade be established prior to treatment with beta blockade?

A

Unopposed alpha receptor–mediated vasoconstriction can cause an extreme rise in blood pressure

63
Q

Why is Phenoxybenzamine generally the preferred agent for alpha blockade in Phaeo?

A

Noncompetitive alpha-adrenergic blocker, so cannot be displaced from alpha receptors by a rise in concentration of endogenous catecholamines (unlike prazosin)

64
Q

What are three genetic syndromes commonly associated with Phaeo?

A

Von Hippel-Lindau (VHL) syndrome
MEN2
Neurofibromatosis type 1 (NF1)

65
Q

What percent of adrenal incidentalomas are functional?

A

20%

66
Q

What is the general algorithm for evaluation of adrenal incidentalomas?

A

Test for hormonal hypersecretion
- if present, consider surgery

If non-functional

  • assess risk based on imaging characteristics ->
  • > over 4cm
  • > over 10 Hounsfield units
  • > delayed CT contrast washout
  • if suspicious, consider surgery

If benign phenotype, monitor =

  • repeat imaging in 12 months
  • biochemical testing for 4-5 years
67
Q

What is the 1st line medical management of Cushing’s syndrome, used when surgical management is not appropriate or unsuccessful?

A

1st line -> ketoconazole (inhibits the first step in cortisol biosynthesis - side-chain cleavage - and, to a lesser extent, the conversion of 11-deoxycortisol to cortisol

2nd line -> add Metarypone (11-beta-hydroxylase inhibitor that blocks the final step in cortisol biosynthesis
or IV Etomidate (blocks 11-beta-hydroxylation of deoxycortisol to produce cortisol)

68
Q

What are the initial screening tests for Cushing’s syndrome?

A

24 hour urinary cortisol or late night salivary cortisol

69
Q

Which medication can be used to achieve medical adrenalectomy in Cushings?

A

Mitotane
= Adrenolytic -> binds to important macromolecules in the mitochondria, causing mitochondrial destruction and necrosis of adrenocortical cells
Used in high doses for adrenal carcinoma

70
Q

What are some contraindications to COCP? (8)

A
  • current or previous venous thromboembolism (VTE)
  • genetic thrombophilia
  • coronary artery disease
  • cerebrovascular disease
  • uncontrolled hypertension
  • severely impaired liver function
  • malignancy of the breast or genital tract
  • migraine with aura
71
Q

Biochemically, how can we tell if a menstrual cycle if ovulatory?

A

Serum progesterone concentration is >20 nmol/L during the midluteal phase (5-10 days prior to menses)

72
Q

For women taking HRT, when do you use cyclical and when do you use continuous?

A

Cyclical ->
- women still having spontaneous menses or LNMP under 2 years ago (may get withdrawal bleed on continuous)

Continuous
- 2 years post menopause

73
Q

What are some non-hormonal options for treating vasomotor symptoms of menopause?

A

Venlafaxine (SNRI)
Paroxetine (SSRI)
Gabapentin
Clonidine

74
Q

How is androgen deficiency diagnosed in men?

A

Must have both the following factors =

  1. Consistent symptoms and signs of androgen deficiency
  2. An unequivocally low early morning plasma testosterone concentration, confirmed by repeat measurement.
75
Q

What effect does obesity have on SHBG?

What effect does age have on SHBG?

A

Obesity decreases SHBG concentrations, thereby decreasing the serum total testosterone concentration

Aging increases SHBG

76
Q

Why should androgen levels not be evaluated in acute illness in men?

A

They are likely to have transient functional secondary hypogonadism

77
Q

How can non-classical CAH be differentiated from PCOS biochemically?

A

NCCAH -> very elevated 17-hydroxyprogesterone level when tested in early morning at follicular phase

Can then be confirmed with ACTH stimulation test -> The Response to ACTH is exaggerated in NCCAH

78
Q

What is the effect of licorice on

A

Inhibits enzyme ->

79
Q

Gene in polyglandular autoimmune syndrome Type 1?

Triad?

A

AIRE gene

Hypoparathyroidism
Chronic mucocutaneous candidiasis
Later -> adrenal insufficiency

80
Q

Common manifestations of polyglandular autoimmune syndrome Type 2?

A

Autoimmune thyroid disease
T1DM
Adrenal insufficiency