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FRACP Shuyu > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

How reproducible is the OGTT

A

65%

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2
Q

How often to have HbA1Cs for

1) diagnosis
2) monitoring

A

MBS rebats:

1) every 12 months for diagnosis
2) 4 times/year for established diabetes

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3
Q

Factors that alter HbA1C

A

1) erythropoiesis: lower erythropoiesis = increased HbA1C and increased erythropoiesis (e.g. EPO administration) = decreased HbA1C
2) Altered Hb - haemoglobinopathies
3) Glycation - ETOH, CKD increased HbA1C, aspirin, vit C decreased HbA1C
4) Erythrocyte destruction - splenectomies increase HbA1C, things that decrease erythrocyte lifespans (splenomegaly) decrease HbA1C
5) Things that affect the assay: Bilirubin, triglycerides

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4
Q

What’s Whipple’s Triad

A

3 clinic criteria that suggests the non diabetic patient’s symptoms may result from an insulinoma.

1) Symptoms known or likely to be caused by hypoglycemia especially after fasting or heavy exercise
2) A low plasma glucose measured at the time of the symptoms
3) Relief of symptoms when the glucose level is raised

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5
Q

What investigations to do for hypoglycaemia in a non diabetic?

A

Insulin

C-peptide

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6
Q

What is C-peptide

A

A byproduct of insulin production. It is a good marker of insulin production.

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7
Q

When to avoid contrast in thyroid disease

A

Multinodular goitre, suppressed TSH, thyrotoxicosis history

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8
Q

What is C-peptide

A

A byproduct of insulin production. It is a good marker of insulin production.

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9
Q

When to avoid contrast in thyroid disease

A

Multinodular goitre, suppressed TSH, thyrotoxicosis history

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10
Q

1st investigation after finding a thyroid nodule clinically

A

TSH

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11
Q

Thyroid nodule and TSH not suppressed

A

Fine-needle aspiration biopsy

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12
Q

Are malignant thyroid nodules taller or wider

A

taller

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13
Q

Adrenal incidentoloma <10 HFU and <4cm

A 
Check functional status
– ARR
– 24h Urinary Catecholamines
– 1 mg Dexamethasone suppression test
• Repeat adrenal CT scan in 6 months
• Then annual CT scans for 1-2 years
• Hormone re-evaluation annually for 5 years
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14
Q

Antihypertensives that do not affect ARR

A

verapamil, prazosin, hydralazine, moxonidine

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15
Q

Antihypertensives that do not affect ARR

A

verapamil, prazosin, hydralazine, moxonidine

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16
Q

What effects would ACE I have on renin?

A

Increase renin

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17
Q

What effects would ACE I have on renin?

A

Increase renin

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18
Q

How frequently to monitor for pituitary microadenomas (<1cm)

A

Re-scan in 12 months; annual scans for 3 years

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19
Q

Next investigation for androgen deficiency

A

LH/FSH

To work out if it’s a testicular (high LH/FSH) or hypothalamo-pituitary (low LH/FSH)

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20
Q

What does prolactinomas do to androgen levels?

A

It suppresses LH and FSH and hence suppresses androgen production

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21
Q

Criteria for striae that discriminates Cushings syndrome from the normal population

A

Reddish purple and 1cm wide

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22
Q

Screening test positive for Cushing’s Syndrome - what next

A

ACTH - to see if the hypercortisolism is ACTH dependent or not
ACTH independent suggests adrenal source

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23
Q

Cushing’s Syndrome + high ACTH - what next

A

High dose dexamethasone suppression tests - suppresses cortisol in Cushing’s Disease patients (temporarily) but not ectopic ACTH producing tumours
OR
Bilateral inferior petrosal sinus sampling - ratio of central to peripheral ACTH of more than 2 in the basal state or more than 3 after CRH stimulation is consistent with Cushing’s disease

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24
Q

DKA criteria

A

Hyperglycaemia (serum glucose >14)
Ketosis
pH <7.3 (bicarb <20 mmol/l)

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25
Q

HHS criteria

A

Hyperglycaemia (serum glucose >30 mmol/l)
Minimal ketosis
Serum osmol>320 mOsm/kg

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26
Q

What medication can result in euglycaemic DKA

A

SGLT2 inihibitor (gliflozin)

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27
Q

HHS mortality compared with DKA

A

3x higher

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28
Q

Most common precipitant of DKA

A

Infection

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29
Q

DKA fluid loss

A

3-6L

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30
Q

HHS fluid loss

A

8-10L

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31
Q

Insulin infusion rate for DKA

A

0.1units/kg/hr until BGL <11.1 then swap to IV dextrose and halve insulin infusion rate

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32
Q

Insulin infusion rate for HHS

A

0.5units/kg/hr until BGL <15 then half insulin infusion rate

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33
Q

Indication for bicarbonate in DKA

A

Low level evidence, may be used in severe DKA pH <7

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34
Q

How long should IV insulin infusion and SC insulin overlap for

A

2 hours

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35
Q

What is ketosis-prone diabetes

A

Also called flatbush diabetes. Common in African ethnicity. A clinical spectrum of patients who develop DKA but does not fit the phenotype of T1DM. They are thought to be diabetes autoantibody negative and have severe insulin resistance +/- reversible beta-cell dysfunction.
These patient can get recovery in their insulin production and do not necessarily remain insulin-dependent. However, they should still be discharged on insulin therapy to be monitored.

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36
Q

What OHG needs to be withheld before the day of surgery

A

SGLT2 inhibitors due to the risk of DKA (at least 2 days, and USA guidelines state 3 days prior surgery).
Metformin needs to be withheld for 24 hours before major surgery

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37
Q

Plan for insulin day prior to surgery

A

Give usual insulin dose day before surgery including nocte basal insulin

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38
Q

Where does SGLT2 inhibitors act

A

They decrease glucose reabsorption in the proximal tubule independent of insulin - leading to glycosuria

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39
Q

Pathophysiology of euglycaemic DKA

A

Reduction in plasma glucose leads to reduction in plasma insulin levels and risk in plasma glucagon.
The lower insulin:glucagon ratio stimulates lipolysis and enhanced lipid oxidation which results in mild ketogenesis. This becomes more pronounced in a lack of carbohydrate availability and the mild ketosis and evolve into ketoacidosis

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40
Q

Mechanism of action if DPPIV inhibitors (gliptins)

A

They inhibit the DPP4 enzyme which inactivates GLP1 and GIP. GLP1 increases glucose uptake by peripheral tissues and decrease hepatic glucose production.

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41
Q

DPPIV adverse effect compared with sulfonylurea

A

DPPIV have no hypoglycaemia because it only stimulates insulin during meals instead of all the time like sulfonylurea. It also causes weight loss instead of weight gain. However, there is no mortality benefit. It is non inferior to sulfonylurea

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42
Q

Mechanism of GLP-1 analogues

A

Insulin sparing agents (use in conjunction with insulin).
E.g. exenatide, dulaglutide, liraglutide
GLP1 increases glucose uptake by peripheral tissues and decrease hepatic glucose production. It also stimulates beta pancreatic cells to produce more insulin

Assoc w weight loss and risk of hypoglycaemia is low

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43
Q

HbA1C targets in pregnancy

A

<6.0

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44
Q

What is foundational therapy in T2DM

A

Metformin

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45
Q

What OHG to avoid in heart failure and T2DM

A

Thiazolidinediones “-glitazone”

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46
Q

Second line in T2DM without cardiovascular disease or weight loss or hypoglycaemia issues

A

sulfonyureas, thiazolidinediones

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47
Q

Polycystic ovary syndrome clinical features

A

hyperandrogenism (clinical, biochemical, or both), ovulatory dysfunction, and polycystic ovarian morphologic features.

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48
Q

FSH, LH, estrogen and testosterone findings in PCOS

A

High LH
Low FSH
Excessive androgen

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49
Q

Biochemical findings that suggest primary ovarian failure

A

Low or normal E2 that is associated with an elevated FSH indicates POI, while low or normal E2 associated with FSH that is normal or low suggests the possibility of secondary (pituitary or hypothalamic) hypogonadism, either structural or functional

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50
Q

What happens to prolactin secretion in pituitary stalk resection?

A

Increased prolactin production because the predominant central control mechanism is inhibitory (Via D2 receptors)

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51
Q

What hormones are produced by the anterior pituitary

A 
Growth hormone
Prolactin
ACTH
TSH
Gonadotropins - FSH and LH
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52
Q

What are the actions of FSH and LH in women and men

A

In women, FSH regulates ovarian follicle development and stimulates ovarian estrogen production. LH mediates ovulation and maintenance of the corpus luteum. In men, LH induces Leydig cell testosterone synthesis and secretion, and FSH stimulates seminiferous tubule development and regulates spermatogenesis.

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53
Q

Amenorrhea/oligomenorrhea, normal uterus outflow tract and negative beta HCG and high FSH

A

Ovarian insufficiency

FSH is a better marker of ovarian failure because of loss of negative feedback effects of both estradiol and the inhibins and because its levels are less variable than those of LH.

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54
Q

Amenorrhea/oligomenorrhea, normal uterus outflow tract and negative beta HCG and low FSH

What to test next and what are the possibilities

A

Test Prolactin next

Ddx: neuroanatomic abnormalities or idiopathic hypogonadotropic hypogonadism

or hypothalamic amenorrhea

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55
Q

Treatment of symptomatic hyperthyroidism during pregnancy

A

Diagnosis within the first trimester should take PTU.
Diagnosis after the first trimester should take carbimazole.

Beta blockers can be used in the short term

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56
Q

What are the actions of FSH and LH in women and men

A

In women, FSH regulates ovarian follicle development and stimulates ovarian estrogen production. LH mediates ovulation and maintenance of the corpus luteum. In men, LH induces Leydig cell testosterone synthesis and secretion, and FSH stimulates seminiferous tubule development and regulates spermatogenesis.

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57
Q

Amenorrhea/oligomenorrhea, normal uterus outflow tract and negative beta HCG and high FSH

A

Ovarian insufficiency

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58
Q

Adverse effects of PTU and carbimazole

A

Minor AEs: pruritus, rash, urticaria, arthralgias, arthritis, fever, abnormal taste sensation, nausea, or vomiting in up to 13 percent of patients

Major AEs: Agranulocytosis, hepatotoxicity (PTU more), ANCA positive vasculitis

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59
Q

Treatment of symptomatic hyperthyroidism during pregnancy

A

Diagnosis within the first trimester should take PTU.
Diagnosis after the first trimester should take carbimazole.

Beta blockers can be used in the short term

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60
Q

What are the 2 most common causes of hyperthyroidism during pregnancy

A

Graves and hCG-mediated hyperthyroidism

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61
Q

Mechanism of action of PTU vs carbimazole

A

They are both thionamide compounds that PTU inhibits the 5’-monodeiodinase that converts thyroxine (T4) to triiodothyronine (T3) in extrathyroidal tissue. They are actively transported into the thyroid gland where they inhibit both the organification of iodine to tyrosine residues in thyroglobulin and the coupling of iodotyrosines

Carbimazole has longer half life, has higher intrathyroid concentrations

62
Q

Treatment of primary adrenal insufficiency and acute illness

A

Increase their normal glucocorticoid dose 3 fold.

Do not require mineralcorticoid because high doses of glucocorticoid has mineralcorticoid receptor effects.

63
Q

What type of medication is biguanides and what are the side effects

A

Metformin
MOA - inhibiting gluconeogenesis, increases insulin-mediated glucose utilization in peripheral tissues (such as muscle and liver), particularly after meals, and has an antilipolytic effect that lowers serum free fatty acid concentrations, thereby reducing substrate availability for gluconeogenesis

Side effect profile: weight loss, maybe improved CVS profile
GI effects (metallic taste in mouth, mild anorexia, nausea, diarrhoea), B12 deficiency (usually not severe), lactic acidosis
64
Q

Difference in clinical manifestations of primary adrenal insufficiency (Addison’s) and secondary adrenal insufficiency

A

Addison’s - loss of both glucocorticoid and mineralocorticoid secretion

Secondary - only glucocorticoid deficiency is present, as the adrenal itself is intact and thus still amenable to regulation by the RAA system.

Adrenal androgen secretion is disrupted in both primary and secondary adrenal insufficiency

65
Q

MOA of sulfonylureas and side effect profile

A

E.g. glicazide

Sulfonylureas bind to the sulfonylurea receptor on the K-ATP channel in the beta pancreatic cells and inhibits them, leading to calcium influx and release of insulin.

Good effects:
Glycemic efficacy — Sulfonylureas usually lower blood glucose concentrations by approximately 20 percent and glycated hemoglobin (A1C) by 1 to 2 percent

Side effects:

  • Hypoglycaemia
  • Weight gain
  • ?negative cardiovascular effects
  • CKD may increase risk of hypoglycaemia
66
Q

Treatment of primary adrenal insufficiency and illness

A

Increase their normal glucocorticoid dose 3 fold.

Do not require mineralcorticoid because high doses of glucocorticoid has mineralcorticoid receptor effects.

67
Q

What type of medication is biguanides and what are the side effects

A

Metformin
MOA - inhibiting gluconeogenesis, increases insulin-mediated glucose utilization in peripheral tissues (such as muscle and liver), particularly after meals, and has an antilipolytic effect that lowers serum free fatty acid concentrations, thereby reducing substrate availability for gluconeogenesis

Side effect profile: weight loss, maybe improved CVS profile
GI effects (metallic taste in mouth, mild anorexia, nausea, diarrhoea), B12 deficiency (usually not severe), lactic acidosis
68
Q

What are anabolic (build up bone) drugs used in osteoporosis

A

full-length parathyroid hormone (PTH 1-84) or its N-terminal fragment, teriparatide (PTH 1-34)

69
Q

MOA of sulfonylureas and side effect profile

A

E.g. glicazide

Sulfonylureas bind to the sulfonylurea receptor on the K-ATP channel in the beta pancreatic cells and inhibits them, leading to calcium influx and release of insulin.

Good effects:
Glycemic efficacy — Sulfonylureas usually lower blood glucose concentrations by approximately 20 percent and glycated hemoglobin (A1C) by 1 to 2 percent

Side effects:

  • Hypoglycaemia
  • Weight gain
  • ?negative cardiovascular effects
  • CKD may increase risk of hypoglycaemia
70
Q

MOA of thiazolidinediones and side effect profile

A

e.g. glitazone

MOA: increase insulin sensitivity by acting on adipose, muscle, and liver to increase glucose utilization and decrease glucose production

Effects:

  • Increased risk of heart failure, weight gain, fluid retention and fractures
  • NOT likely to cause hypoglycaemia
  • Cause weight gain
71
Q

Other non glycaemic effects of SGLT2 inhibitors

A

Decrease BP and weight.

Do not cause hypoglycaemia as the glucose lowering effect is independent of insulin

72
Q

denosumab MOA

A

Prevents RANKL binding to RANK and prevents osteoclast differentiation and activity

73
Q

amiodarone induced thyrotoxicosis types and treatments

A

Type 1 - iodine induced hyperthyroidism
- normally has underlying predisposition: toxic nodules/Graves’ disease; treat with thionamide

Type 2 - inflammatory/destructive thyroiditis
- treat with glucocorticoids

74
Q

What conditions does not respond to carbimazole

A

subacute viral thyroidisitis

type 2 inflammatory amiodarone inducd thyrotoxicosis

75
Q

wolff chaikoff effect

A

protective mechanism
Iodine excess -> reduced expression of Na-iodide symporter and inhibition of H2O2 generation

-> escape to Jod-Basedow phenomenon

76
Q

Amiodarone TFT pattern

A

early phase - mild TSH rise

prolonged therapy - TSH normalises, tend to low TSH, free T4 normal-high, normal T3

77
Q

Amiodarone induced hypothyroidism treatment

A

levothyroxine and mostly does not need to cease amiodarone

78
Q

differentiating between amiodarone induced thyroiditis type 1 vs type 1

A

thyroid U/S with colour flow doppler sonography: reduced/absent vascularity in type 2

AIT that develops quickly after commencement of amiodarone is more likely to be type 1
AIT that develops after drug cessation is more likely to be type 2

free T4 may be disproportionally higher in type 2 due to massive release of preformed thyroid hormone

79
Q

Risk factor for developing graves’ opthalmopathy

A 
smoking
thyroid peroxidase antibodies have no bearing on the develpment of graves opthalmopathy
pre-tibial myxedema
duration of graves
TSH receptor Ab titre
Advancing age
80
Q

what is thyroid bruit specific for

A

Graves (not multinodular goitre)

81
Q

what are the specific signs for graves opthalmopathy

A

proptosis, periorbital oedema, conjunctival oedema, opthalmoplegia

where as lid retraction is due to increased sympathetic system

82
Q

thyroiditis on thyroid uptake scan

A

no uptake

iodine induced thyrotoxicosis also has no uptake

83
Q

what will give diffusely decreased technetium 99m pertechnetate uptake

A

hasimoto’s iodinated contrast, excess iodine, amiodarone, subacute thyroiditis, painless thyroiditis, tactitious thyrotoxicosis, struma ovarii, hyperfunctioning thyroid cancer mets

84
Q

painful thyroiditis

A

subacute/de Quervain’s thyroiditis
- post viral (usually URTI)

infections/supprative thyroiditis

  • systemically unwell
  • TFTs usually normal
  • USS +/- aspiration
85
Q

painless thyroiditis

A

Hashimoto’s thyroiditis/lymphocytic thyroiditis

Postpartum thyroiditis

  • normally within 3 months but up to 1 year
  • increased risk with higher TPO Ab titre

Drugs
- Amiodarone, lithium, check point inhibitors, TKIs, IFN-alpha

86
Q

when is pregnancy thyrotoxicosis

A

up to 16 weeks

87
Q

what is associated with gestational thyrotoxicosis

A

hyperemesis gravidarum

88
Q

heterophile antibodies in thyroid disease

A

assay interference in relation to antibodies

usually assos with TSH rise

89
Q

clinically picture of TSHoma and TRH

A

mild sx of hyperthyroidism
goitres mostly present
normal TSH
high T4

90
Q

what is the MOA of potassium iodide

A

prevents release of pre-formed thyroid effect

91
Q

what kind of calcification in thyroid lesions are concerning

A

microcalcification

macrocalcification is not concerning

92
Q

what HLA allele is most associated with T1DM

A

DR3 and DR4 (in combination)

93
Q

Treatment target for T1DM - general population (HbA1C)

A

<7.0

94
Q

Treatment target for T1DM pregnancy or planning pregnancy (HbA1C)

A

<7.0

95
Q

Treatment target for T1DM recurrent severe hypoglycaemia or hypoglycaemia unawareness

A

<8.0

96
Q

which OHG has shown efficacy in T1DM for glycaemic control

A

SGLT2

97
Q

in what population does calcium and vitamin D have the greatest effect for primary prevention of fractures?

A

institutionalised elderly - no effect in free living individuals

98
Q

what are the 3 main actions of the parathyroid hormone

A
  1. Increased bone resorption (osteoclast breakdown), which occurs within minutes after PTH secretion increases.
  2. Increased intestinal calcium absorption mediated by increased production of calcitriol, the most active form of vitamin D, which occurs days after PTH secretion increases.
  3. Decreased urinary calcium excretion due to stimulation of calcium reabsorption in the distal tubule, which occurs within minutes after PTH secretion increases
99
Q

Where is bone density loss the greatest in primary hyperparathyroidism

A

vertebra > femoral > radius

100
Q

Management of inoperable PHPT

A
  1. Oestrogens
  2. SERMs
  3. Alendronate
  4. Cinacalcet (calcimimetics) - only reduces serum Ca and PTH levels for up to 12 months, No effect on BMD
101
Q

what antipsychotic gives a picture of hyperparathyroidism

A

lithium

102
Q

hypercalcaemia with low urinary calcium diagnosis w family hx of same

A

Familial hypocalciuric hypercalcemia - mutation in the calcium sensing receptor; autosomal dominant inheritance

103
Q

hypocalcaemia with high urinary calcium w family hx of same

A

autosomal dominant hypocalcaemia; treat with calcitriol

104
Q

biochemical findings of osteomalacia

A

If due to vit D deficiency:

  • high ALP (increased osteoblastic activity)
  • low vit D
  • low/normal calcium
  • secondary hyperparathyroidism
  • low phosphate
105
Q

renal phosphate wasting and increased fibroblast growth factor 23

A

tumour induced osteomalasia and hypophosphataemia

benign mesenchymal tumour

106
Q

which arcuate nucleus nerves make you hungry and suppresses hunger

A

NPY - want to eat

CART - suppresses hunger

107
Q

What is P1NP in osteoporosis

A

a marker of bone formation

synthesised by osteoblasts

108
Q

what is the most potent bisphosphonate available?

A

zoledronic acid

109
Q

how long should bisphosphonates be

A 
high risk (low hip T-score, hx fracture) - continuation of treatment for up to 10 years oral and 6 years IV
non-high risk - 3-5 years and a drug holiday of 2-3 years can be considered
110
Q

what population has the greatest incidence of osteonecrosis of the jaw?

A

oncology patients as the frequency of bisphosphonates is much higher
only 0.001% in the osteoporosis patient population

111
Q

what is the PBS criteria for teriparatide?

A

BMD T score <3.0
2 or more fractures due to minimal trauma
At least 1 new symptomatic fracture after at least 1 months of continuous treatment with antiresorptive therapy at adequate doses

112
Q

MOA denosumab

A

mAb to RANK-ligant - an osteoclast differentiating factor

113
Q

the cessation of which anti-resorptive therapy would increase the risk of rebound fractures significantly?

A

denosumab - bisphosphantes shoudl be considered to prevent or reduce the rebound increase in bone turnover

114
Q

BP target in diabetes

A

<140/90

115
Q

at what age should statins be implemented for all diabetic patients?

A

> 40 yr

116
Q

next step to lower LDL after statin

A

ezetimibe

117
Q

the effect of intensive glycaemic control in type 2 diabetes on macrovascular, microvascular and mortality

A
  • no significant effect on macrovascular
  • decreases microvascular events
  • increases mortality
118
Q

what is the best marker/index of diabetic kidney disease progression

A

GFR

albuminemia is non specific

119
Q

why is there an initial drop in eGFR when starting SGLT2 inihibitors

A

increased tone of afferent arteriole and decreased intragomerular pressure

120
Q

screening of diabetic kidney disease in T2DM

A

Yearly from diagnosis (ACR + eGFR)

121
Q

Diagnosis of acromegaly

A
  1. IGF-1
  2. OGTT for GH suppression if IGF-1 equivocal
  3. Pituitary MRI to differentiate between pituitary and extra-pituitary acromegaly
122
Q

Acromegaly treatment

A
  1. Resection - selective trans-sphenoidal microadenomectomy vs total hypophysectomy +/- radiotherapy
  2. Medical - somatostatin analogue therapy (octreotide, pasireotide); possible role for adjunctive dopaminergic drug, GH receptor antagonist 3rd line (pegvisomant)
123
Q

How does manifest ectopic ACTH present differently from Cushing’s disease?

A

Pigmentation
Hypokalaemia
Very high cortisol and ACTH
Severe myopathy

(Occult ectopic ACTH may closely resemble Cushing’s disease)

124
Q

Treatment of Cushing’s disease

A
  1. Resection/irradiation of pituitary/bilateral adrenals
  2. Medical preparation pre-operatively: metyrapone, ketoconazole, mifepristone
  3. Medical treatment if failed other therapy - pasireotide
125
Q

What is Carney complex?

A

Autosomal dominant condition with PRKAR1A mutations (tumour suppressor gene)

Presents with hyperpigmented skin and endocrine excess

126
Q

Which test for Cushing’s syndrome is not accurate in woman on oral oestrogen

A

dexamethasone suppression test because of increased corticosteroid-binding globulin

127
Q

How to classify micro vs macroprolactinoma

A

Macro = >1cm

128
Q

Management of prolactinomas - micro and macro

A
  1. Micro = dopaminergic agent (bromocriptine, cabergolin)

2. Macro = medication +/- surgery with adjunctive radiotherapy

129
Q

Pathology in central diabetes insipidus

A

Hypothalamic damage

Vasopressin/ADH deficiency

130
Q

How to differentiate between central and nephrogenic diabetes insipidus

A

central responds to Pitressin or DDVAP

131
Q

Management of hyperkalaemia in adrenal failure

A

IV calcium gluconate or bicarbonate. NOT insulin/glucose or resonium

132
Q

Management of primary hyperaldosteronism and unilateral adrenal tumour on CT

A

<40 yr - adrenalectomy

>40 yr - adrenal vein sampling -> if lateralisation then medical prep with spironolactone and adrenalectomy

133
Q

Management of Graves’ disease

A

Based on patient preference
Low risk can have antithyroid drugs (<40, small goitres, low titre TRABs, during pregnancy)
Older patients/high risk have a higher risk of relapse and should consider ablative therapy

I131 may exacerbate opthalmopathy
Surgery is good for obstructive goitre

134
Q

Management of multinodular goitre/toxic adenoma

A

Both should get ablative therapy intead of thionamide therapy as remission is unlikely.

Toxic adenoma is particularly suited to I131
MNG can have either depending on seizure of goitre, obstructive symptoms or suspicion of malignancy

135
Q

Indications for treatment of subclinical hyperthyroidism

A

TSH <0.1mL
Osteoporosis/heart disease
>65 years
MNG

136
Q

Management of thyroid storm

A 
HDU/ICU
Propanolol
PTU (lowers T3 levels quicker)
Steroids
Cholestyramine
PLEX
137
Q

When to treat subclinical hypothyroidism

A

TSH >10
Treat if pregnant or contemplating pregnancy
Goitre, hyperlipidaemia, depression

138
Q

Treatment of subacute thyroiditis

A

NSAIDS +/- prednisolone
BBlocker for symptoms
Thionamides ineffective

139
Q

Is hyperechoeic or hypoechoic worse prognosis for thyroid nodules?

A

Hypoechoic

140
Q

Which thyroid nodules to FNA?

A

Non-hot nodules on Tc99m uptake scan
>2cm and not cyst
1-2 cm based on TI-RADS 3-5

<1cm repeat evaluation in 6-12 months

141
Q

What thyroid cancers may be amendable to a partial thyroidectomy?

A

<4cm young patients with no adverse features

142
Q

General management of thyroid cancer

A
  1. Total thyroidectomy
  2. Remnant ablation with I131
  3. Surveillance with thyroglobulin measurement
  4. Stimulated thyroglobulin
  5. Whole body iodine scans
    Neck US
  6. TKI therapy for non-iodine avid recurrent and progressive disease
143
Q

What cancer is PCOS associated with?

A

Endometrial carcinoma

144
Q

Treatment of infertility in PCOS

A
  1. Lifestyle modificaiton (weight loss)
  2. Letrozole (aromatase inhibitor)
  3. Clomiphene
  4. Metformin
  5. Gonadotrophin therapy
  6. IVF
145
Q

What to exclude in patient with hyperandrogenism and virilization?

A

Androgen secreting tumour

146
Q

Cutaneous manifestations of Turner syndrome

A 
Small fingernails
Brown spots (nevi)
147
Q

Cardiac manifestations of Turner Syndrome

A 
Coarctation of aorta
Bicuspid aortic valve
Mitral valve prolapse
IHD
Dissection
ECHO every 3-5 years
148
Q

What condition is FMR1 mutation implicated in?

A

Fragile X

149
Q

Most likely cause of Cushing’s syndrome in ACTH dependent Cushing’s syndrome with normal MRI scan of the pituitary fossa

A

still pituitary tumour that’s small and not seen on MRI

150
Q

What dietary intake is associated with hypokalaemia in primary hyperaldosteronism

A

high salt intake

FRACP Shuyu (65 decks)

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