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RACP 2024 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What serology supports a diagnosis of type 1 diabetes?

A
  • low or undetectable c-peptide levels
  • anti-GAD5
  • insulin autoantibody
  • Anti-IA-2, anti-IA-2B (tyrosine phosphatases)
  • anti-ZnT8
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2
Q

What HLA types are strongly associated with Type 1 diabetes?

A

HLA-DR3
HLA-DR4

(HLA-DR2 = protective)

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3
Q

What is the most common autoimune disease associated with type 1 diabetes?

A

Autoimmune thyroid disease

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4
Q

What is the most common form of auotimmune polyendocrine syndrome?

A

Type 2 (polygeneic, Addison’s, Type 1 diabetes, chronic thyroiditis)

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5
Q

What are features of autoimmune polyendocrine syndrome type 1?

A
  • AR inheritance
  • AIRE gene on Chr 21
  • asplenism
  • commonly: canididaisis, hypoparathyroidism, Addisons
  • also associated with type 1 diabetes
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6
Q

What are features of autoimmune polyendocrine syndrome type 2?

A
  • polygeneic
  • addison’s disease, type 1 diabetes, chronic thyroiditis
  • female predominance
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7
Q

What processes are enhanced by insulin?

A
  • glucose uptake into muscle and adipose
  • glycolysis
  • glycogen synthesis
  • protein synthesis
  • K+ and phosphate uptake
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8
Q

What processes are inhibited by insulin?

A
  • gluconeogenesis
  • glycogenolysis
  • lipolysis
  • ketoneogenesis
  • proteolysis
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9
Q

What effects does insulin have on the liver?

A
  • inhibits glycogenolysis
  • inhibits ketoneogenesis
  • inhibits gluconeogenesis
  • promotoes glycogen synthesis
  • increases triglyceride synthesis and VLDL formation
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10
Q

What effects does insulin have on muscle cells?

A
  • promotes amino acid transport
  • increases ribosomal protein synthesis
  • promotes glucose transprt
  • induces glycogen synthesis
  • inhibits phosphorylase
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11
Q

What effects does insulin have adipose tissue?

A
  • induces lipoprotein liase to hydrolyze triglycerides in circulating lipoprotein to deliver fatty acids to adipocytes
  • promotes glucose transport into cell, allowing esterification of fatty acids
  • inhibits intracellular lipase
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12
Q

What are the benefits of insulin analogues over human insulin?

A
  • less hypoglycaemia
  • less weight gain
  • lower HbA1c
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13
Q

What is the typical starting dose of insulin for a type 1 diabetic?

A

0.5 units/kg/day
50% basal dose

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14
Q

What are the insulin carbohydrate ratio and insulin sensitivity factor?

A

Insulin carbohydrate ratio: how many grams of carb are covered by 1 unit of insulin

Insulin sensitivity factor: how much 1 unit of rapid acting insulin with lower a blood glucose over 2-4 hours

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15
Q

What is the effect of metformin in type 1 diabetes?

A
  • small reduction in weight and lipids
  • no effect on HbA1c
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16
Q

What is the target HbA1c in type 1 diabetes?

A

Individualised but typically 7% (53 mmol/mol)

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17
Q

What is the lag between interstitial and capillary glucose levels?

A

10 minutes

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18
Q

What is the diagnostic criteria of diabetic keotacidosis?

A
  • BSL > 11 or known diabetes
  • Ketones > 3.0 or 2+ ketonuria
  • venous pH < 7.3 or HCO3 < 15
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19
Q

What features identify severe DKA?

A
  • ketones > 6
  • pH < 7.2 or HCO3 < 5
  • K < 3.5
  • GCS < 12
  • Sats < 92%
  • SBP < 90
  • HR > 100 or < 60
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20
Q

What are the management principles of DKA?

A
  • correct hypovolaemia and dehydration with IV fluids
  • restore carbohydrate metabolism with IV insulin (+ Q1H BSL)
  • monitor and correct electrolyte deficiencies especially potassium
  • investigate and treat precipitant
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21
Q

What 8 factors contribute to the pathogenesis of type 2 diabetes?

A
  1. decreased insulin secretion
  2. Increased glucagon secretion
  3. Increased hepatic glucose production
  4. Neurotransmitter dysfunction
  5. Decreased glucose uptake by muscle
  6. Increased glucose reabsorption in kidney
  7. Increased lipolysis
  8. Decreased incretin effect in intestine
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22
Q

What are the complications fo diabetes?

A

Microvascular:
- retinopathy (non proliferative, pre proliferative and proliferative)
- Nephropathy
- Neuropathy (glove and stocking = distal symmetric neuropathy, multineuritis multiplex, autonomic)

Macrovascular:
- brain
- heart
-extremities

Autonomic:
- cardiovascular
- gastrointestinal
- sudomotor
- genitourinary

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23
Q

What are the definitions of microalbuminuria and clinical albuminuria?

A

microalbuminuria = 3-30 mg/mmol

clinical albuminuria = >3 mg/mmol

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24
Q

What is the lieftime risk of a diabetic developing a foot ulcer?

A

25% (15-34%)

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25
Q

What diabetes complications contribute to diabetic foot disease?

A
  • somatic sensory neuropathy
  • somatic motor neuropathy
  • autonomic neuropathy
  • peripheral artery disease
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26
Q

What are treatment options for type 2 diabetes?

A

1st line = diet + exercise
2nd line = metformin (biguanide)
3rd line:
- sulphonylurea (gliclazide, glipizide)
- DDP-IV inhibitors (vildagliptin)
- Alpha glucosidase inhibitors (acarbose)
- thiazolidinediones (Pioglitazone)
- SGLT2 inhibitors (empagliflozin)
- GLP-1 receptor agonists (dulaglutide)
- insulin

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27
Q

What is the mechanism of action of SGLT2i?

A

Impair the reabsorption of glucose in the proximal tubule of the kidneys

(SGLT2 is responsible for 90% glucose reabsorption)

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28
Q

What are the benefits of SGLT2i?

A
  • lower HbA1c
  • weight loss
  • lower BP
  • decrease MACE
  • decrease HF hospitalisations
  • reno protective
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29
Q

What are the risks of SGLT2i?

A

-GU infections
- DKA
- amputations
- fractures
- volume depletion
- AKI

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30
Q

What dose of SGLTi is associated with CV benefit?

A

10 mg for both empagliflozin and dapagliflozin

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31
Q

What eGFR must patients have before commencing SGLT2i?

A

Empagliflozin > 30
Dapagliflozin > 25

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32
Q

What is the mechanism of DKA with SGLT2i use?

A

Result in relative insulin deficiency due to lowering of plasma glucose, which results in increased action of glucagon

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33
Q

What is the mechansim of action of GLP1 receptor agonists?

A
  • increase insulin secretion (decrease glucagon)
  • increase glucose uptake in muscle and adipose
  • increase natriuresis of kidney
  • decrease appetite
  • delays gastric emptying
  • reduces gastric acid secretion
  • increase HR, contractility and decrease BP
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34
Q

What GLP-1 receptor agonists have demonstrated CV benefit?

A

Dulaglutide
Semaglutide

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35
Q

What are risks of GLP-1 receptor agonists?

A
  • acute pancreatitis
  • hypoglycaemia
  • accumulation in renal impairment (dulaglutide >15, semaglutide >30)
  • increase in HR
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36
Q

What endocrine factors contribute to PCOS?

A
  • abnormal pulsatile GnRH release
  • causes elevated LH and FSH levels
  • results in ovary dysfunction: hyperandrogenism and follicular arrest
  • insulin resistance
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37
Q

What is the Rotterdam criteria for the diagnosis of PCOS?

A

Any 2 of 3 features:
- hyperandrogensim ( clinical = acne, hair loss, hirsutism, biochemical = non diagnostic on hormonal contraception)
- ovulatory dysfunction (primary amenorrhoea or irregular cycles)
- polycystic ovaries (follicle number per ovary >20)

38
Q

What diagnoses need to be excluded to make a diagnosis of PCOS?

A
  • nonclassical congenital adrenal hyperplasia (17-OH-progesterone)
  • Androgen-secreting tumours (androgen profile)
  • Hyperprolactinaemia
  • thyroid disorders
  • drug induced androgen excess
  • syndromes of severe insulin resistance
  • Cushing syndrome
  • hypogonadotrophic hypogonadism
39
Q

What is the role of anti-mullerian hormone in the diagnosis of PCOS?

A

As an alternative to pelvic ultrasound where a diagnosis of PCOS is not otherwise met with the Rotterdam criteria

40
Q

How can hirsutism be treated in PCOS?

A
  • COCP = most effective, increases SHBG which binds free androgens
  • Androgen blockade = spirinolactone, cyproterone acetate
  • metformin
  • non pharmacological
41
Q

How can menstrual irregularities be treated in PCOS?

A
  • cocp
  • POP
  • mirena
  • cyclical progestin (aiming 4 bleeds/year for endometrial protection)
42
Q

How can infertility be treated in PCOS?

A
  • letrozole to promote ovulation
  • GnRH agonist with USS if fails to ovulate
  • IVF
43
Q

How should metabolic disease be treated in PCOS?

A
  • CVD risk assessment and management of risk factors as per guideline
  • screening for T2DM (OGTT)
  • weight management
  • smoking cessation
44
Q

What is the typical pattern of puberty in women?

A
  1. Thelarche = breast pudding
  2. Pubarche = pubic ahir
  3. Menarche = menstruation starts
45
Q

Amenorrhoea asscoiated with low oestrogen, low FSH and no hypothalamic-pituitary pathology is typically due to what cause?

A

Hypogonadotrophic hypogonadism

46
Q

Amennprrhoea presenting with normal oestrogen, normal FSH and normal prolactin is typically due to what cause?

A

PCOS

47
Q

Amenorrhoea presenting with low oestrogen and high FSH is typically due to what cause?

A

Gonadal failure

48
Q

What is the DICER1 syndrome?

A

AD associated with Sertoli-Leydig tumour of ovaries with androgenism and multi-nodular goitre

49
Q

What are clinical features of functional hypothalamic amenorrhoea?

A
  • stress, weight loss and excercise
  • low LH, FSH and oestrogen
50
Q

How is functional hypothalamic amenorrhoea treated?

A
  • lifestyle advice
  • CBT
  • oestrogen replacement
  • ovulation induction or IVF or IUI for pregnancy
51
Q

What are the anatomical relations to the pituitary gland?

A

-Located in sella turcica
-Has anterior and posterior lobes
-Anterior conntected to hypothalamus by hypothalamo-hypophyseal portal system (venous)
- posterior connected to hypothalamus by axons
- located above optic chiasm
- ICA and CN nuclei of III, IV, V1, V2, anf VI located laterally

52
Q

What is the best imaging modality for the pituitary?

A

MRI (T1 and T2)

53
Q

What size in a pituitary microadenoma?

A

< 1 cm

54
Q

What are the 6 hormones made by the hypothalamus?

A
  • CRH (ACTH)
  • TRH (TSH)
  • GnRH (LH, FSH)
  • GHRH (GH)
  • Somatostatin (inhibits GH)
  • Dopamine (inhibits Prolactin)
55
Q

What are the 6 hormones made by the anterior pituitary?

A
  • ACTH (adrenal, cortisol)
  • TSH (thyroid, fT4 and fT3)
  • LH (gonads)
  • FSH (gonads)
  • GH (liver, IGF-1)
  • prolactin (breast)
56
Q

What hormones are released by the posterior pituitary?

A

Oxytocin (contracts uterus, releases milk)
Vasopressin

57
Q

What hormone acts on V1 and V2 receptors and what effect do these have?

A

Vasopressin (AVP)

V1 = vasoconstriction

V2 = AQP2 insertion and water reabsorption collecting duct

58
Q

What hormone is typically lost first following pituitary irradiation?

A

Growth hormone

59
Q

What are clinical features of low ACTH?

A

Lethargy
Anorexia
Postural dizziness

60
Q

What are clinical features of low GH?

A

Increased fat mass
Reduced muscle mass
Reduced vitality
Poor quality of life
Social isolation

61
Q

How is ACTH deficiency diagnosed?

A
  • Low early morning cortisol with low/N ACTH
  • Failure to respond to short synacthen test (requires several weeks for adrenals to atrophy)
  • insulin tolerance test (gold standard) with failure of cortisol to rise
62
Q

What tests support a diagnosis of TSH deficiency?

A

Low fT4 and low/N TSH

63
Q

What tests support LH/FSH deficiency?

A
  • Man: low T, low/N LH and FSH
  • pre menopause: low oestradiol, low/N LH and FSH
  • post menopause: low/N LH and FSH (oestradiol already low)
64
Q

What tests support GH deficiency?

A
  • insulin tolerance test
  • glucagon stimulation test
    (both measure GH response to stimulation)
    (IGF-1 not sensitive)
65
Q

How is ACTH deficiency managed?

A

Replace with 10-20 mg hydrocortisone in 2-3 doses/day
(don’t need mineralocorticoid replacement)

66
Q

What is sick day plan for ACTH deficiency?

A
  • double or triple hydrocortisone
  • 100 mg subcut or IM if cant swallow
67
Q

How is TSH deficiency managed?

A

Thyroxine 1.6 microgram/kg/day, aiming fT4 to half normal upper range
(don’t use TSH to titrate as will always be low)

68
Q

How is FSH/LH deficiency treated?

A

Men: Testosterone 1g IM Q12weekly or 50 mg 1% transdermal OD

Woman: Transdermal oestrogen + progesterone

69
Q

How is GH deficiency treated?

A

Subcut GH nocte aiming IGF-1 in normal range

70
Q

What is the Copeptin stimulation test?

A

Test to diagnose AVP deficiency

Copeptin is cleaved from AVP precursor 1:1, should increase after hypertonic saline or arginine stimulation

71
Q

How is AVP deficiency treated?

A

Desmopressin = V2 selective

72
Q

What are the indications for treatment of non-functioning pituitary adenomas?

A

Visual loss
Features of mass effect

Typically transphenoidal hypophysectomy
Transcranial for large tumours

73
Q

What is the most common complication of pituitary radiotherapy?

A

Hypopituitarism

74
Q

What are complications of acromegaly?

A

Hypertension
Diabetes
OSA
Cardiomyopathy
Colonic polyps/cancer
Carpal tunnel syndrome
Arthritis

75
Q

What is the most common secretory pituitary adenoma?

A

Prolactinoma

76
Q

How is acromegaly diagnosed?

A
  • IGF-1
  • 75g OGTT (GH fails to suppress)
  • MRI pituitary
77
Q

How is acromegaly treated?

A

1st line = transsphenoidal surgery
2nd line = somatostain analogue targeting SST2 (octreotide, lanreotide Q28 days)

3rd line:
- carbegoline if co-secretes prolactin
- pasireotide (SST5, causes hyperglycaemia)
- pegvisomant (GH receptor antagonist, no effect on adenoma)
- radiotherapy

78
Q

What is macroprolactin and how can it be differentiated from true hyperprolactinaemia?

A

Macroprolactin = Ig that binds prolactin and makes it inactive, results in raised levels on measurement

If add polythethylene glycol will bind large complex and only measure free prolactin

79
Q

How can adenoma size help assess for prolactinoma vs stalk compression?

A

Stalk compression = macroadenoma with prolactin 2-5x ULN

Macroprolactinoma = macroadenoma + prolactin 10x ULN

Microprolactinoma = microadenoam with prolactin 2-5x ULN

80
Q

How are prolactinomas treated?

A

1st line Dopamine agonists:
- bromocripitne (D1 + D2)
- cabergoline (D2)

2nd line = transsphenoidal hypophysectomy

3rd line = radiotherapy

81
Q

What are side effects of dopamine agonists used to treat prolactinomas?

A
  • acute: nausea, postural hypotension
  • impulse control disorders
  • cardio valvulopathy (only high dose cabergoline due to 5HT3 receptors)
82
Q

What proprotion of Cushing syndrome is due to pituitary adenoma?

A

70%
(adrenal 20%)

83
Q

What are clinical features of Cushing syndrome?

A

Central adiposity
Moon facies
Buffalo hump
Supraclavicular fullness
Thin skin
Proximal muscle weakness
Facial plethora
Violaceous striae

84
Q

What are complications of Cushing’s syndrome?

A

Hypertension
Diabetes
VTE
Osteoporosis
Fungal infections
Mood change
IHD

85
Q

How is Cushing syndrome diagnosed?

A

Dexamethasone suppression test
OR late night salivary cortisol
OR 24h urinary free cortisol

ACTH level
CT adrenals if ACTH low

If ACTH level normal/high:
- MRI pituitary
- high dose (8 mg) dexamethasone suppression test if macroadenoma
- inferior petrosal sampling if micro or no adenoma
- CT CAP or gadolinium PET if above consistent with ectopic

86
Q

What result on inferior petrosal sinus sampling indicates a pituitary source for Cushing’s syndrome?

A

Central to peripheral ACTH ration >3 post CRH

87
Q

How is Pituitary Cushing’s treated?

A

1st line = transsphenoidal surgery

88
Q

How does thyroid hormone resistance present and what is it’s cause?

A

Hyperthyroidism or hypothyroidism

Mutation in thyroid hormone receptor beta, need higher fT3 to switch off TSH production

89
Q

How are TSHoma diagnosed and treated?

A

High T4,T3 with High/N TSH
+/- macroadenoma on MRI
Raised SHBG

1st line = transsphenoidal surgery
2nd line = octreotide

90
Q

What is the main differential diagnoses for post partum hypopituitarism?

A
  • Sheehan syndrome
  • lymphocytic hyophysitis (homogenous mass on MRI with thickened stalk)
91
Q
A

RACP 2024 (15 decks)

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