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1
Q

How often is HbA1c checked?

A

Every 3-6 months until stable

Then 6 monthly

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2
Q

What are the target HbA1cs?

A

Lifestyle: <48mmol
Lifestyle + metformin: <48mmol
Otherwise: <53mmol

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3
Q

What is the metformin pathway of T2DM management?

A
  1. Metformin
  2. Metformin + gliptin/sulfonylurea/pioglitazone/SGLT2 inhibitor
  3. 3 of the above OR insulin
  4. Metformin + sulphonylurea + GLP-1 mimetic
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4
Q

What is the HbA1c threshold for adding another hypoglycaemic agent?

A

58mmol

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5
Q

What is the level of HbA1c dependent on?

A

Red blood cell lifespan

Average blood glucose concentration

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6
Q

Which conditions mean HbA1c is lower than expected?

A

Sickle cell
G6PD deficiency
Hereditary sphreocytosis

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7
Q

Which conditions mean HbA1c is higher than expected?

A

Vit B12/folic acid def
IDA
Splenectomy

(increased RBC lifespan)

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8
Q

How do you calculate the average plasma glucose from HbA1c?

A

2x HbA1c - 4.5

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9
Q

What is T2DM is a symptomatic patient?

A

Fasting glucose >7mmol

Random or post OGTT >11.1

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10
Q

What is T2DM in an asymptomatic patient?

A

FG>7 or random/post OGTT>11.1

On 2 separate occasions

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11
Q

What is impaired fasting glucose?

A

Fasting glucose 6.1-7mmol

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12
Q

What is impaired glucose tolerance?

A

Fasting glucose <7mmol AND

OGTT 2 hour value 7.8-11.1mmol

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13
Q

What can be added in T1DM patients with BMI over 25?

A

Metformin

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14
Q

Which is the first hormone secreted in response to hypoglycaemia?

A

Glucagon

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15
Q

What are the characteristics of MODY?

A

Patients younger than 25 years
Autosomal dominant
Lack of ketosis
Good response to sulfonylurea

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16
Q

What is the most common type of MODY?

A

MODY 3 - defect in HNF-1 alpha gene

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17
Q

What is MODY 3 associated with?

A

Increased risk of HCC

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18
Q

What is the pathophysiology of DKA?

A

Uncontrolled lipolysis which results in an excess of free fatty acids which are converted to ketone bodies

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19
Q

What is the diagnostic criteria of DKA?

A

Glucose >11mmol or known DM
pH<7.3
Bicarb<15
Ketones>3 or urine ketones +++

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20
Q

What is the management of DKA?

A

Fluid resuscitation +/- K
IV insulin 0.1IU/kg/hr
Once BM<15 - start 5% dextrose

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21
Q

What should happen with a patient’s normal insulins when in DKA?

A

Continue long acting insulin

Omit short acting insulin

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22
Q

When should a patient be switched to normal insulins post DKA?

A

Eating and drinking

After first meal

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23
Q

Name 5 complications of DKA.

A 
Hypokalaemia
Cerebral oedema
Arrhythmias
ARDS
AKI
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24
Q

What is the pathophysiology of HHS?

A

Hyperglycaemia –> osmotic diuresis
Volume depletion –> raised serum osmolality –> hyperviscosity
electrolyte disturbances

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25
Q

What is the diagnostic criteria of HHS?

A

Hypovolaemia
Hyperglycaemia >30mmol without ketonaemia or acidosis
Raised serum osmolality >320mosmol/kg

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26
Q

What is the treatment of HHS?

A

IV 0.9% saline

Fixed rate insulin 0.05IU/kg/hr

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27
Q

What are the features of thyroid MALT lymphoma?

A

Painless goitre

Non-functional thyroid tumour

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28
Q

90% Hashimoto’s thyroiditis patients have which antibody?

A

anti-TPO

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29
Q

How does subacute De Quervain’s thyroiditis present?

A

Occurs following a viral infection

Typically presents with hyperthyroidism, painful goitre, raised ESR

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30
Q

How is De Quervain’s thyroiditis diagnosed?

A

Thyroid scintigraphy - globally reduced uptake of iodine-131

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31
Q

What is the treatment of De Quervain’s thyroiditis?

A

Self limiting

NSAIDs for pain

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32
Q

What are the biochemical abnormalities in non thyroidal illness?

A

Low TSH, low thyroxine, low T3

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33
Q

What is the most common type of thyroid cancer?

A

Papillary

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34
Q

What cell does medullary thyroid cancer originate from?

A

C cells (parafollicular) which produce calcitonin

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35
Q

Which syndrome is medullary thyroid cancer associated with?

A

MEN 2a and 2b

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36
Q

What is the treatment of papillary and follicular thyroid cancer?

A

Total thyroidectomy
Followed by radio-iodine I-131
Yearly thyroglobulin levels

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37
Q

Which antibodies are diagnostic of Graves’ disease?

A

TSH receptor stimulating antibodies (present in 90%)

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38
Q

What percentage of Graves’ patients have eye problems?

A

30%

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39
Q

What are other signs of Graves’ disease?

A

Pretibial myxoedema
Thyroid acropachy, which is a triad of: digital clubbing, soft tissue swelling of hands and feet, periosteal new bone formation

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40
Q

What percentage of Graves’ patients have positive anti-TPO and anti-thyroglobulin antibodies?

A

Anti-TPO: 75%

Anti-thyroglobulin: 30%

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41
Q

What is the cause of subclinical hyperthyroidism?

A

Excessive thyroxine

Multinodular goitre

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42
Q

What are risk factors for thyroid eye disease?

A

Smoking

Radio-iodine

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43
Q

What is the treatment of thyroid eye disease?

A

Steroids
Topical lubricants
Radiotherapy

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44
Q

What is the treatment of myxoedemic coma?

A

Hydrocortisone and levothyroxine

Treated as presumed adrenal insufficiency until ruled out

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45
Q

What are the features of MEN type 1?

A

Pancreatic endocrine tumours
Pituitary tumours
Primary hyperparathyroidism

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46
Q

What are the features of MEN type 2a?

A

Primary hyperparathyroidism
Phaeochromocytoma
Medullary thyroid cancer
RET oncogene

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47
Q

What are the features of MEN type 2b?

A 
Marfinoid body habitus
Neuromas
Phaeochromocytoma
Medullary thyroid cancer
RET oncogene
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48
Q

What is the most common cause of primary hyperaldosteronism?

A

Bilateral idiopathic adrenal hyperplasia

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49
Q

What are the other causes of primary hyperaldosteronism?

A 
Adrenal adenoma (Conn's)
Adrenal carcinoma
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50
Q

What are the features of primary hyperaldosteronism?

A

Hypokalaemia
Hypertension
High aldosterone, low renin

51
Q

How is bilateral adrenal hyperplasia differentiated from Conn’s syndrome?

A

CT abdomen

Adrenal vein sampling

52
Q

What is the treatment of bilateral adrenocortical hyperplasia?

A

Spironalactone

53
Q

What are the features of hypocalcaemia?

A

Tetany
Perioral paraesthesia
Chronic: depression, cataracts

54
Q

What are Trousseau’s and Chvostek’s sign in hypocalcaemia?

A

Trousseau’s: carpal spasm if brachial artery is occluded

Chvostek’s: tapping over parotid causes facial muscles to twitch

55
Q

What is seen on ECG in hypocalcaemia?

A

Prolonged QT

56
Q

When is calcium chloride used in hypocalcaemia?

A

Haemodynamically unstable or liver failure

Gluconate must be hepatically metabolized before the calcium becomes available

57
Q

What is the cause of secondary hyperaldosteronism?

A

High levels of renin

e.g. in nephrotic syndrome, heart failure, liver failure

58
Q

How can you differentiate the hypertension and hypokalaemia in Cushing’s syndrome, bilateral renal artery stenosis, and Liddle syndrome?

A

Cushing’s: high aldosterone, low renin

Bilateral renal artery stenosis: high aldosterone, high renin

Liddle syndrome: low aldosterone, low renin

59
Q

What is the threshold for chronic over acute hyponatraemia?

60
Q

What are the causes of hypovolaemic hyponatraemia?

A

Dehydration
Diuretic stage of renal failure
Diuretics
Addisonian crisis

61
Q

What is the cause of euvolaemic hyponatraemia?

62
Q

What is the cause of hypervolaemic hyponatraemia?

A

Heart failure
Liver failure
Nephrotic syndrome

63
Q

What is the treatment of chronic hyponatraemia?

A

Hypovolaemic: isotonic saline

Euvolaemic: fluid restrict 500-1000ml/day, consider demeclocycline/vaptans

Hypervolaemic: fluid restrict 500-1000ml/day, consider loop diuretics/vaptans

64
Q

What happens if sodium falls after administration of isotonic saline in hyponatraemia?

A

Suggests SIADH

65
Q

What is the treatment of acute hyponatraemia with severe symptoms?

66
Q

What is a complication of treating hyponatraemia?

A

Osmotic demyelination syndrome/cerebral pontine myelinolysis

67
Q

How do vaptans work in hyponatraemia?

A

Act on V1 and V2 receptors causing vasoconstriction and selective water diuresis

68
Q

What are the irreversible symptoms of cerebral pontine demyelinosis?

A 
Dyarthria
Dysphagia
Quadraparesis
Seizures
Coma
69
Q

How does demeclocycline work in SIADH?

A

Inhibits G-protein coupled receptor signalling downstream of ADH binding to the renal vasopressin V2 receptors

Thus inducing nephrogenic diabetes insipidus

70
Q

What is the management of SIADH?

A

Mild: fluid restrict
Mod/sev: IV 3% hypertonic saline
Resistant: demeclocycline

71
Q

What metabolic abnormality is seen in Cushing’s syndrome?

A

Hypokalaemic metabolic alkalosis

72
Q

How is Cushing’s syndrome diagnosed?

A

Overnight dexamethasone suppression test - morning cortisol not suppressed
High 24 urinary free cortisol

73
Q

In Cushing’s syndrome, how is a non ACTH-dependent cause diagnosed?

A

Suppressed ACTH in 9am and midnight plasma ACTH and cortisol levels

74
Q

What are the results of CRH stimulation in pituitary and adrenal/ectopic sources of Cushing’s syndrome?

A

Pituitary: cortisol rises

Adrenal/ectopic: no change in cortisol

75
Q

How is ACTH pituitary adenoma diagnosed?

A

High dose dexamethasone test

Cortisol and ACTH suppressed

76
Q

Why is eplenerone less likely to cause gynaecomastia than spironalactone?

A

Eplenerone does not inhibit free testosterone binding to androgen receptors on breast tissue

77
Q

Why does prednisolone cause neutrophilia?

A

Demargination of neutrophils via the endovascular lining
Delayed migration of neutrophils into tissue
Releases of immature neutrophils from bone marrow

78
Q

What are 5 causes of hypoadrenalism?

A 
TB
Metastases
Waterhouse-Friderichsen syndrome
HIV
Anti-phospholipid syndrome
79
Q

What are the features of Addison’s?

A 
N+V, weakness, weight loss
Hyperpigmentation
Vitiligo
Low Na and High K
Loss of pubic hair and libido secondary to androgen deficiency
Hypotension and hypoglycaemia
80
Q

How is Cushing’s disease differentiated from pseudo-Cushing’s?

A

Insulin stress test

In normal pituitary function, GH and cortisol should rise

81
Q

What is the pathophysiology of PCOS?

A

Hyperinsulinaema

High levels of LH

82
Q

How does empty sella syndrome present?

A

Symptoms of hypopituitarism

83
Q

Hypokalaemia and normotension are seen in which syndromes?

A

Gitelman’s

Bartter’s

84
Q

What are 6 causes of raised prolactin?

A 
Pregnancy
Prolactinoma
Physiological
PCOS
Primary hypothyroidism
Phenothiazines, metoclopramide, domperidone
85
Q

What are the causes of hypertriglyceridaemia?

A 
DM
Obesity
Alcohol
CKD
Thiazides, BB, unopposed oestrogen
Liver disease
86
Q

What are the causes of hypercholesterolaemia?

A

Nephrotic syndrome
Cholestasis
Hypothyroidism

87
Q

What is the inheritance of androgen insensitivity syndrome?

A

X-linked recessive

88
Q

What is the pathophysiology of androgen insensitivity syndrome?

A

End-organ resistance to testosterone

Genotypically male children have a female phenotype

89
Q

What are the features of androgen insensitivity syndrome?

A

Primary amenorrhoea
Undescended testes
Breast development may occur as a result of conversion of testosterone to oestradiol

90
Q

How is phaeochromocytoma diagnosed?

A

24h urinary metanephrinesW

91
Q

What are the causes of primary hyperparathyroidism?

A

80% solitary adenoma
15% hyperplasia
4% multiple adenoma
1% carcinoma

92
Q

Why does peptic ulceration and hypertension occur in primary hyperparathyroidism?

A

Hypercalcaemia

Ca stimulates gastrin release

Ca causes vasoconstriction

93
Q

What are the biochemical results seen in primary hyperparathyroidism?

A

High Ca
High-normal PTH
Low PO4

94
Q

When is surgery indicated in primary hyperparathyroidism?

A

Symptomatic
Calcium>2.85
End organ disease

95
Q

What are the causes of secondary hyperparathyroidism?

A

CKD - lack of vit D hydroxylation by kidneys

Vit D deficiency

96
Q

What are the biochemical abnormalities seen in secondary hyperparathyroidism?

A

Low-normal Ca
High PTH
High PO4
Low Vit D

97
Q

What is the treatment of secondary hyperparathyroidism?

A

Phosphate binders

Calcium/vit D supplementation

98
Q

What are the manifestations of renal bone disease?

A

Osteitis fibrosa cystica
Osteomalacia
Osteoporosis

99
Q

What are the biochemical abnormalities seen in tertiary hyperparathyroidism?

A 
High-normal Ca
High PTH
Low-normal PO4
Low-normal Vit D
High ALP
100
Q

What is the treatment of tertiary hyperparathyroidism?

A

Parathyroidectomy

101
Q

How is benign familial hypocalciuric hypercalcaemia diagnosed?

A

Urine calcium: creatinine clearance ratio <0.01

102
Q

Where is growth hormone secreted?

A

Somatotroph cells of anterior pituitary

103
Q

What stimulates and inhibits secretion of growth hormone?

A

Stimulated: GnRH pulses from hypothalamus, sleep, exercise

Inhibits: glucose, somatostatin

104
Q

How is acromegaly diagnosed?

A

Serum IGF-1 with serial GH measurements

OGTT confirms diagnosis if IGF-1 raised

105
Q

What is the management of acromegaly?

A

Trans-sphenoidal surgery

Somatostatin analogue octreotide or SC pegvisomant (GH receptor antagonist)

106
Q

What are 4 complications of acromegaly?

A

HTN
Diabetes
Cardiomyopathy
Colorectal Ca

107
Q

What are the features of insulinoma?

A

Hypoglycaemia

Weight gain

108
Q

How is insulinoma diagnosed?

A

High insulin
Raised proinsulin:insulin ratio
High C peptide
72 hour fast

109
Q

When is metformin contraindicated?

110
Q

What are the side effects of metformin?

A

Diarrhoea

Lactic acidosis

111
Q

Which class of hypoglycaemics are used for patients with an erratic lifestyle?

A

Meglitinides

112
Q

How do sulfonylureas lower blood glucose?

A

Bind to beta cell receptors

(Close K channel –> depolarises cell –> opens VG Ca channels –> increases intracellular Ca)

Leads to insulin secretion

Also stimulates glycolytic pathway

113
Q

What are the side effects of sulfonyureas?

A 
Weight gain
Severe hypos
Teratogenic
SIADH
Bone marrow suppression
114
Q

How do meglitinides such as repaglinide work?

A

Increase pancreatic insulin secretion by blocking K channel of beta cells

115
Q

Which diabetes drug is an agonist to the PPAR-gamma receptor (controls adipocyte differentiation and function) therefore reduces peripheral insulin resistance?

A

Pioglitazone

116
Q

What are the side effects of pioglitazone?

A 
Weight gain
Increased fracture risk
Fluid retention
liver impairment
Bladder Ca
117
Q

What is the mechanism of action of DPP-4 inhibitors such as sitagliptin?

A

Increases insulin, lowers glucagon

Reduce the peripheral breakdown of incretins such as GLP-1

118
Q

Which DPP-4 inhibitor is linked with ischaemic heart disease?

A

Saxagliptin

119
Q

What is GLP-1?

A

A hormone released by small intestine in response to PO glucose load

120
Q

How do GLP-1 mimetics work?

A

Activate GLP-1 receptor to increase insulin, lower glucagon, slow gastric emptying

121
Q

What is a favourable feature of GLP-1 mimetics and SGLT-2 inhibitors?

A

Prevent weight gain/lose weight

122
Q

What are the side effects of GLP-1 mimetics such as exenatide?

A

GI disturbance

Acute pancreatitis

123
Q

How do SGLT-2 inhibitors work?

A

Reduce glucose reabsorption in PCT by reversibly inhibiting sodium-glucose co-transporter 2

124
Q

What are the side effects of canagliflozin?

A

Genital thrush –> Fournier’s gangrene
Increased risk of euglycaemic ketoacidosis
Increased risk of lower limb amputation

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